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miR-124 Targets EGFR and Attenuates Growth and Invasion in Bladder Cancer Cells
Kuo-Pao Chen1, Tsai-Lan Liao2, Fei-Ting Hsu3
1Department of Family Medicine, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.
Background/Aim:
The epidermal growth factor receptor (EGFR) is a key driver in bladder cancer progression. This study investigated the tumor-suppressive role of miR-124-3p and its regulatory effect on EGFR.
Materials And Methods:
TSGH8301 and T24 bladder cancer cells were treated with the EGFR inhibitor erlotinib or transfected with an miR-124-3p mimic. Cell viability, proliferation, migration, and invasion were assessed using MTT, colony formation, and transwell assays. EGFR targeting was confirmed via Western blot, immunofluorescence, and luciferase reporter assays.
Results:
Erlotinib and miR-124-3p both reduced cell viability and proliferation. miR-124-3p significantly inhibited EGFR phosphorylation and expression, suppressed migration and invasion, and downregulated the EGFR downstream targets MMP2, MMP9, and VEGF-A. Luciferase assays confirmed the direct binding of miR-124-3p to EGFR 3'UTR.
Conclusion:
miR-124-3p suppresses bladder cancer cells progression by directly targeting and inactivating EGFR, thereby impairing cell proliferation, migration, and invasion. These findings highlight miR-124-3p as a potential therapeutic agent in EGFR-driven bladder cancer.
Insights
MicroRNA-124-3p acts as a tumor suppressor in bladder cancer by targeting the epidermal growth factor receptor (EGFR). This microRNA inhibits cancer cell proliferation, migration, and invasion, offering potential therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epidermal growth factor receptor (EGFR) is a critical factor in bladder cancer progression.
- Dysregulation of microRNAs plays a significant role in various cancers, including bladder cancer.
Purpose of the Study:
- To investigate the tumor-suppressive function of miR-124-3p in bladder cancer.
- To determine the regulatory relationship between miR-124-3p and EGFR in bladder cancer cells.
Main Methods:
- Utilized bladder cancer cell lines (TSGH8301, T24).
- Treated cells with EGFR inhibitor erlotinib or miR-124-3p mimic.
- Assessed cell viability, proliferation, migration, and invasion using MTT, colony formation, and transwell assays.
- Confirmed EGFR targeting through Western blot, immunofluorescence, and luciferase reporter assays.
Main Results:
- Both erlotinib and miR-124-3p reduced cell viability and proliferation.
- miR-124-3p significantly inhibited EGFR phosphorylation and expression.
- miR-124-3p suppressed cancer cell migration and invasion, downregulating MMP2, MMP9, and VEGF-A.
- Luciferase assays confirmed direct binding of miR-124-3p to the EGFR 3'UTR.
Conclusions:
- miR-124-3p effectively suppresses bladder cancer progression by directly targeting and inactivating EGFR.
- This microRNA impairs cancer cell proliferation, migration, and invasion.
- miR-124-3p represents a promising therapeutic candidate for EGFR-driven bladder cancer.
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