Abstract
Background BMPER has been reported to be associated with the biological behavior of a few malignant tumors, but the mechanism is still unclear. We aimed to detect BMPER expression in ovarian epithelial tumor tissues and its effects on their biological behaviors, as well as to elucidate the possible mechanism. Methods BMPER expression in ovarian epithelial tumor tissues was detected by immunohistochemistry. BMPER expression in ovarian cancer cell lines was inhibited via RNA interference. Changes in the malignant behaviors of ovarian cancer cells were detected by MTT, wound healing, Transwell, and flow cytometry assays. Changes in proteins in the MAPK and autophagy-related signaling pathways were detected by Western blot analysis. Results The expression of BMPER was significantly upregulated in ovarian epithelial malignant tumors and was related to increased lymph node metastasis and lower survival rate. High BMPER expression is an independent risk factor for poor prognosis in patients. Inhibition of BMPER inhibited the proliferation, invasion, and migration of ovarian cancer cells and promoted apoptosis. In addition, BMPER downregulation decreased the expression of PCNA, Bcl-2, MMP2, and MMP9 and increased the expression of Bax. Moreover, the levels of p-ERK, p-MEK, and the autophagy-related protein p-mTOR were decreased, and Beclin 1 levels and the LC3II/I ratio were increased. Conclusions Our findings indicated that BMPER is closely related to poor prognosis in ovarian cancer. BMPER plays a role in promoting the malignant biological behavior of tumor cells through the MAPK and autophagy-related signaling pathways.
Highlights
Epithelial ovarian cancers are the most common type of ovarian malignancy in female reproductive organs
High BMPER expression was associated with lymph node metastasis, and the proportion of patients with high BMPER expression in the lymph node metastasis positive group was higher than that in the lymph node metastasis negative group (P < 0:05)
The results showed that after BMPER expression was downregulated, the levels of p-ERK, p-MEK, and p-mechanistic target of rapamycin (mTOR) proteins decreased while Beclin 1 levels and the LC3II/I ratio increased, indicating that the mitogen-activated protein kinase (MAPK) signaling pathway was inhibited after interference with BMPER expression but that autophagyrelated pathways were promoted upon BMPER knockdown (Figures 5(a) and 5(b))
Summary
Epithelial ovarian cancers are the most common type of ovarian malignancy in female reproductive organs Their mortality rate is high due to the absence of obvious symptoms during the early stages and a lack of reliable screening methods and specific biomarkers [1]. BMPER is a secretory glycoprotein expressed by endothelial precursor cells and is highly expressed in the lung, brain, prostate, appendix, and liver of adults It plays an important role in normal embryonic growth and development and participates in regulating the BioMed Research International. We aimed to detect BMPER expression in ovarian epithelial tumor tissues and its effects on their biological behaviors, as well as to elucidate the possible mechanism. BMPER plays a role in promoting the malignant biological behavior of tumor cells through the MAPK and autophagy-related signaling pathways
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
