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lncTUG1/miR-144-3p affect the radiosensitivity of esophageal squamous cell carcinoma by competitively regulating
Pan Wang1, Zhuanbo Yang2, Ting Ye3,4
1Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No.17 Panjiayuannanli, Beijing, 100021, China.
Background:
Long noncoding RNAs (lncRNAs) are involved in the progression of various cancers and affect the response to radiotherapy. This study focused on clarifying the underlying mechanism by which lncTUG1 affects the radiosensitivity of esophageal squamous cell carcinoma (ESCC).
Methods:
lncTUG1, miR-144-3p and MET expression levels were detected in ESCC tissues and cells by qRT-PCR. Western blotting was used to examine the protein levels of MET, p-AKT and EGFR. The dual-luciferase reporter system and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncTUG1 and miR-144-3p or miR-144-3p and MET. MTT, colony formation and flow cytometry assays were applied to examine the behavioral changes in EC9706 and KYSE30 cells.
Results:
lncTUG1 was upregulated in ESCC cells and tissues, and lncTUG1 expression was associated with an advanced pathological stage. The bioinformatics analysis revealed that lncTUG1 could specifically bind to miR-144-3p, which was downregulated in ESCC. There was a negative correlation between lncTUG1 and miR-144-3p. LncTUG1 inhibition retarded proliferation and colony formation and induced apoptosis in ESCC cells. Moreover, lncTUG1 knockdown dramatically improved the effect of radiotherapy on ESCC development both in vivo and in vitro. Furthermore, MET was revealed as a downstream target of miR-144-3p and is downregulated by it. LncTUG1 promoted the progression of ESCC and elevated radiotherapy resistance in ESCC cells, accompanied by a high level of MET expression. Moreover, we found that knockdown of lncTUG1 enhanced the radiosensitivity of ESCC cells via the p-AKT signaling pathway.
Conclusion:
Our results indicate that lncTUG1 enhances the radiotherapy resistance of ESCC by lowering the miR-144-3p level and modulating the MET/EGFR/AKT axis.
Insights
Long noncoding RNA TUG1 (lncTUG1) promotes esophageal squamous cell carcinoma (ESCC) progression and radioresistance by downregulating miR-144-3p and activating the MET/EGFR/AKT pathway. Inhibiting lncTUG1 enhances radiosensitivity in ESCC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) play a role in cancer development and radiotherapy response.
- Esophageal squamous cell carcinoma (ESCC) radiosensitivity is a critical factor in treatment efficacy.
Purpose of the Study:
- To elucidate the mechanism by which lncTUG1 influences the radiosensitivity of ESCC.
- To investigate the regulatory role of lncTUG1 in ESCC progression and radioresistance.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blotting were used to measure expression levels of lncTUG1, miR-144-3p, MET, p-AKT, and EGFR.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays confirmed molecular interactions.
- Cell proliferation, colony formation, apoptosis, and in vivo/in vitro radiotherapy effects were assessed.
Main Results:
- lncTUG1 was upregulated in ESCC and correlated with advanced stage.
- lncTUG1 directly binds to miR-144-3p, leading to its downregulation.
- MET is a downstream target of miR-144-3p; lncTUG1 promotes MET expression, activating the AKT pathway and conferring radioresistance.
- lncTUG1 knockdown inhibited ESCC cell proliferation, induced apoptosis, and significantly enhanced radiosensitivity.
Conclusions:
- lncTUG1 enhances ESCC radioresistance by suppressing miR-144-3p and modulating the MET/EGFR/AKT axis.
- Targeting lncTUG1 represents a potential therapeutic strategy to improve radiotherapy outcomes in ESCC.
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