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      MUC3A promotes the progression of colorectal cancer through the PI3K/Akt/mTOR pathway

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          Abstract

          Mucin 3A (MUC3A) is overexpressed in colorectal cancer (CRC) and associated with poor prognosis, but the related mechanism remains unclear. Our study found that MUC3A promotes the progression of CRC by activating the PI3K/Akt/mTOR signaling pathway. Knockout of MUC3A significantly inhibited the proliferation of CRC cells and induced G1 phase arrest by upregulating p21 protein, an important cell cycle regulator. Moreover, knockout of MUC3A significantly inhibited invasion ability and enhanced the sensitivity to the chemotherapeutic agent 5-FU. Furthermore, we found that knockout of MUC3A repressed the PI3K/Akt/mTOR pathway through RNA-seq. Treatment with the PI3K/Akt/mTOR pathway inhibitor rapamycin successfully eliminated the difference in proliferation, invasion and chemoresistance between MUC3A knockout cells and control cells. Our study suggests that MUC3A is a potential oncogene that promotes the proliferation, invasion, and chemotherapy resistance of CRC. Moreover, CRC patients with high expression of MUC3A may benefit from rapamycin treatment. 

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          The online version contains supplementary material available at 10.1186/s12885-022-09709-8.

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          PI3K/Akt/mTOR inhibitors in cancer: At the bench and bedside

          Ali Alzahrani (2019)
          Article 0 comments Cited 352 times – based on 0 reviews     Review now
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            Rapamycin passes the torch: a new generation of mTOR inhibitors.

            Don Benjamin, Marco Colombi, Christoph Moroni … (2011)
            Mammalian target of rapamycin (mTOR) is an atypical protein kinase that controls growth and metabolism in response to nutrients, growth factors and cellular energy levels, and it is frequently dysregulated in cancer and metabolic disorders. Rapamycin is an allosteric inhibitor of mTOR, and was approved as an immuno-suppressant in 1999. In recent years, interest has focused on its potential as an anticancer drug. However, the performance of rapamycin and its analogues (rapalogues) has been undistinguished despite isolated successes in subsets of cancer, suggesting that the full therapeutic potential of targeting mTOR has yet to be exploited. A new generation of ATP-competitive inhibitors that directly target the mTOR catalytic site display potent and comprehensive mTOR inhibition and are in early clinical trials.
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              Targeting mTOR for cancer therapy

              Hui Hua, Qingbin Kong, Hongying Zhang … (2019)
              Mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. mTOR is usually assembled into several complexes such as mTOR complex 1/2 (mTORC1/2). In cooperation with raptor, rictor, LST8, and mSin1, key components in mTORC1 or mTORC2, mTOR catalyzes the phosphorylation of multiple targets such as ribosomal protein S6 kinase β-1 (S6K1), eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), Akt, protein kinase C (PKC), and type-I insulin-like growth factor receptor (IGF-IR), thereby regulating protein synthesis, nutrients metabolism, growth factor signaling, cell growth, and migration. Activation of mTOR promotes tumor growth and metastasis. Many mTOR inhibitors have been developed to treat cancer. While some of the mTOR inhibitors have been approved to treat human cancer, more mTOR inhibitors are being evaluated in clinical trials. Here, we update recent advances in exploring mTOR signaling and the development of mTOR inhibitors for cancer therapy. In addition, we discuss the mechanisms underlying the resistance to mTOR inhibitors in cancer cells.
              Article 0 comments Cited 331 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Minghua Yu: minghua_md@fudan.edu.cn
                Journal
                Journal ID (nlm-ta): BMC Cancer
                Journal ID (iso-abbrev): BMC Cancer
                Title: BMC Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2407
                Publication date (Electronic): 2 June 2022
                Publication date PMC-release: 2 June 2022
                Publication date Collection: 2022
                Volume: 22
                Electronic Location Identifier: 602
                Affiliations
                GRID grid.477929.6, Department of Oncology, , Fudan University Pudong Medical Center, Shanghai Pudong Hospital, ; 2800 Gongwei Road, Shanghai, 201399 China
                Article
                Publisher ID: 9709
                DOI: 10.1186/s12885-022-09709-8
                PMC ID: 9161576
                PubMed ID: 35655161
                SO-VID: db67e930-e796-4bf2-9e4d-ebb52152da7c
                Copyright © © The Author(s) 2022
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 16 February 2022
                Date accepted : 27 May 2022
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: muc3a,colorectal cancer,pi3k,akt,mtor pathway,cell cycle,cancer progression
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: muc3a, colorectal cancer, pi3k, akt, mtor pathway, cell cycle, cancer progression

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