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"Mahkota Dewa as a traditional plant has been commonly used as traditional cancer medication. However, themechanism of usage is not yet clear. The objective of this study was to know the mechanism of the protection effect ofMahkota Dewa on Benzo(a)pyrene (BaP) induced cytotoxicity in CCRF-CEM cell line. The result showed BaP inducedcell death with in CCRF-CEM cell line was dose-dependent but not based on time-course. Exposure of this cell for 24 hwith variation of dose between 5-20 μM increased the percentage of apoptosis to about 15%. On the other hand,Mahkota Dewa itself has dose-dependently induced cytotoxicity and has no effect in the inhibition of BaP exposure.Phosphorylation of p38 MAPK in both BaP and Mahkota Dewa induced cytotoxicity has been seen but the involvementof oxidative stress is unclear. However, in other cancer cell line SH-SY5Y human neuroblastoma cells, the inhibitionefffect of Mahkota Dewa in BaP exposure has been seen and no cytotoxicity effect appeared in this cell line. Inconclusion, Mahkota Dewa has induced apoptosis in CCRF-CEM cancer cell line but not in SH-SY5Y cell line, so ithas a potential anticancer effect; Mahkota Dewa, however, requires more researches on DNA level using other type ofcancer to observe the mechanism.Efek Penghambatan Mahkota Dewa (Phaleria macrocarpa) pada Sitotoksisitas CCRF-CEM Cell Lines yangTerpajan oleh Benzo(a)pyrene. Mahkota Dewa adalah tumbuhan tradisional yang umumnya digunakan sebagai obatkanker tradisional. Namun belum terdapat kejelasan mengenai mekanisme penggunaannya. Tujuan penelitian ini adalahuntuk mengetahui mekanisme efek proteksi Mahkota Dewa pada sitotoksisitas CCRF-CEM cell line yang terpajan olehBenzo(a)pyrene. Hasil penelitian menunjukkan kematian sel dalam CCRF-CEM cell line yang diinduksi oleh BaPterjadi secara dependen terhadap dosis, tetapi bukan didasari oleh jangka waktunya. Paparan sel ini dibiarkan selama 24jam dengan dosis bervariasi antara 5-20 μM dan mengakibatkan peningkatan persentase apoptosis sampai sekitar 15%.Di lain pihak, Mahkota Dewa itu sendiri telah menginduksi sitotoksisitas secara dependen terhadap dosis, dan tidakditemukan efek terhadap penghambatan paparan BaP. Fosforilasi p38 MAPK baik dalam BaP dan sitotoksisitas yangterpajan oleh Mahkota Dewa telah terlihat. Akan tetapi keterlibatan stress oksidatif tidak jelas terlihat. Meskipundemikian, dalam cell line kanker lainnya seperti SH-SY5Y sel neuroblastoma manusia, efek penghambatan MahkotaDewa dalam paparan BaP telah terlihat dan tidak terdapat adanya efek sitotoksisitas yang muncul di cell line ini.Sebagai kesimpulan, Mahkota Dewa telah menginduksi apoptosis pada cell line kanker CCRF-CEM. Namun apoptosistidak diinduksi pada SH-SY5Y cell line sehingga tumbuhan ini berpotensi memiliki efek antikanker. Meskipundemikian, perlu lebih banyak penelitian mengenai Mahkota Dewa pada level DNA dengan menggunakan jenis kankerlainnya agar mekanismenya dapat diobservasi."

"ABSTRAKMahkota Dewa as a traditional plant has been commonly used as traditional cancer medication. However, the mechanism of usage is not yet clear. The objective of this study was to know the mechanism of the protection effect of Mahkota Dewa on Benzo(a)pyrene (BaP) induced cytotoxicity in CCRF-CEM cell line. The result showed BaP induced cell death with in CCRF-CEM cell line was dose-dependent but not based on time-course. Exposure of this cell for 24 h with variation of dose between 5-20 μM increased the percentage of apoptosis to about 15%. On the other hand, Mahkota Dewa itself has dose-dependently induced cytotoxicity and has no effect in the inhibition of BaP exposure.Phosphorylation of p38 MAPK in both BaP and Mahkota Dewa induced cytotoxicity has been seen but the involvement of oxidative stress is unclear. However, in other cancer cell line SH-SY5Y human neuroblastoma cells, the inhibition efffect of Mahkota Dewa in BaP exposure has been seen and no cytotoxicity effect appeared in this cell line. In conclusion, Mahkota Dewa has induced apoptosis in CCRF-CEM cancer cell line but not in SH-SY5Y cell line, so it has a potential anticancer effect; Mahkota Dewa, however, requires more researches on DNA level using other type of cancer to observe the mechanism."

