microRNA-206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α-positive ovarian cancer cells

Abstract

The expression levels of estrogen receptor (ER α) are closely associated with estrogen-dependent growth, invasion and response to endocrine therapy in ERα-positive ovarian cancer. However, the underlying regulatory mechanisms remain to be fully understood. Previous studies have demonstrated that ERα is a direct target of microRNA (miR)-206. miR-206 has been found to be an important tumor suppressor in several cancer types, including ovarian, gastric and laryngeal cancer. However, the specific role of miR-206 in ovarian cancer remains unclear. The aim of the present study was to investigate the role of miR-206 in ER-a positive ovarian cancer in vitro. The present study demonstrated that miR-206 is significantly downregulated in ERα-positive but not ERα‑negative ovarian cancer tissues, compared with normal ovarian epithelium tissue. It was also found that the expression of miR-206 was decreased in ERα-positive ovarian cancer cell lines, CAOV-3 and BG-1, compared with normal ovarian epithelium tissues. This suggests that miR-206 may play a role in ERα-positive ovarian cancer cells via an estrogen-dependent mechanism. Further analysis revealed that 17β-E2 treatment significantly promoted cellular proliferation and invasion of estrogen-dependent CAOV-3 and BG-1 cells, which could be reversed by the introduction of miR-206 mimics. In conclusion, the present study suggests that miR-206 has an inhibitory role in estrogen-dependent ovarian cancer cells. Thus, miR-206 may be a promising candidate for the endocrine therapy of ERα-positive ovarian cancer.

Overexpression of miR-206 suppresses glycolysis, proliferation and migration in breast cancer cells via PFKFB3 targeting

“…miR-206 was found to be significantly downregulated in ERa-positive but not ERa-negative ovarian cancer tissues, compared with normal ovarian epithelium tissue [22]. It was also found that the expression of miR-206 was decreased in ERa-positive ovarian cancer cell lines [22].…”

MiR-25 promotes ovarian cancer proliferation and motility by targeting LATS2

“…Aberrantly altered expression of miRNAs has been found in several cancers including OC, and many miRNAs have been identified as prognostic markers for some cancers [7,8]. In OC, miRNAs act as either oncogenes or tumor suppressor [9,10]. MiR-25 has been found to be increased in OC; however, its detailed role remains unclear [11].…”

Prognostic significance of combined microRNA-206 and CyclinD2 in gastric cancer patients after curative surgery: A retrospective cohort study

“…Recent studies using highthroughput technology such as miRNA oligonucleotide arrays and quantitative real-time polymerase chain reaction (PCR) for validation have observed the abnormal expression of miR-206 in various human cancer types such as rhabdomyosarcoma (RMS), laryngeal cancer, breast cancer, lung cancer, hepatocellular carcinoma, gastric cancer, endometrial endometrioid carcinoma (EEC) and HeLa cells [14][15][16][17][18][19][20][21]. Especially, Yang et al [19] reported that miR-206 expression was significantly downregulated in gastric cancer tissues when compared with normal adjacent mucosa, and its downregulation might be a potent prognostic marker of this disease; Ren et al [22] revealed that miR-206 could suppress gastric cancer cell growth and metastasis; Zhang et al [23] also confirmed that miR-206 could suppress gastric cancer cell proliferation at least partially through targeting CyclinD2 (CCND2), a crucial regulator in cell cycle progression.…”