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Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway
BACKGROUND: 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. METHODS: Experiments were completed in the Medical Research and Inno...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Tehran University of Medical Sciences
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9273497/ https://www.ncbi.nlm.nih.gov/pubmed/35866106 http://dx.doi.org/10.18502/ijph.v51i2.8685 |
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author | Zhuang, Biao Ni, Xiong Min, Zhijun Wu, Dejun Wang, Tingfeng Cui, Peng |
author_facet | Zhuang, Biao Ni, Xiong Min, Zhijun Wu, Dejun Wang, Tingfeng Cui, Peng |
author_sort | Zhuang, Biao |
collection | PubMed |
description | BACKGROUND: 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. METHODS: 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 CKMT2-AS1 was knocked down by shRNA transfection. RESULTS: We found CKMT2-AS1 was the most significant=0.0105 for SW480 and P=0.0071 for HCT116) difference lncRNA between colorectal cancer treated with autophagy inducer and colorectal cancer without any treatment. Effective shRNA-CKMT2-AS1 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-CKMT2-AS1 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-CKMT2-AS1 compared to the cells treated with autophagy inducer of autophagy inducer + shRNA-NC. CONCLUSION: Enhancing the expression of CKMT2-AS1 will become a promising strategy to prevent the progress of colorectal cancer. |
format | Online Article Text |
id | pubmed-9273497 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Tehran University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-92734972022-07-20 Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway Zhuang, Biao Ni, Xiong Min, Zhijun Wu, Dejun Wang, Tingfeng Cui, Peng Iran J Public Health Original Article BACKGROUND: 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. METHODS: 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 CKMT2-AS1 was knocked down by shRNA transfection. RESULTS: We found CKMT2-AS1 was the most significant=0.0105 for SW480 and P=0.0071 for HCT116) difference lncRNA between colorectal cancer treated with autophagy inducer and colorectal cancer without any treatment. Effective shRNA-CKMT2-AS1 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-CKMT2-AS1 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-CKMT2-AS1 compared to the cells treated with autophagy inducer of autophagy inducer + shRNA-NC. CONCLUSION: Enhancing the expression of CKMT2-AS1 will become a promising strategy to prevent the progress of colorectal cancer. Tehran University of Medical Sciences 2022-02 /pmc/articles/PMC9273497/ /pubmed/35866106 http://dx.doi.org/10.18502/ijph.v51i2.8685 Text en Copyright © 2022 Zhuang et al. Published by Tehran University of Medical Sciences https://creativecommons.org/licenses/by-nc/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International license (https://creativecommons.org/licenses/by-nc/4.0/). Non-commercial uses of the work are permitted, provided the original work is properly cited. |
spellingShingle | Original Article Zhuang, Biao Ni, Xiong Min, Zhijun Wu, Dejun Wang, Tingfeng Cui, Peng Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title | Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title_full | Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title_fullStr | Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title_full_unstemmed | Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title_short | Long Non-Coding RNA CKMT2-AS1 Reduces the Viability of Colorectal Cancer Cells by Targeting AKT/mTOR Signaling Pathway |
title_sort | long non-coding rna ckmt2-as1 reduces the viability of colorectal cancer cells by targeting akt/mtor signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9273497/ https://www.ncbi.nlm.nih.gov/pubmed/35866106 http://dx.doi.org/10.18502/ijph.v51i2.8685 |
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