"ABSTRAKManifestasi klinis yang menonjol pada demam berdarah dengue adalah kebocoran plasma karena gangguan pada sel endotel vaskular. Anti NS-1 dapat bereaksi silang dengan Protein Disulfide Isomerase (PDI) pada sel endotel. Jambu biji biasa digunakan untuk mengatasi gejala dengue namun belum pernah ada penelitian secara in vitro untuk mengetahui mekanisme senyawa aktif yaitu lycopene yang terdapat di dalamnya. Tujuan penelitian ini adalah untuk mengetahui apakah lycopene dapat menurunkan apoptosis yang ditandai dengan Annexin V dan Heme oxygenase -1 (HO-1). Penelitian ini menggunakan kultur Human Umbillical Vein Endothelial Cells (HUVEC) yang diberi stimulasi anti NS-1 dan terdiri atas 5 perlakuan yaitu kontrol positif, kontrol negatif, dan lycopene dosis 0.5, 1 dan 2 μM. Kontrol positif adalah HUVEC yang diberi anti NS-1 dan basitrasin karena basitrasin sudah diketahui bekerja sebagai anti PDI dan dapat menghambat apoptosis. Kontrol negatif adalah kultur HUVEC yang diberi anti NS-1 tanpa perlakuan lycopene. Hasil penelitian menunjukkan bahwa hanya Annexin V pada kontrol positif menunjukkan hasil yang rendah secara bermakna dibandingkan perlakuan lainnya. Hal ini menunjukkan bahwa lycopene dengan dosis 0.5, 1 dan 2 μM tidak dapat menghambat apoptosis. Kadar HO-1 pada semua perlakuan tidak menunjukkan perbedaan bermakna. Hal ini menunjukkan bahwa baik basitrasin maupun lycopene tidak mempengaruhi metabolisme HO-1. Dapat disimpulkan bahwa senyawa lycopene dengan dosis dosis 0.5, 1 dan 2 μM tidak menunjukkan pengaruh dalam apoptosis sel endotel setelah terjadi infeksi dengue.

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ABSTRACTProminent clinical manifestation of dengue hemorrhagic fever is plasma leakage due to malfunction of endothelial cells. There is cross reaction between anti NS-1 and Protein Disulfide Isomerase (PDI) on endothelial cells. Psidium guajava is commonly used to improve condition in dengue symptoms but there is no research yet that study the in vitro mechanism how lycopene, a compound in Psidium guajava, works in this case. So this study aimed to know whether lycopene will decrease apoptosis of endothelial cells marked by Annexin V and Heme oxygenase-1 (HO-1) This study used Human umbillical vein endothelial cells (HUVEC) that given anti NS-1 stimulation and consisted of positive control, negative control and lycopene treatment with 0.5, 1 and 2 μM dose. Positive control is HUVEC with anti NS-1 and bacitracin that known act as anti PDI and inhibit apoptosis. Negative control is HUVEC with anti NS-1. Results showed that Annexin V only in positive control had lower Annexin V significantly compared to other treatments. This showed that lycopene 0.5,1 and 2 μM was not able to inhibit apoptosis. HO-1 in all treatments did not show significant difference. This showed that either bacitracin nor lycopene did not give effect to HO-1 metabolism. It was concluded that lycopene with 0.5, 1 dan 2 μM dose has no effect in endothelial cell apoptosis after dengue infection."

