BACKGROUND/AIMS: SUZ12 and EZH2 are two main components of polycomb repressive complex 2 (PRC2) that is known to be of great importance in tumorigenesis. EZH2 has been reported to play a vital role in pathogenesis of human cancer. However, whether SUZ12 has equivalent roles in tumorigenesis has not been demonstrated. Here, we investigated a possible role of SUZ12 for the proliferation of gastric cancer cells. METHODS: Western-blot analysis was used to detected the levels of SUZ12, H3K27me3, EZH2 and p27 in ten gastric cell lines. SUZ12 was depleted by RNA interference. Cell cycle was detected by flow cytometry. Luciferase assays was to analyze whether miR-200b directly regulate SUZ12. RESULTS: We found that SUZ12 depletion mediated by RNA interference (RNAi) led to a reduction of gastric cell numbers and arrested the cell cycle at G1/S point. As an important G1/S phase inhibitory gene, p27 is re-induced to some extent by SUZ12 knockdown. Furthermore, we demonstrated that SUZ12 was directly downregulated by miR-200b. CONCLUSION: We provide evidence suggesting that SUZ12 may be a potential therapeutic target for gastric cancer.
BACKGROUND/AIMS: SUZ12 and EZH2 are two main components of polycomb repressive complex 2 (PRC2) that is known to be of great importance in tumorigenesis. EZH2 has been reported to play a vital role in pathogenesis of humancancer. However, whether SUZ12 has equivalent roles in tumorigenesis has not been demonstrated. Here, we investigated a possible role of SUZ12 for the proliferation of gastric cancer cells. METHODS: Western-blot analysis was used to detected the levels of SUZ12, H3K27me3, EZH2 and p27 in ten gastric cell lines. SUZ12 was depleted by RNA interference. Cell cycle was detected by flow cytometry. Luciferase assays was to analyze whether miR-200b directly regulate SUZ12. RESULTS: We found that SUZ12 depletion mediated by RNA interference (RNAi) led to a reduction of gastric cell numbers and arrested the cell cycle at G1/S point. As an important G1/S phase inhibitory gene, p27 is re-induced to some extent by SUZ12 knockdown. Furthermore, we demonstrated that SUZ12 was directly downregulated by miR-200b. CONCLUSION: We provide evidence suggesting that SUZ12 may be a potential therapeutic target for gastric cancer.
Authors: Ming Zhang; Yuxuan Wang; Sian Jones; Mark Sausen; Kevin McMahon; Rajni Sharma; Qing Wang; Allan J Belzberg; Kaisorn Chaichana; Gary L Gallia; Ziya L Gokaslan; Greg J Riggins; Jean-Paul Wolinksy; Laura D Wood; Elizabeth A Montgomery; Ralph H Hruban; Kenneth W Kinzler; Nickolas Papadopoulos; Bert Vogelstein; Chetan Bettegowda Journal: Nat Genet Date: 2014-10-12 Impact factor: 38.330