Journal
ONCOLOGY REPORTS
Volume 33, Issue 4, Pages 1745-1752Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2015.3763
Keywords
endometrial carcinoma; OCT4-pg5; miR-145; OCT4; proliferation
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Funding
- National Natural Science Foundation of China (NSFC) [81272883, 81202044, 81370074, 81172478]
- Science and Technology Commission of Shanghai Municipality (STCSM) [12ZR1447600]
- Shanghai Municipal Public Health Bureau [XYQ2013119]
- Shanghai Jiaotong University [BXJ201339]
- Shanghai Jiaotong University
- grant of 'Chenxin plan' from Shanghai Jiaotong University
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OCT4 plays a critical role in the maintenance of stem cell pluripotency and proliferation, and is overexpressed in multiple human tumors, including endometrial cancer. OCT4 expression can be modulated by miR-145 and the OCT4 pseudogene 5 (OCT4-pg5), which share similar binding sites in the OCT4 3'-untranslated region. The goal of the present study was to evaluate the interaction between miR-145 and OCT4-pg5 on OCT4 expression in endometrial cancer. We assessed OCT4-pg5 expression in 14 benign endometrium and 29 endometrial carcinoma samples. Furthermore, miR-145 mimic transfection was performed to explore its effect on OCT4-pg5 and OCT4 expression, and small interfering RNA (siRNA)-mediated knockdown of OCT4 was conducted to determine whether the effect of OCT4-pg5 on cellular growth was OCT4-dependent. We observed that OCT4-pg5 was abnormally activated in the endometrial carcinomas, and that overexpression of OCT4-pg5 contributed to enhanced cell proliferation and OCT4-PI3K/AKT-cyclin D1 signaling. Moreover, the miR-145 mimic depleted OCT4 expression, Whereas elevated OCT4-pg5 restored OCT4 expression and OCT4-PI3K/AKT-cyclin D1 signaling. In conclusion, these data indicate that OCT4-pg5 can act as an RNA sponge to protect OCT4 transcripts from being inhibited by miR-145, providing novel insight into the control of OCT4 expression.
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