"Tujuan Studi ini adalah untuk mengetahui pengaruh hipoksia terhadap pola ekspresi gen HIF-1α pada jantung tikus serta mengamati timbulnya apoptosis pada kardiomiosit akibat hipoksia sistemik.Metode Hewan coba (tikus Sprague-Dawley) dibagi secara acak menjadi 7 kelompok (n= 4 per kelompok): kelompok kontrol normoksia (oksigen atmosfir), dan beberapa kelompok hipoksia yang ditempatkan dalam sungkup-hipoksik (kadar O2 8%) selama 1, 3, 7, 14, 21, dan 28 hari. Pemeriksaan ekspresi gen HIF-1α dilakukan dengan real-time PCR dan apoptosis dengan metode TUNEL.Hasil Dibandingkan dengan kelompok normoksia, ekspresi gen HIF-1α meningkat secara bertahap sejalan dengan lamanya hipoksia dan mencapai puncak pada hari ke-21. Tidak ada sel yang terlabel dengan cara TUNEL pada kelompok kontrol. Dibandingkan dengan kontrol, indeks apoptotik meningkat sejalan dengan lamanya hipoksia. Tidak ada hubungan bermakna antara peningkatan ekspresi HIF-1α dengan peningkatan indeks apoptotik.Kesimpulan Hipoksia sistemik kronik mengakibatkan peningkatan ekspresi mRNA HIF-1α dan apoptosis pada kardiomiosit.

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AbstractAim This study explored the expression of HIF-1α in hypoxic cardiac muscle in mice, and observed the evidence of apoptosis in hypoxia induced cardiomyocyte.Methods Male Sprague-Dawley rats, were randomized into 7 groups (n= 4 per group): control normoxia group that was exposed to atmospheric oxygen and hypoxia groups that were housed in hypoxic chambers (O2 level 8%) for 1, 3, 7, 14, 21, and 28 days respectively. Animals were sacrificed, hearts were rapidly excised, total RNA was extracted with an mRNA isolation kit and the expression of HIF-1α mRNA was then detected by real-time RT-PCR. Apoptosis was assessed by TUNEL method.Results For rat in hypoxia group, the expression of HIF-1α mRNA in cardiac myocytes was clearly up-regulated compared to the control normoxia group. Further, HIF-1α expression level elevated gradually and reached a peak at 21 days of hypoxia. No cell labeled by the TUNEL method was detected in the control group. Compared with the control group, the apoptotic index was significantly increased in the hypoxia group (P < 0.05). There was no significant correlation between the elevation of HIF-1α mRNA and the elevation of apoptotic index.Conclusion Systemic chronic hypoxia caused the elevation of HIF-1α mRNA and apoptosis in cardiac myocytes."

"Kanker serviks termasuk salah satu jenis kanker dengan tingkat prevalensi kasus yang tinggi di Indonesia. Berdasarkan GLOBOCAN 2020, ditemukan 36.633 (36% dari total kasus kanker pada wanita) kasus kanker serviks baru dan 21.003 kematian. Pengobatan terhadap kanker serviks saat ini masih menimbulkan efek samping seperti resistensi obat pada sejumlah kasus sehingga diperlukan alternatif pengobatan. Salah satu senyawa yang memiliki potensi antikanker, yaitu Eucalyptol. Eucalyptol adalah senyawa utama dalam tumbuhan eukaliptus seperti Eucalyptus globulus. Studi pengaruh konsentrasi eucalyptol terhadap viabilitas dan deteksi apoptosis sel HeLa dilakukan dengan konsentrasi 25, 50, 100 dan 200 μg/mL. Uji viabilitas dengan WST-1 menunjukkan bahwa variasi konsentrasi eucalyptol tersebut belum dapat menekan viabilitas sel HeLa (p>0,05 dengan uji ANOVA). Selanjutnya, deteksi apoptosis (menggunakan pewarna Annexin V-FITC) dengan mikroskop fluoresens menunjukkan bahwa variasi konsentrasi eucalyptol dapat menginduksi apoptosis dibandingkan nekrosis. Meskipun demikian, belum dilakukan pengamatan pada sel hidup sehingga tidak diketahui persentase sel apoptosis dan nekrosis dalam populasi total. Pengujian lanjutan dengan pewarna DAPI yang mewarnai sel hidup dan metode kuantifikasi lainnya untuk validasi hasil pengamatan dengan mikroskop fluoresens diperlukan.

