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MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2
Background/Aims:
MicroRNAs (miRNAs) play an essential role in the tumorigenesis of gastric carcinoma (GC). MiR-429 has been recently reported to inhibit GC growth, but the underlying mechanisms are not clear.
Methods:
Here, we studied the levels of miR-429 and anti-apoptotic protein Bcl-2 in GC specimens. We performed bioinformatics analyses and used luciferase-reporter assay to analyze the relationship between miR-429 and Bcl-2 in GC cells. Cell survival upon Fluorouracil treatment was analyzed in a CCK assay. Cell apoptosis was measured by flow cytometry based FITC Annexin V apoptosis detection assay.
Results:
MiR-429 levels were significantly decreased and Bcl-2 levels were significantly increased in GC specimens, compared to the paired adjacent non-tumor gastric tissue. Moreover, the levels of miR-429 and Bcl-2 inversely correlated in GC specimens. MiR-429-low subjects had an overall inferior survival, compared to miR-429-high subjects. Bioinformatics analyses showed that miR-429 targeted the 3'-UTR of Bcl-2 mRNA to inhibit its translation, which was confirmed by luciferase-reporter assay. Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against apoptosis induced by Fluorouracil, while depletion of miR-429 augmented it.
Conclusion:
Our data suggest that miR-429 suppression in GC promotes Bcl-2-mediated cancer cell survival against chemotherapy-induced cell death. Re-expression of miR-429 levels in GC cells may enhance cancer apoptosis during chemotherapy.
Insights
MicroRNA-429 (miR-429) suppression in gastric cancer (GC) increases the survival of cancer cells by upregulating Bcl-2. Restoring miR-429 may enhance chemotherapy effectiveness by promoting apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are critical regulators in gastric carcinoma (GC) tumorigenesis.
- MiR-429 has shown potential in inhibiting GC progression, but its precise mechanisms remain elusive.
Purpose of the Study:
- To investigate the role of miR-429 in gastric cancer.
- To elucidate the relationship between miR-429 and the anti-apoptotic protein Bcl-2 in GC.
- To determine the impact of miR-429 on chemotherapy response in GC cells.
Main Methods:
- Quantification of miR-429 and Bcl-2 levels in GC tissues.
- Bioinformatics analysis and luciferase-reporter assays to confirm miR-429 targeting of Bcl-2.
- Cell viability (CCK assay) and apoptosis (flow cytometry) assays following Fluorouracil treatment.
Main Results:
- Decreased miR-429 and increased Bcl-2 levels were observed in GC tissues, with an inverse correlation.
- MiR-429 directly targets Bcl-2 mRNA, inhibiting its translation.
- Overexpression of miR-429 sensitized GC cells to Fluorouracil-induced apoptosis, while miR-429 depletion enhanced cell survival.
Conclusions:
- Suppression of miR-429 in GC contributes to chemoresistance by promoting Bcl-2-mediated cell survival.
- Re-establishing miR-429 levels in GC cells could be a therapeutic strategy to enhance apoptosis during chemotherapy.
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