lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR‑145/p70S6K1 and p53 pathway

  • Authors:
    • Ming Wang
    • Liang Wang
    • Xiang He
    • Jinhua Zhang
    • Zhongcheng Zhu
    • Mingyun Zhang
    • Xingde Li
  • View Affiliations

  • Published online on: December 2, 2019     https://doi.org/10.3892/ijo.2019.4929
  • Pages: 327-336
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The long non‑coding RNA colon cancer‑associated transcript 2 (CCAT2) is abnormally expressed in various types of malignant tumor tissues and considered to be an oncogene, including for esophageal cancer (EC). Radiotherapy is an important and widely used cancer treatment. However, some patients with EC do not respond to radiotherapy. This study was designed to investigate effects of CCAT2 expression on radiotherapy dynamics for EC cells and to explore underlying molecular mechanisms. Reverse transcription‑quantitative PCR was used to measure CCAT2 expression in EC tissues, normal esophageal mucosa, EC cells and normal human esophageal epithelial cells. TUNEL assays were used to assess the effect of CCAT2 on X‑ray‑induced apoptosis of EC cells. Protein expression was detected by western blot. CCAT2 was highly expressed in EC tissues and EC cells, and was negatively associated with radiotherapy efficacy in patients with EC. In vitro, knockdown of CCAT2 enhanced radiosensitivity of EC cells and promoted apoptosis by increasing Bax/Bcl2 and active‑caspase 3/caspase 3 following X‑ray treatment. In addition, CCAT2 negatively regulated miR‑145 and P70 ribosomal protein S6 kinase 1 (p70S6K1) expression, and inhibited phosphorylation of Akt, ERK and p70S6K1 in EC cells. After X‑ray treatment, CCAT2 negatively regulated protein levels of p53, P21 and c‑Myc. These results showed that CCAT2 promoted the radiotherapy resistance of EC cells via negative regulation of the miR‑145/p70S6K1 and the p53 signaling pathways and associated elements may be potential targets for improving the sensitivity of EC radiotherapy.

Related Articles

Journal Cover

January 2020
Volume 56 Issue 1

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
APA
Wang, M., Wang, L., He, X., Zhang, J., Zhu, Z., Zhang, M., & Li, X. (2020). lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR‑145/p70S6K1 and p53 pathway. International Journal of Oncology, 56, 327-336. https://doi.org/10.3892/ijo.2019.4929
MLA
Wang, M., Wang, L., He, X., Zhang, J., Zhu, Z., Zhang, M., Li, X."lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR‑145/p70S6K1 and p53 pathway". International Journal of Oncology 56.1 (2020): 327-336.
Chicago
Wang, M., Wang, L., He, X., Zhang, J., Zhu, Z., Zhang, M., Li, X."lncRNA CCAT2 promotes radiotherapy resistance for human esophageal carcinoma cells via the miR‑145/p70S6K1 and p53 pathway". International Journal of Oncology 56, no. 1 (2020): 327-336. https://doi.org/10.3892/ijo.2019.4929