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Cervical cancer is one type of cancer with a high case prevalence rate in Indonesia. Based on GLOBOCAN 2020, found 36,633 (36% of total cancer cases in women) new cervical cancer cases and 21,003 deaths. Treatment of cervical cancer is currently still causing side effects such as drug resistance in a number of cases so that alternative treatment is needed. One of the compounds that have anticancer potential is Eucalyptol. Eucalyptol is the main compound in eucalyptus plants such as Eucalyptus globulus. The study of the effect of eucalyptol concentration on the viability and detection of apoptosis of HeLa cells was carried out at concentrations of 25, 50, 100 and 200 g/mL. The viability test with WST-1 showed that the variation in eucalyptol concentration had not been able to suppress HeLa cell viability (p>0.05 by ANOVA test). Furthermore, detection of apoptosis (using Annexin V-FITC dye) by fluorescent microscopy showed that variations in eucalyptol concentration could induce apoptosis rather than necrosis. However, no observations have been made on living cells so that the percentage of apoptotic and necrotic cells in the total population is unknown. Further testing with DAPI dye that stains living cells and other quantification methods for validation of observations by fluorescent microscopy is required.

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"Pseudomonas aeruginosa is a Gram negative bacterium that can cause fatal infection in immunocompromised patient. This is an opportunist pathogen which is associated with some dental infections. Pseudomonas aeruginosa produces pyocyanin that functions as an important virulent factor in bacterial invasion. It can be identified in the lesion tissue and capable to induce cellular damage in endothelial cell, respiratory, neutrophil, and lymphocytes. B lymphocyte plays a significant role in the immune response of periapical infection; however, its cellular and molecular response to pyocyanin is unclear.

Objective: To investigate cellular responses of B lymphocyte to the exposure of pyocyanin and the role of caspase-3 in its molecular mechanism.

Methods: B lymphocytes (Raji cells) were cultured, and in five replications were exposed to various concentrations of pyocyanin for 24 h. MTT assay was performed to analyze the cytotoxicity effect of pyocyanin. Cell morphological analysis using phase contrast microscope were done in separate experiments. Immunocytochemical analysis was carried out for the identification of active caspase-3 protein expression, to study the mechanism involved in pyocyanin induced cellular damage.

Results: It showed that cell viability was decreased in pcyocyanin-treated groups. Pyocyanin induced cell death on B lymphocyte in a dose-dependent manner. Statistical analysis using ANOVA demonstrated significant difference between groups with p=0.000. Nuclear fragmentation was observed in pyocyanin-induced cell death; furthermore, caspase-3 was expressed clearly in cell cytoplasm after 24 h incubation.

Conclusion: Pyocyanin is capable of inducing cell death on B lymphocyte. Caspase-3 may play an important role in the molecular mechanism of pyocyanin-induced cell death."

"Oral commensal bacterium Streptococcus sanguinis may find in periodontal lesions, deep seated infection, and infective endocarditis that are usually dominated by anaerobes. This bacterium caused cell death on some cells but host responses to this species remained unclear. Objective: This study was aimed to detect cell morphologicalchange and role of caspase-3 in cell death mechanism induced by S. sanguinis. Methods: HeLa cells as representative model for oral epithelial cells were exposed to 107 cells/ml bacteria for 48 h. Morphological change was observed microscopically after hematoxyline-eosin staining. Expression of active caspase-3 was examined by immunocytochemical analysis after cell stimulation for 36 and 48 h with wild type supragingival S. sanguinis. Doxorubicin (0.5625 μg/ml) was used as positive control for caspase-3 activation. Results: The results showed cell shrinkage of bacterial-treated cells; and active caspase-3 molecules were detected after 36 and 48 hours cell stimulation. Conclusion: This study would suggest cell shrinkage and caspase-3-dependent apoptotic cell death induced by S. sanguinis."

