Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway

Colorectal cancer (CRC) has not only seriously affected people's lives, but also burdened the government healthcare system. Long non-coding RNAs (lncRNA) have attracted more and more attention in the cancer study field. Experiments were completed in the Medical Research and Innovation Center of...

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Veröffentlicht in:Iranian journal of public health 2022-02, Vol.51 (2), p.327-335
Hauptverfasser: Zhuang, Biao, Ni, Xiong, Min, Zhijun, Wu, Dejun, Wang, Tingfeng, Cui, Peng
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Sprache:eng
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Zusammenfassung:Colorectal cancer (CRC) has not only seriously affected people's lives, but also burdened the government healthcare system. Long non-coding RNAs (lncRNA) have attracted more and more attention in the cancer study field. Experiments were completed in the Medical Research and Innovation Center of Shanghai Pudong Hospital, China from 2019 to 2020. Cell cycle was detected by western blot analyzing and flow cytometry. Apoptosis analysis were determined using flow cytometry or western blot analysis. LncRNA was knocked down by shRNA transfection. We found was the most significant=0.0105 for SW480 and =0.0071 for HCT116) difference lncRNA between colorectal cancer treated with autophagy inducer and colorectal cancer without any treatment. Effective shRNA- was also designed. Following, we found the treatment of autophagy inducer and autophagy inducer + shRNA-NC were able to suppress the proliferation of both SW480 and HCT116 cells. In addition, the treatment of autophagy inducer + shRNA- significantly reduced the apoptosis of SW480 and HCT116 cells induced by autophagy. Furthermore, we found the phosphorylation of mTOR, AKT was enhanced in SW480, and HCT116 cells treated with autophagy inducer + shRNA- compared to the cells treated with autophagy inducer of autophagy inducer + shRNA-NC. Enhancing the expression of will become a promising strategy to prevent the progress of colorectal cancer.
ISSN:2251-6085
2251-6093
2251-6093
DOI:10.18502/ijph.v51i2.8685