Effect of miR-301a/PTEN pathway on the proliferation and apoptosis of cervical cancer

Abstract

The aim of this study was to evaluate the effect of the miR-301a/PTEN pathway in cervical cancer. miR-301a and PTEN expression were measured by quantitative real-time PCR (qRT-PCR) in tissues samples and HeLa cells. PTEN protein level was determined by Western blotting. Dual reporter luciferase assay was performed to validate PTEN as a direct target of miR-301a. The gain- and loss-of function assay was performed by miR-301a overexpression and silencing. Cell proliferation was monitored by cell counting Kit-8 (CCK-8). Cell apoptosis was quantitated by flow cytometry. SPSS was used to analyze the significant difference in the treatments. miR-301a demonstrated a significantly higher expression in cervical carcinoma tissues compared with the paired non-carcinoma tissues (n = 12), while PTEN expression was found to be significantly lower in cervical carcinoma tissues than their paired non-carcinoma tissues (n = 12). In addition, PTEN was identified as the direct target of miR-301a. Moreover, overexpression of miR-301a significantly promoted HeLa cells proliferation and anti-apoptosis which had a reverse pattern after PTEN overexpression. Our results confirm PTEN as a direct target of miR-301a in HeLa cells and suggest that miR-301a/PTEN pathway contributes to the development and progression of cervical cancer.

Phosphatase and Tensin Homolog (PTEN) of Japanese Flounder—Its Regulation by miRNA and Role in Autophagy, Apoptosis and Pathogen Infection

“…In our study, we found that interference with pol-miR-novel_547, which resulted in enhanced PoPTEN expression, significantly promoted the apoptosis of flounder cells, implying an involvement of pol-miR-novel_547 and PoPTEN in the regulation of apoptosis. This observation is in line with the pro-apoptotic role of PTEN in mammals [ 36 , 92 , 93 , 94 ].…”

MicroRNA‑301a/ZNRF3/wnt/β‑catenin signal regulatory crosstalk mediates glioma progression

“…miR-301a participates in the cancer progression by directly targeting a large number of tumor suppressor genes, such as PTEN, RUNX family transcription factor 3 (RUNX3) and septin 7 ( 7 , 11 , 13 ). Accumulating evidence has demonstrated that miR-301a is innately associated with cancer cell proliferation, invasion and drug resistance by targeting PTEN in cervical cancer, malignant melanoma and pancreatic cancer ( 7 , 8 , 10 ). In the present study, according to bioinformatic predictions and experimental assays, it was identified that ZNRF3 was a functional target of miR-301a in GBM cell lines.…”

“…In the last few decades, along with the extensive identification and study of novel non-coding RNAs, such as long non-coding RNAs and circular RNAs, miRNA-mediated network dysregulations have been found to serve significant roles in the development and progression of malignancies, including gliomas (5,6). Previous studies have reported that miR-301a is markedly upregulated in a variety of cancer types, including melanoma, cervical, breast, pancreatic and colorectal cancer (CRC), indicating that it has an oncogene potential (7)(8)(9)(10)(11). For instance, miR-301a mediates breast cancer proliferation and invasion by directly targeting forkhead box F2, BCL2 binding component 3, PTEN and collagen type II α 1 chain (9).…”

Inhibiting microRNA‐301b suppresses cell growth and targets RNF38 in cervical carcinoma

“…In addition, under hypoxia, miR‐301a and miR‐301b, two hypoxia responsive miRNAs were significantly upregulated in prostate cancer cells, and high expression of miR‐301a and miR‐301b resulted in elevated autophagy and increased radio resistance in LNCaP cells 19 . Moreover, miR‐301a was reported upregulated in cervical carcinoma, and overexpressed miR‐301a could significantly promote HeLa cell proliferation by inhibiting PTEN expression 20 . In this study, miR‐301b was also found elevated in cervical carcinoma tumors and cell lines compared with the control, and inhibiting miR‐301b significantly suppressed cervical carcinoma cell growth, which was similar to other reported functions of miR‐301b in other tumors that all acted as an oncogene.…”