"Latar belakang : Glioblastoma Multiforme (GBM) merupakan kanker otak primer yang paling umum terjadi pada orang dewasa dan merupakan glioma yang paling agresif yang diklasifikasikan oleh WHO sebagai tingkat keempat dari astrositoma. Penatalaksanaan utama GBM dengan operasi disertai dengan kemoradiasi memberikan rata-rata harapan hidup sekitar 14,6 bulan saja, ini disebabkanpertumbuhan tumor yang difus disertai tingginya resistensi. Apoptosis, dinamakan juga “kematian sel terprogram” merupakan mekanisme kematian sel yang berperan penting dalam terapi kanker dan menjadi target utama dalam berbagai tehnik terapi kanker. Dua jalur utama apoptosis adalah jalur intrinsik yang melibatkan mitokondria dan jalur ekstrinsik yang diinduksi oleh ikatan ligan dengan reseptornya. Rotenon, inhibitor rantai respirasi kompleks I mitokondria dapat menyebabkan peningkatan kadar superoksida (ROS) endogen sehingga menginduksi jalur apoptosis intrinsik melalui lepasnya sitokrom C dan agen-agen proapoptotik ke sitosol. Rotenon bersifat lipofilik dan dapat menembus sawar darah otak dengan mudah, menjadikannya kandidat yang menarik untuk digunakan pada terapi GBM. Hingga kini mekanisme apoptosis yang disebabkan oleh rotenon pada GBM masih belum jelas diketahui, karena itu penelitian ini bertujuan untuk menelusuri jalur-jalur apoptosis yang timbul akibat induksi rotenon pada galur sel Glioblastoma Multiforme T98G. Metode : Penelitian eksperimental in vitro menggunakan kultur galur sel Glioblastoma Multiforme T98G yang diinduksi stres oksidatif dengan rotenon dosis 10μM, 20μM, dan 40μM selama enam jam, selanjutnya dilakukan identifikasi morfologi sel menggunakan inverted mikroskop. Identifikasi jalur apoptosis intrinsik dengan cara menganalisis ekspresi protein sitokrom-C dan protein kaspase-9menggunakan metode sandwich ELISA (Enzyme Linked Immuno Assay) serta identifikasi jalur apoptosis ekstrinsik dengan menganalisis ekspresi mRNA TRAIL (Tumor Necrosis Factor Related Apoptosis Inducing Ligand) menggunakan q-RTPCR (quantitative-reverse transcriptase-Polymerase Chain Reaction) selain itudilakukan pula elektroforesis hasil amplifikasi cDNA TRAIL pada agarosa 2%. Analisis statistik dilakukan menggunakan uji Mann Whitney pada tingkat kepercayaan 95%. Hasil : Induksi rotenon 10 μM pada galur sel T98G menyebabkan meningkatnya kadar sitokrom C yang tidak disertai meningkatnya kadar kaspase-9 dan ekspresimRNA TRAIL. Kadar sitokrom C turun menjadi setara dengan kadar pada sel kontrol saat induksi rotenon 20μM disertai meningkatnya kadar kaspase-9 dan ekspresi mRNA TRAIL yang bermakna. Sedangkan Induksi rotenon 40μM menyebabkan turunnya kadar sitokrom C, kaspase-9 dan mRNA TRAIL. Pada pemeriksaan elektroforesis hasil RT-PCR kami mendapatkan varian TRAIL sepanjang sekitar 300 bp yang ikut teramplifikasi bersama varian sTRAIL (soluble TRAIL) sepanjang 232 bp. Varian TRAIL panjang ini nampak ditranskripsi lebih banyak saat dilakukan induksi rotenon hingga 20μM sementara varian pendek transkripsinya nampak semakin berkurang.Kesimpulan : Pada penelitian kami, induksi rotenon 20μM dapat menyebabkan terinduksinya jalur apoptosis intrinsik yang melibatkan kaspase serta jalur apoptosis ekstrinsik melalui pengaturan post transkripsi mRNA TRAIL pada galur sel Glioblastoma Multiforme T98G.

