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"Sel kanker adalah sel yang berproliferasi secara progresif, dan salah satu dasar pengendaliannya hingga saat ini yaitu dengan menghambat kemampuan proliferasinya melalui intervensi sintesis nukleotida purin/pirimidin menggunakan analog purin/pirimidin. Avidin, suatu protein yang ditemukan pada putih telur, diketahui dapat mengikat biotin dengan sangat kuat, yang merupakan koenzim pada reaksi karboksilasi, suatu tahapan penting di biosintesis de novo nukleotida purin. Studi sebelumnya membuktikan bahwa viabilitas dan proliferasi sel mononuklear darah tepi (SMDT) dapat dihambat dengan penambahan avidin yang diakibatkan gangguan ketersediaan biotin. Studi ini bertujuan melihat efek pemberian avidin terhadap sel kanker kolorektal HT-29 dilihat dari viabilitas, proliferasi, ekspresi gen dan protein cyclin D1, serta siklus sel. Penelitian dilakukan dengan mengultur sel kanker kolorektal HT-29 dengan avidin, lalu dianalisis viabilitas, proliferasi, ekspresi gen dan protein cyclin D1, serta siklus selnya pada 24, 48, dan 72 jam. Didapatkan hasil bahwa avidin menghambat viabilitas dan proliferasi sel HT-29, serta menurunkan ekspresi gen dan protein cyclin D1 pada sel HT-29, namun tidak memengaruhi transisi fase G0/G1 ke fase S siklus sel HT-29.

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Cancer cells are progressively proliferating cell, and up to now, one way to control its proliferation is by intervening the formation of purine/pyrimidine nucleotide using its purine/pyrimidine analog. Avidin, a protein from white egg, known to bind biotin strongly, whereas biotin is an important coenzyme in carboxylation reaction, a key step in purine nucleotide de novo pathway. Previous study showed that viability of peripheral blood mononuclear cells (PBMC) was reduced and its proliferation was inhibited caused by lack of biotin due to avidin administration. This study aims to observe the effect of avidin administration to HT-29 cells viability, proliferation, cyclin D1gene and protein expression, also the cell cycle. The experiment done by culturing HT-29 cells, then its viability, proliferation, cyclin D1 gene and protein expression, also the cell cycle analyzed at 24, 48, and 72 hours. The result showed that avidin halted HT-29 cells viability and proliferation, also lower its cyclin D1 gene and protein expression, but did not affect the transition between G0/G1 phase to S phase on HT-29 cell cycle"

"Pendahuluan: Sindroma ovarium polikistik (SOPK) merupakan masalah reproduksi yang sering terjadi pada perempuan usia reproduksi, namun hingga saat ini etiopatogenesis SOPK masih belum jelas. Penelitian ini bertujuan menganalisis peran sel granulosa folikel ovarium dalam etiologi SOPK, keterkaitan genotip FSHR Asn680Ser dengan patogenesis SOPK dan peran gen CYP19A1(aromatase) dalam patogenesis SOPK. Metode: Penelitian ini menggunakan desain penelitian analitik observasional berbentuk studi seran lintang (cross sectional study) dan dilakukan di Departemen Biologi FKUI, Klinik Yasmin-RSCM Kencana dan Laboratorium terpadu FKUI pada tahun 2011-2014. Sebanyak 142 subyek penelitian (66 pasien SOPK dan 76 pasien bukan SOPK) terlibat dalam penelitian ini. Sampel penelitian berupa darah tepi dan cairan folikel ovarium yang diaspirasi ketika proses ovum pick up sebagai sumber sel granulosa. Dilakukan isolasi DNA untuk analisis RFLP polimorfisme FSHR Asn680Ser, dilakukan kultur sel granulosa untuk mengetahui kemampuan proliferasi sel granulosa dan analisis ekspresi mRNA aromatase sel granulosa dengan metode RT-qPCR. Hasil: Indeks proliferasi sel dan ekspresi mRNA aromatase sel granulosa pada kelompok SOPK lebih rendah secara bermakna dibandingkan bukan SOPK (p<0,05). Tidak ditemukan perbedaan bermakna distribusi genotip FSHR Asn680Ser antara kelompok SOPK dan bukan SOPK (p>0,05), tidak ditemukan perbedaan bermakna antara kadar hormon FSH basal berdasarkan variasi genotip FSHR Asn680Ser pada kelompok SOPK dan bukan SOPK (p>0,05). Tidak ditemukan perbedaan yang bermakna indeks proliferasi sel granulosa berdasarkan variasi genotip FSHR Asn680Ser baik pada kelompok SOPK maupun bukan SOPK (p>0,05). Tidak terdapat korelasi antara indeks proliferasi sel granulosa dengan ekspresi mRNA aromatase (p>0,05). Kesimpulan: Indeks proliferasi sel dan tingkat ekspresi mRNA aromatase sel granulosa kelompok SOPK menurun dibandingkan kelompok bukan SOPK. Genotip FSHR Asn680Ser tidak menentukan kerentanan individu untuk menderita SOPK. Kadar hormon FSH basal dan indeks proliferasi sel granulosa tidak berbeda antara kelompok SOPK dan bukan SOPK berdasarkan variasi genotip FSHR Asn680Ser. Tidak ada korelasi antara indeks proliferasi sel dengan ekspresi mRNA aromatase sel granulosa pada penelitian ini.

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Introduction: Polycystic ovary syndrome (PCOS) is a common reproductive problem in women at reproductive age, but until now aetiopathogenesis of PCOS has not been fully understood. The objective of this study was to analyse interrelationship between proliferation of ovarian follicular granulosa cells, CYP19A1 expression and polymorphism at codon 680 of FSHR towards the etiology of PCOS.

Methods: Observational analytic in the form of cross-sectional study was used in this research. The study was carried out between 2011-2014 at the Department of Biology, Integrated laboratory of Faculty of Medicine University of Indonesia and Yasmin clinic at the Cipto Mangunkusumo Hospital. A total of 142 subjects (66 patients with PCOS and 76 patients without PCOS) were involved in this study. Granulosa cells for culture were obtained from ovarian follicular fluid and total RNA was isolated from the cells. DNA samples were extracted from peripheral blood. Granulosa cell proliferation index was determined by counting under a phase-contrast microscope. CYP19A1 expression was measured by qRT-PCR, whereas polymorphism at Asn680Ser FSHR was performed by RFLP.

Result: Cell proliferation index and CYP19A1 mRNA expression levels in the granulosa cells of the PCOS group was significantly lower than non-PCOS (p < 0.05). There was no significant difference found in Asn680Ser FSHR genotype distribution between PCOS and non-PCOS group (p > 0.05). Based on Asn680Ser FSHR genotype variation, no significant difference was found between basal FSH hormone levels in the PCOS and non- PCOS group (p > 0.05) and FSHR genotype variation did not correlate with granulosa cell proliferation index between PCOS and non-PCOS group (p > 0.05). Moreover, there was no correlation between the granulosa cell proliferation index with aromatase mRNA expression levels (p > 0.05).

Conclusion: Cell proliferation index and CYPA1 expression of granulosa cells in PCOS group were lower compared to the non PCOS group although no correlation was found between the two parameters. Asn680Ser FSHR genotype did not correlate with individual susceptibility to PCOS. FSHR genotype variation did not correlate with basal FSH levels and granulosa cell proliferation index between PCOS and non-PCOS."