2017Die PharmazieOpen access

miR-152-5p inhibits proliferation and induces apoptosis of liver cancer cells by up-regulating FOXO expression

Donny L.F. Chang, Wei Wei, Zhiwu Yu, Cun‐Wei Qin

Open full text 17 citations

Abstract

Currently, a lot of microRNAs (miRNAs) have been confirmed to be closely related with liver cancer occurrence and development. This study was aimed to explore the role of miR-152-5p in liver cancer. HepG2 and MHCC97 cells were transfected with miR-152-5p mimic, inhibitor or corresponding scramble controls, respectively. The expression level of miR-152-5p in transfected cells was detected by qPCR. Cell viability, apoptosis, migration and invasion of miR-transfected cells were measured to determine the effect of miR-152-5p on the activity of hepatoma cells. The protein expressions of fork head transcription factor O (FOXO) and apoptosis related factors in miR-transfected cells were detected by western blot assay. In addition, western blot was used to detect the relationship of FOXO expression and mainly factors of the JNK signaling pathway after concurrent treatment with miR-152-5p mimic and JNK inhibitor. The results showed that the miR-152-5p was effectively overexpressed or repressed in both HepG2 and MHCC97 cells. Overexpression of miR-152-5p inhibited cell viability, promoted apoptosis, and reduced migration and invasion. In these cells, miR-152-5p overexpression activated the expression of apoptosis-related factors and upregulated the expression of FOXO by activating the phosphorylation of mainly factors in the JNK pathway. miR-152-5p might be a potential anti-tumor factor for liver cancer treatment.

Open-access reader

About this research paper

What this paper is about

Currently, a lot of microRNAs (miRNAs) have been confirmed to be closely related with liver cancer occurrence and development. This study was aimed to explore the role of miR-152-5p in liver cancer. HepG2 and MHCC97 cells were transfected with miR-152-5p mimic, inhibitor or corresponding scramble controls, respectively. The expression level of miR-152-5p in transfected cells was detected by qPCR. Cell viability, apoptosis, migration and invasion of miR-transfected cells were measured to determine the effect of miR-152-5p on the activity of hepatoma cells. The protein expressions of fork head transcription factor O (FOXO) and apoptosis related factors in miR-transfected cells were detected by western blot assay. In addition, western blot was used to detect the relationship of FOXO expression and mainly factors of the JNK signaling pathway after concurrent treatment with miR-152-5p mimic and JNK inhibitor. The results showed that the miR-152-5p was effectively overexpressed or repressed in both HepG2 and MHCC97 cells. Overexpression of miR-152-5p inhibited cell viability, promoted apoptosis, and reduced migration and invasion. In these cells, miR-152-5p overexpression activated the expression of apoptosis-related factors and upregulated the expression of FOXO by activating the phosphorylation of mainly factors in the JNK pathway. miR-152-5p might be a potential anti-tumor factor for liver cancer treatment.

Why it matters

OpenAlex reports 17 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Currently, a lot of microRNAs (miRNAs) have been confirmed to be closely related with liver cancer occurrence and development. This study was aimed to explore the role of miR-152-5p in liver cancer. HepG2 and MHCC97 cells were transfected with miR-152-5p mimic, inhibitor or corresponding scramble controls, respectively. The expression level of miR-152-5p in transfected cells was detected by qPCR. Cell viability, apoptosis, migration and invasion of miR-transfected cells were measured to determine the effect of miR-152-5p on the activity of hepatoma cells. The protein expressions of fork head transcription factor O (FOXO) and apoptosis related factors in miR-transfected cells were detected by western blot assay. In addition, western blot was used to detect the relationship of FOXO expression and mainly factors of the JNK signaling pathway after concurrent treatment with miR-152-5p mimic and JNK inhibitor. The results showed that the miR-152-5p was effectively overexpressed or repressed in both HepG2 and MHCC97 cells. Overexpression of miR-152-5p inhibited cell viability, promoted apoptosis, and reduced migration and invasion. In these cells, miR-152-5p overexpression activated the expression of apoptosis-related factors and upregulated the expression of FOXO by activating the phosphorylation of mainly factors in the JNK pathway. miR-152-5p might be a potential anti-tumor factor for liver cancer treatment.

Key concepts: Transfection, Apoptosis, Western blot, Viability assay, microRNA, Cancer research, Cell growth, Cancer cell

Related papers

Back to paper searchBrowse research topicsOriginal source
miR-152-5p inhibits proliferation and induces apoptosis of liver cancer cells by up-regulating FOXO expression — Research Paper | ScholarLens