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Background : Glioblastoma Multiforme (GBM) is the most common primary brain tumor in adults and the most aggressive gliomas classified by WHO as grade IV astrocytoma. Primary treatment of GBM is surgery followed by Chemoradiation give

the median survival only for about 14,6 months, this is due to difusse tumor growth with high therapy resistance. Apoptosis, named as “programmed cell death” is a mechanism of cell death that plays an important role in the treatment of cancer and

being a primary target of many cancer treatment strategies. There are two central pathways of apoptosis, the intrinsic pathway that involves the mitochondria and the extrinsic pathway induced by ligands binding to the death receptors. Rotenone,

respiratory chain inhibitor complex I mitochondria may increase endogenous superoxide (ROS) levels that induce intrinsic apoptotic pathway by release of cytochrome-C and several proapoptotic agents to cytosol. Rotenone is a lipophilic

compound and could easily cross the Blood Brain Barrier that makes rotenone become an interesting candidate for GBM therapy. Up to now, the apoptosis mechanism induced by rotenone in GBM is not well known yet, therefore we aim to investigate the apoptosis pathways in Glioblastoma Multiforme T98G cell line

induced by rotenone. Methods : This experimental study in vitro using GBM T98G cell line cultured in complete DMEM medium. We induced oxidative stress for six hours with 10 μM, 20 μM and 40 μM of rotenone respectively. After harvested, the cell morphology was identified using inverted microscope. We identified the intrinsic apoptotic pathway by analyzing the expression of cytochrome C protein and Caspase-9 protein using

sandwich ELISA method, furthermore we identified the extrinsic apoptotic pathway by analyzing the expression of mRNA TRAIL using q-RT-PCR followed by gel electrophoresis to confirm the amplification of cDNA TRAIL. Statistical analysis was performed by Mann Whitney test with 95% confidence intervals. Results : Rotenone treatment of T98G resulted in increase of cytochrome C by 10μM of rotenone but no increase of caspase-9 and mRNA TRAIL. While rotenone 20 μM showed relative decrease of cytochrome C and increase of caspase-9 expression together with significant increase of the mRNA TRAIL expression (p<0,05) and induction with 40μM showed decrease of cytochrome C, caspase-9 and mRNA TRAIL expression. In the electrophoresis examination of the RT-PCR product we obtain an isoform of TRAIL (length about 300 bp) was coamplified along with our isoform (soluble TRAIL, length about 232 bp). This long isoform band become more dens in samples induced by rotenone 20μM, while the short isoform was gradually missing. Conclusions : In our study, 20μM of rotenone was able to induced both the intrinsic apoptotic pathway by caspase dependent mechanism and the extrinsic apoptotic pathway through post transcriptional regulating of mRNA TRAIL in Glioblastoma Multiforme T98G cell line."

