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Updated: Mar 30, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-122 inhibits cancer cell malignancy by targeting PKM2 in gallbladder carcinoma
Wei Lu1,2, Yijian Zhang1,3, Linzhu Zhou4
1Department of General Surgery, Xinhua Hospital, Affiliated to Shanghai Jiao Tong University, School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, People's Republic of China.
Abstract:
Gallbladder cancer (GBC) is one of the lethal diseases of digestive system. Increasing evidence prompt that microRNAs (miRs) might provide a novel therapeutical target for malignant disease. The antitumor effect of miR-122 to GBC is worth to be investigated. miR-122 expression level in GBC tissue sample and cell lines were assayed by qRT-PCR. miR-122 mimics were transfected for upregulation of miR-122 expression. Cell function was assayed by CCK8, flow cytometry, wound healing assay, migration assay, and invasion assay. The target genes of miR-122 were predicated by TargetScan online program and verified by western blot and luciferase report gene assay. miR-122 was decreased in GBC tissue and cell lines. The exogenous introduction of miR-122 exhibits multiple antitumor effect in GBC cell proliferation, invasion, and metastasis. Further studies revealed that the PKM2 was a regulative target of miR-122 in GBC cell. miR-122 also inhibits TGF-β-induced epithelium mesenchymal transformation of GBC cell by downregulating PKM2 expression. These findings suggest that miR-122 plays an important role in tumorigenesis of GBC through interfering PKM2, highlighting its usefulness as a potential therapeutic agent in GBC.
Insights
MicroRNA-122 (miR-122) is significantly decreased in gallbladder cancer (GBC). Restoring miR-122 levels inhibits GBC cell proliferation, invasion, and metastasis, suggesting its therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gallbladder cancer (GBC) is a lethal digestive system malignancy.
- MicroRNAs (miRs) are emerging as potential therapeutic targets for cancers.
- The role of miR-122 in GBC warrants investigation.
Purpose of the Study:
- To investigate the expression of miR-122 in GBC.
- To evaluate the antitumor effects of miR-122 in GBC.
- To identify the molecular targets of miR-122 in GBC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for miR-122 expression analysis.
- Transfection with miR-122 mimics to upregulate expression.
- Cell function assays (CCK8, flow cytometry, wound healing, migration, invasion).
- Bioinformatic prediction (TargetScan) and experimental validation (Western blot, luciferase assay) of target genes.
Main Results:
- miR-122 expression was significantly decreased in GBC tissues and cell lines.
- Exogenous miR-122 introduction suppressed GBC cell proliferation, invasion, and metastasis.
- PKM2 was identified as a direct target gene of miR-122 in GBC.
- miR-122 inhibited TGF-β-induced epithelial-mesenchymal transition (EMT) by downregulating PKM2.
Conclusions:
- miR-122 functions as a tumor suppressor in GBC.
- miR-122 targets PKM2, impacting GBC cell behavior and EMT.
- miR-122 represents a promising therapeutic candidate for GBC treatment.
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