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MicroRNA-122 overexpression suppresses the colon cancer cell proliferation by downregulating the astrocyte elevated

Sarubala Malayaperumal¹, Sushmitha Sriramulu¹, Ganesan Jothimani¹

¹Faculty of Allied Health Sciences, Chettinad Academy of Research and Education, Chettinad Hospital and Research Institute, Chennai, India.

Annals of Medicine

|April 10, 2025

Abstract

Background:

MicroRNAs (miRNAs) are small non-coding RNAs that regulate essential cellular functions, such as cell adhesion, proliferation, migration, invasion, and programmed cell death, and therefore, alterations in miRNAs can contribute to carcinogenesis. Previous studies have shown that miRNA-122 is abundant in the liver and regulates cell proliferation, migration, and apoptosis. However, the expression pattern and mechanism of actions of miR-122 remain primarily unknown in colon cancer.

Methods:

In this study, we analyzed The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) database to assess the clinical significance of astrocyte elevated gene-1 (AEG-1)/metadherin (MTDH) and miR-122 in colon cancer. MiR-122 overexpression studies were performed in HCT116, SW480, and SW620 cell lines. Dual-luciferase assay was carried out to confirm the interaction between AEG-1 and miR-122. In vivo-JetPEI-transfection reagent was used for in-vivo transient transfection of miR-122 in the AOM/DSS-induced colon tumor mouse model.

Results:

Our results demonstrate that miR-122 was downregulated in colon cancer cells, and it influences the expressions of apoptotic factors and inflammatory cytokines. MiR-122 overexpression in HCT116, SW480, and SW620 cells showed upregulation of Caspase 3, Caspase 9, and BAX and decreased expression of BCL2, which are pro-apoptotic and anti-apoptotic members that maintain a ratio between cellular survival and cell death. In vivo transient transfection of miR-122 mimic in AOM/DSS induced colon tumor mouse model showed less inflammation and disease activity. The TCGA-COAD data indicated that AEG-1 expression was higher in patients with low expression of miR-122 and lower AEG-1 expression in patients with higher expression miR-122.

Conclusion:

Our findings highlight the key role of miR-122 in the high grade of colonic inflammation, and possibly in colon cancer, and the use of miR-122 mimic might be a therapeutic option.

Insights

MicroRNA-122 (miR-122) is downregulated in colon cancer, impacting apoptosis and inflammation. Restoring miR-122 may offer a therapeutic strategy for colon inflammation and cancer.

Area of Science:

Oncology
Molecular Biology
Gene Regulation

Background:

MicroRNAs (miRNAs) are crucial regulators of cellular processes, and their dysregulation is linked to cancer.
miRNA-122 (miR-122) is known for its role in liver function but its function in colon cancer is largely unexplored.

Purpose of the Study:

To investigate the clinical significance and mechanism of miR-122 in colon cancer.
To assess the relationship between miR-122 and astrocyte elevated gene-1 (AEG-1) in colon adenocarcinoma.

Main Methods:

Analysis of The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) database.
MiR-122 overexpression in colon cancer cell lines (HCT116, SW480, SW620).
Dual-luciferase assay to confirm AEG-1 and miR-122 interaction.
In vivo studies using an AOM/DSS-induced colon tumor mouse model.

Main Results:

MiR-122 was found to be downregulated in colon cancer cells.
Overexpression of miR-122 modulated apoptotic factors (upregulating Caspase 3, Caspase 9, BAX; downregulating BCL2) and reduced inflammation in vivo.
AEG-1 expression inversely correlated with miR-122 expression in TCGA-COAD data.

Conclusions:

MiR-122 plays a significant role in colon inflammation and potentially in colon cancer development.
MiR-122 mimics represent a potential therapeutic avenue for managing colon inflammation and cancer.

Read full analysis

Keywords:

AEG-1/MTDH TCGA-COAD apoptosis colon cancer inflammatory cytokines miR-122

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