Abstract
Altered expression of miR-182 has been observed in various types of human cancer. The purpose of this study was to investigate the expression of miR-182 and its role in prostate cancer (PCa). Expression of miR-182 and ST6GALNAC5 in tumor tissues and the Du145 PCa cell line was analyzed. Cell proliferation assay, colony formation assay, transwell assay, and wound healing assay were performed. The impact of miR-182 on tumor growth was investigated using a xenograft model. The results indicated that expression of miR-182 was higher in PCa tissues and cell lines, while ST6GALNAC5 was decreased. Downregulating miR-182 significantly inhibited the capacities of proliferation and invasion of PC3 and Du145 cells. ST6GALNAC5 was demonstrated to be a target of miR-182 by luciferase assay, and western blot results indicated PI3K/Akt pathway was involved in miR-182 associated effects on PC3 and Du145 cells. The animal experiment suggested that knockdown of miR-182 inhibited tumor growth. Our study proved that miR-182 participated in the proliferation and invasion of PCa cells via mediating expression of ST6GALNAC5 and established a miR-182/ST6GALNAC5/PI3K/AKT axis in regulation of tumor progression. Our investigation provided a basis for further exploration of the application of miR-182 or ST6GALNAC5-associated therapies for PCa patients.
Highlights
Human prostate cancer (PCa) is one of the most common malignant tumors, especially for aging males, and frequently known as the fourth most prevalent cause of cancer-related mortality worldwide [1,2]
Expression pattern of miR-182 and ST6GALNAC5 in PCa cell lines and tissues miR-182 was significantly higher in PCa tissues compared with adjacent noncancerous tissues (Figure 1A)
PCa cell lines exhibited a statistically higher level of miR-182 than normal human prostate epithelial (NHPE) (Figure 1D), which was in accordance with what we found in PCa and paired noncancerous tissues
Summary
Human prostate cancer (PCa) is one of the most common malignant tumors, especially for aging males, and frequently known as the fourth most prevalent cause of cancer-related mortality worldwide [1,2]. Despite major improvements of diagnosis and therapy strategies, the clinical benefits are still unsatisfactory [2]. Most patients experience recurrence and poor prognosis after the standard treatments [2]. Studies have revealed that the high recurrence rate is mainly due to invasion, migration, and proliferation capacities of PCa cells [1,2]. Aberrant alterations at the protein and gene levels have been recognized as one of the reasons for high invasion, migration, and proliferation of tumor cells, the inherent molecular underpinnings are still unclear [3,4,5,6,7]. The mechanisms underlying the poor prognosis as well as novel therapeutic strategies of PCa must be explored
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