Accumulating evidence has demonstrated that microRNAs (miRNAs) play critical roles in cancer initiation and development by functioning either as oncogenes or as tumor suppressors. The role of microRNA-449a (miR-449a) in endometrial cancer remains unclear. We examined the levels of miR-449a and miR-449b in benign endometrium, type I and type II endometrial cancer tissues by quantitative real-time polymerase chain reaction. To further investigate the roles of miR-449a in regulating the behavior of endometrial cancer cells, we overexpressed miR-449a in the endometrial cancer cell line HEC-1B, which had low endogenous miR-449a expression. We analyzed the effects of miR-449a overexpression on CDC25 expression, proliferation, invasion and apoptosis of HEC-1B cells. We found that miR-449a and miR-449b levels were markedly reduced in type II endometrial cancer tissues but not in type I endometrial cancer tissues compared with normal endometrium. Overexpression of miR-449a significantly inhibited the proliferation, invasion and clonogenic survival of HEC-1B cells. MiR-449a overexpression also induced apoptosis in HEC-1B cells. In addition, real-time RT-PCR and western blot analysis showed that CDC25A expression was suppressed by miR-449a overexpression. Our results suggest that miR-449a may act as a tumor suppressor by targeting CDC25A in endometrial cancer.

PurposeCapsid protein L2 is the minor capsid protein of human papillomavirus 16 (HPV16). Although L2-based vaccines were developed, the therapeutic effect of recombinant viral capsid protein L2 (rVL2) was still to be illustrated.MethodsWe used glucose uptake and lactate production assay to verify the inhibitory effect of rVL2 on the glucose metabolism in cervical cancer cells. Secondly, we performed gene-chip assay, RT-PCR, and Western blot to determine the role of ITGB7/C/EBPβ signaling pathway in rVL2-mediated glucose metabolism in vitro. Finally, we used an animal model to verify the function of rVL2 in cervical cancer.ResultsWe found that rVL2 reduced glucose uptake and lactate production levels in cervical cancer cells, which caused the inhibition of cell proliferation. rVL2 decreased the expression levels of key metabolic enzymes, including GLUT1, LDHA, and ALDOA, to affect cell metabolism in cervical cancer cells by inhibiting ITGB7/C/EBPβ signaling pathway in vitro and in vivo.ConclusionThese results demonstrated the vital role of rVL2 in the glycolysis-induced cell growth and proliferation via suppressing ITGB7/C/EBPβ signaling axis.

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