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LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4
Chunxiang Li1, Hengchang Liu2, Ran Wei2
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, Beijing, People's Republic of China.
Background/Aims:
Long non-coding ribonucleic acids (lncRNAs) are involved in the progression of cancers and affect the response to radiation therapy. This study was to investigate the mechanism of lncRNA EGOT in the radiosensitivity of rectal cancer.
Methods:
The mRNA expression of EGOT, miR-211-5p and ErbB4 in rectal cancer tissues and cells was detected by qRT-PCR. The protein expression of ErbB4 was detected by Western blot. Dual-luciferase reporter assay and ribonucleic acid immunoprecipitation (RIP) were used to confirm the interaction between EGOT and miR-211-5p or miR-211-5p and ErbB4. Transfection technology was used to down-regulate and up-regulate the expression of EGOT and miR-211-5p in rectal cancer cells, respectively. MTT, colony formation and flow cytometry were used to detect the effect of EGOT and miR-211-5p on proliferation, invasion, migration and apoptosis of rectal cancer cells.
Results:
The expression of EGOT was up-regulated in rectal cancer tissues and cells, and the expression of EGOT was related to the late stage of pathology. EGOT knockdown inhibited the proliferation and colony formation of rectal cancer cells and induced the apoptosis of rectal cancer cells. Moreover, EGOT knockdown was significantly enhanced the effects of radiotherapy on rectal cancer in vivo and in vitro. Furthermore, EGOT was found to serve as a sponge of miR-211-5p, and ErbB4 was a downstream target of miR-211-5p. EGOT enhanced the expression of ErbB4 by regulating miR-211-5p. MiR-211-5p inhibitor restored the effect of EGOT knockdown on the radiosensitivity of rectal cancer.
Conclusion:
Down-regulation of EGOT could inhibit the growth of rectal cancer cells by regulating the miR-211-5p/ErbB4 axis and improve the radiosensitivity of rectal cancer cells. EGOT may be a new therapeutic target for rectal cancer.
Insights
Down-regulating long non-coding RNA EGOT inhibits rectal cancer growth and enhances radiosensitivity by targeting the miR-211-5p/ErbB4 pathway. This suggests EGOT is a potential therapeutic target for rectal cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Long non-coding RNAs (lncRNAs) play a role in cancer progression and influence radiation therapy response.
- Rectal cancer radiosensitivity is a critical factor in treatment efficacy.
Purpose of the Study:
- To elucidate the mechanism of lncRNA EGOT in modulating radiosensitivity in rectal cancer.
- To investigate the potential of EGOT as a therapeutic target for rectal cancer.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot to assess gene and protein expression.
- Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) to confirm molecular interactions.
- Cell proliferation, invasion, migration, and apoptosis assays (MTT, colony formation, flow cytometry) following EGOT and miR-211-5p manipulation.
Main Results:
- EGOT expression was elevated in rectal cancer tissues and correlated with advanced pathological stages.
- EGOT knockdown suppressed rectal cancer cell proliferation and colony formation while inducing apoptosis.
- EGOT acts as a molecular sponge for miR-211-5p, leading to increased ErbB4 expression; miR-211-5p inhibition reversed the effects of EGOT knockdown on radiosensitivity.
Conclusions:
- Downregulation of EGOT inhibits rectal cancer cell growth and enhances radiosensitivity via the miR-211-5p/ErbB4 axis.
- EGOT represents a promising novel therapeutic target for improving rectal cancer treatment outcomes.
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