J Gynecol Oncol | Volume 2, Issue 2 | Research Article | Open Access
Yanfei L1,2, Haoying P2, Jin Z2, Zhongping N1* and Junwei S1,3*
1Zhoupu Hospital, Shanghai University of Medicine and Health Sciences, China 2School of Medical Technology, Shanghai University of Medicine and Health Sciences, China 3Eastern Hospital, Tongji University, China
Fulltext PDFObjectives: Cervical cancer is the most common gynecological cancer in the world and is one of the leading causes of cancer related death among women. EFEMP2, an extracellular matrix protein that could be easily detected in serum, plays key roles in several cancers formation and progression. However, its role in cervical cancer remains to be determined. Methods: We have analyzed differentially expressed genes between Long-Term Survivors (LTSs) and Short-Term Survivors (STSs) using edgeR. The EFEMP2 shRNA plasmids were prepared and the EFEMP2 knockdown cervical cancer cell lines were constructed. The functions of EFEMP2 on cervical cancer were evaluated in vitro and in vivo and the molecular mechanism was investigated by western blotting, etc. Results: The genes associated with the Extracellular Matrix (ECM) were significantly downregulated in LTSs group compared with STSs. Low expression of EFEMP2 was positively associated with longer survival of cervical cancer patients. Knockdown of EFEMP2 not only suppressed the cell proliferation of cervical cancer cells in vitro, but inhibited the tumor growth in vivo. Moreover, EFEMP2 knockdown suppressed the expression of several genes related to promoting-proliferation by inhibiting AKT signaling. Conclusion: EFEMP2 functions as an oncogene to promote cell proliferation of cervical cancer, and it is a promising biomarker and therapy target for human cervical cancer.
Extracellular Matrix; EFEMP2; Cervical Cancer; Tumor Biomarkers; AKT Signaling
Yanfei L, Haoying P, Jin Z, Zhongping N, Junwei S. Inhibition of EFEMP2 Suppresses the Cell Proliferation of Cervical Cancer Cells via AKT Signaling. J Gynecol Oncol. 2019; 2(2): 1015.