MiR-136 triggers apoptosis in human gastric cancer cells by targeting AEG-1 and BCL2
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Updated: Feb 2, 2026

Establishment of Gastric Cancer Patient-derived Xenograft Models and Primary Cell Lines
Published on: July 19, 2019
1Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province, China. dechunli12@hotmail.com.
Objective:
Gastric cancer is the second most prevalent cancer across the globe and accounts for about 10% of new cancer cases. It is one among the leading causes of cancer-related deaths around the world. Recently, microRNAs have been identified as important therapeutic targets for the treatment of several cancers owing to their potential to target multiple genes and hinder several biological processes such as proliferation and apoptosis. In the current study, we investigated the potential of miR-136 as therapeutic target for gastric cancer.
Materials And Methods:
Total RNA was isolated by RNeasy RNA isolation kit and cDNA was prepared byRevertAid cDNA synthesis kit. The transcript analysis was carried out by quantitative RT-PCR. The transfection of miR-136 mimics or plasmids was carried out by using the Lipofectamine 2000 reagent. Apoptosis was detected by DAPI and acridine orange/ethidium bromide (AO/EB) staining. Protein expression was examined by Western blotting.
Results:
The results indicated that the expression of miR-136 is significantly downregulated in gastric cancer cells. Transfection and subsequent overexpression of miR-136 in gastric cancer cells significantly promoted apoptosis as evident from DAPI and OA staining. In silico analysis revealed AEG-1 and BCL2 to be the potential targets of miR-136. Therefore, the expression of AEG-1 and BCL2 was determined in untreated control, cisplatin treated control and miR-136 transfected AGS gastric cancer cells. The results revealed that overexpression of miR-136 expression causes significant downregulation of AEG-1 and BCL2 protein expression.
Conclusions:
Taken together, we conclude that miR-136 promotes apoptosis in gastric cancer cells by targeting AEG-1 and BCL2. Therefore, miR-136 may prove as a potential therapeutic target for the treatment of gastric cancer.
Insights
MicroRNA-136 (miR-136) is downregulated in gastric cancer. Overexpressing miR-136 promotes apoptosis by targeting AEG-1 and BCL2, suggesting miR-136 as a potential therapeutic target for gastric cancer.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Gastric cancer is a leading cause of cancer-related deaths globally.
- MicroRNAs are emerging as critical regulators of cancer development and potential therapeutic targets.
- The role of miR-136 in gastric cancer pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the expression levels of miR-136 in gastric cancer.
- To determine the therapeutic potential of miR-136 in gastric cancer treatment.
- To identify the molecular targets of miR-136 in gastric cancer cells.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for transcript analysis.
- Transfection of miR-136 mimics/plasmids using Lipofectamine 2000.
- Apoptosis assays (DAPI, acridine orange/ethidium bromide staining) and Western blotting for protein expression analysis.
Main Results:
- miR-136 expression was significantly downregulated in gastric cancer cells.
- Overexpression of miR-136 promoted apoptosis in gastric cancer cells.
- miR-136 directly targeted and downregulated AEG-1 and BCL2 protein expression.
Conclusions:
- miR-136 induces apoptosis in gastric cancer cells through targeting AEG-1 and BCL2.
- Restoring miR-136 levels represents a promising therapeutic strategy for gastric cancer.
- Further research into miR-136-based therapies for gastric cancer is warranted.
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