"[ABSTRAKLatar Belakang: Kanker prostat adalah kanker yang paling umum pada pria. Kanker terjadi karena hilangnya kontrol atas proliferasi sel dan apoptosis sehingga sel berproliferasi terus menerus tanpa ada kematian sel. Apoptosis diregulasi oleh beberapa protein tertentu diantaranya protein keluarga Bcl-2 dan protein kanal. Perkembangan kanker prostat memerlukan transformasi dari sel epitel yang normal menjadi sel ganas yang kehilangan kemampuan untuk mengakumulasi zinc. Salah satu efek utama zinc adalah mencegah pertumbuhan sel kanker prostat dengan menginduksi apoptosis dengan memfasilitasi proses pembentukan pori Bax yang memulai apoptogenesis mitokondria. Selain keluarga Bcl-2, VDAC1 juga berperan penting dalam proses apoptosis. Beberapa penelitian menyatakan Bcl-2 mempunyai kaitan erat dengan VDAC1 terkait proses apoptosis dan protein pro-apoptotik Bax juga secara langsung berinteraksi dengan VDAC yang kemudian menginduksi keluarnya sitokrom c dari membran mitokondria.Tujuan: Mengevaluasi ekspresi mRNA dari gen mengkode keluarga protein Bcl-2 (Bax dan Bcl-2) dalam proses apoptogenesis pada galur sel kanker prostat yg diinduksi oleh zinc; Mengevaluasi ekspresi mRNA dari gen VDAC1 dalam proses apoptogenesis pada galur sel kanker prostat yang diinduksi oleh zinc; Menganalisis hubungan antara ekspresi VDAC1 dengan protein keluarga Bcl-2 pada apoptogenesis galur sel kanker prostat.Desain: Penelitian ini menggunakan eksperimental in vitro dan analisis statistikMetode: Untuk memperbanyak galur sel kanker prostat (PC3) dilakukan kultur sel, kemudian diberi perlakuan dengan tiga kelompok (kontrol, zinc 20 μM dan staurosporin 0,16 μM). Selanjutnya dilakukan isolasi RNA dan elektroforesis RNA untuk mengetahui keutuhan RNA. Terakhir dilakukan qRT PCR yang kemudian datanya dianalisis secara statistika.Hasil: Ekspresi Bax, Bcl-2 dan VDAC1 pada galur sel kanker prostat (PC-3) yang diberi perlakuan zinc mengalami penurunan dibandingkan dengan kontrol (tidak diberi perlakuan). Akan tetapi penurunan ekspresi tersebut tidak bernilai signifikan karena nilai p > 0,05 (nilai signifikansi Bax = 0,309; nilai signifikansi Bcl-2 = 0,236; nilai signifikansi VDAC1 = 0,437). VDAC1 mempunyai korelasi yang signifikan (p < 0,05) dengan Bax (p = 0,01) dibandingkan dengan Bcl-2 (p = 0,118).Kesimpulan: Terjadi perubahan ekspresi pada setiap gen (Bax, Bcl-2 dan VDAC1) pada galur sel kanker prostat yang diberi perlakuan zinc dengan yang tidak diberi perlakuan, akan tetapi tidak bernilai signifikan. VDAC1 mempunyai korelasi yang bermakna dengan Bax dan mempunyai korelasi yang tidak bermakna dengan Bcl-2.

ABSTRACT

Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2.;Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2., Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2.]"

"Latar Belakang : Kanker payudara adalah kanker kedua tersering pada wanita denganangka kcmatian yang tinggi. Keganasan, cherno-resistance, dan kegagaJan tempi untuk menyembuhkan kanker payudara disebabkan oleb adanya sel punca kanker payudara (BCSCs). BCSCs mengekspresikan multigen untuk kelangsungan hidup, kemampuan self-renewal, dan kemampuan bennetastasis. LingkWlgan hipoksia memicu sel tumor untuk mengekspresikan gen pro-survival dan beradaptasi secara metabolik terhadap stres, sehingga memlcu pertumbuhan sel kanker.Inhibitor of Apoptosis Prolein(lAP), mengatur supresi apoptosis, kontrol pembelahan sel, dan promosi angiogenesis.Ekspresi gen survivin sangat tinggi di sei tumor Wltuk kclangsungan hidup.perkembangan tumor dan keganasan. Survivin sangat papuler dijadikan sebagai gen target kanker. Mendalami peran SUrYivin dalam kondisi hipoksia akan menjanjikanmanfaat terapeutik yang lebih baik. Dalam percobaan ini, ekspresi survivin akan diamati di BCSCs yang dibiakkan dalam media bebas serum yang diberi perlakuan hipoksia 1%dengan periode berbeda.Mctode : Sel punca diekstrak dari kanker payudara, kemudian diberi perlakuan hipoksia. RNA kemudian diisolasi dan diukur dengan spectrophotometry Wltuk menentukan kadar kemumian sampeL Setelah itu, One-Step qRT-PCR dilakukan untuk mendapatkan hasH ekspresi relatif gen survivin. Produk peR tersebut kemudian diproses dengan electrophoresis uotuk memastikan gen yang telat diamplifikasi.HasH : Kadar ekspresi gen survivin rnengalami penurunan di sci pWlca kanker payudara selama proses hypoxia dengan interval yang berbeda.Kesimpulan : Sci punca kanker payudara yang diberi perlakuan hypoxia yang berbedamenunjukkan kadar ekspresi gen survi.vin yang rendah. Ada kemungkinan bahwa seItersebut telah berdiferensiasi dalam popuJasi sel puncak. Penelitian tambahan perlu dilaksanakan untuk memastikan aktivitas apoptosis di sel puncak kanker payudara dalam kondisi hypoxia."