Effect of RNA Interference of BID and BAX mRNAs on Apoptosis in Granulosa Cell-derived KGN Cells

• Published in: Journal of Reproduction and Development Vol. 58; no. 1; pp. 112 - 116
• Main Authors: SAI, Takafumi, MATSUDA, Fuko, GOTO, Yasufumi, MAEDA, Akihisa, SUGIMOTO, Miki, GAO, Hong-Mei, Abul Khair Mohammad Ahan KABIR, LI, Jun-You, MANABE, Noboru
• Format: Journal Article
• Language: English
• Published: Japan THE SOCIETY FOR REPRODUCTION AND DEVELOPMENT 2012
• Subjects: Apoptosis; Bax protein; BCL-2-associated X protein (BAX); bcl-2-Associated X Protein - biosynthesis; BH3 Interacting Domain Death Agonist Protein - biosynthesis; BH3-interacting domain death agonist (BID); BID protein; Cell Line, Tumor; Female; Gene expression; Granulosa cells; Granulosa Cells - metabolism; Humans; Mitochondrion-dependent type II apoptosis; Ovaries; Polymerase chain reaction; Reverse transcription; RNA Interference; RNA interference (RNAi); RNA-mediated interference; Signal Transduction; siRNA; Tumor cell lines; Western blotting; X protein
• ISSN: 0916-8818; 1348-4400
• DOI: 10.1262/jrd.11-121H

In mitochondrion-dependent type II apoptosis, BH3-interacting domain death agonist (BID) and BCL-2-associated X protein (BAX) promote death ligand and receptor-mediated cell death. In porcine ovaries, the levels of BID and BAX increase in follicular granulosa cells during atresia. In the present study, to confirm the pro-apoptotic activity of BID and BAX in granulosa cells, we examined the effect of RNA interference of BID or BAX on apoptosis using a human ovarian granulosa tumor cell line, KGN. By reverse transcription polymerase chain reaction (RT-PCR) and Western blotting, expression of BID and BAX was detected in KGN cells. Then, we suppressed BID and BAX mRNA expression in KGN cells using small interfering RNA (siRNA). When BID or BAX was suppressed, a significant decrease in the apoptotic cell rate was noted. In granulosa-derived cells, BID and BAX showed pro-apoptotic activity. These results suggest that BID and BAX act as signal-transducing factors in mitochondrion-dependent type II apoptosis.