4.5 Article

LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4

Journal

ONCOTARGETS AND THERAPY
Volume 14, Issue -, Pages 2867-2878

Publisher

DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S256989

Keywords

EGOT; miR-211-5p; ErbB4; rectal cancer; radiosensitivity

Funding

  1. National Natural Science Foundation of China [81972196]
  2. National Key Research and Development Program of the Ministry of Science and Technology of China [2016YFC1303201, 2016YFC0905 300, 2018YFC1315000]
  3. Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences [2018PT32012]
  4. CAMS Innovation Fund for Medical Sciences (CIFMS) [2017-I2M-1-006, 2019-I2M-2-002]
  5. Beijing Hope Run Special Fund from Cancer Foundation of China [LC2017A19]

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This study revealed that EGOT was up-regulated in rectal cancer tissues and cells, and its knockdown inhibited proliferation, colony formation, and induced apoptosis of rectal cancer cells. Additionally, down-regulation of EGOT improved the radiosensitivity of rectal cancer cells by regulating the miR-211-5p/ErbB4 axis. EGOT may serve as a potential therapeutic target for rectal cancer.
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.

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