Literature DB >> 35083552

Regulatory effects of lncRNAs and miRNAs on the crosstalk between autophagy and EMT in cancer: a new era for cancer treatment.

Lihui Si1, Zecheng Yang2, Lu Ding3, Duoduo Zhang4.   

Abstract

PURPOSE: Autophagy and EMT (epithelial-mesenchymal transition) are the two principal biological processes and ideal therapeutic targets during cancer development. Autophagy, a highly conserved process for degrading dysfunctional cellular components, plays a dual role in tumors depending on the tumor stage and tissue types. The EMT process is the transition differentiation from an epithelial cell to a mesenchymal-like cell and acquiring metastatic potential. There is evidence that the crosstalk between autophagy and EMT is complex in cancer. In recent years, more studies have shown that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are involved in autophagy, EMT, and their crosstalk. Therefore, accurate understanding of the regulatory mechanisms of lncRNAs and miRNAs in autophagy, EMT and their interactions is crucial for the clinical management of cancers.
METHODS: An extensive literature search was conducted on the Google Scholar and PubMed databases. The keywords used for the search included: autophagy, EMT, crosstalk, lncRNAs, miRNAs, cancers, diagnostic biomarkers, and therapeutic targets. This search provided relevant articles published in peer-reviewed journals until 2021. Data from these various studies were extracted and used in this review.
RESULTS: The results showed that lncRNAs/miRNAs as tumor inhibitors or tumor inducers could regulate autophagy, EMT, and their interaction by regulating several molecular signaling pathways. The lncRNAs/miRNAs involved in autophagy and EMT processes could have potential uses in cancer diagnosis, prognosis, and therapy.
CONCLUSION: Such information could help find and develop lncRNAs/miRNAs based new tools for diagnosing, prognosis, and creating anti-cancer therapies.
© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Entities:  

Keywords:  Autophagy; Cancer; EMT; LncRNAs; MiRNAs

Mesh:

Substances:

Year:  2022        PMID: 35083552     DOI: 10.1007/s00432-021-03892-0

Source DB:  PubMed          Journal:  J Cancer Res Clin Oncol        ISSN: 0171-5216            Impact factor:   4.553


  142 in total

Review 1.  Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease.

Authors:  Hervé Acloque; Meghan S Adams; Katherine Fishwick; Marianne Bronner-Fraser; M Angela Nieto
Journal:  J Clin Invest       Date:  2009-06-01       Impact factor: 14.808

2.  EMT in cancer.

Authors:  Thomas Brabletz; Raghu Kalluri; M Angela Nieto; Robert A Weinberg
Journal:  Nat Rev Cancer       Date:  2018-01-12       Impact factor: 60.716

Review 3.  Targeting noncoding RNAs in disease.

Authors:  Brian D Adams; Christine Parsons; Lisa Walker; Wen Cai Zhang; Frank J Slack
Journal:  J Clin Invest       Date:  2017-03-01       Impact factor: 14.808

4.  Upholding a role for EMT in pancreatic cancer metastasis.

Authors:  Nicole M Aiello; Thomas Brabletz; Yibin Kang; M Angela Nieto; Robert A Weinberg; Ben Z Stanger
Journal:  Nature       Date:  2017-07-05       Impact factor: 49.962

5.  SQSTM1/p62 regulates the expression of junctional proteins through epithelial-mesenchymal transition factors.

Authors:  Matthieu Bertrand; Valérie Petit; Ashish Jain; Raymonde Amsellem; Terje Johansen; Lionel Larue; Patrice Codogno; Isabelle Beau
Journal:  Cell Cycle       Date:  2015       Impact factor: 4.534

6.  Autophagy induction impairs migration and invasion by reversing EMT in glioblastoma cells.

Authors:  Myriam Catalano; Giuseppina D'Alessandro; Francesca Lepore; Marco Corazzari; Sara Caldarola; Cristina Valacca; Fiorella Faienza; Vincenzo Esposito; Cristina Limatola; Francesco Cecconi; Sabrina Di Bartolomeo
Journal:  Mol Oncol       Date:  2015-05-13       Impact factor: 6.603

7.  Inhibition of the PI3K/AKT/mTOR pathway activates autophagy and compensatory Ras/Raf/MEK/ERK signalling in prostate cancer.

Authors:  Dominika E Butler; Christopher Marlein; Hannah F Walker; Fiona M Frame; Vincent M Mann; Matthew S Simms; Barry R Davies; Anne T Collins; Norman J Maitland
Journal:  Oncotarget       Date:  2017-05-23

Review 8.  LncRNAs as Regulators of Autophagy and Drug Resistance in Colorectal Cancer.

Authors:  Mercedes Bermúdez; Maribel Aguilar-Medina; Erik Lizárraga-Verdugo; Mariana Avendaño-Félix; Erika Silva-Benítez; Cesar López-Camarillo; Rosalío Ramos-Payán
Journal:  Front Oncol       Date:  2019-10-02       Impact factor: 6.244

9.  miR-506 regulates epithelial mesenchymal transition in breast cancer cell lines.

Authors:  Himanshu Arora; Rehana Qureshi; Woong-Yang Park
Journal:  PLoS One       Date:  2013-05-22       Impact factor: 3.240

Review 10.  Recent insights into the function of autophagy in cancer.

Authors:  Ravi Amaravadi; Alec C Kimmelman; Eileen White
Journal:  Genes Dev       Date:  2016-09-01       Impact factor: 11.361

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  4 in total

Review 1.  Context-Dependent Regulation of Gene Expression by Non-Canonical Small RNAs.

Authors:  Kinga Plawgo; Katarzyna Dorota Raczynska
Journal:  Noncoding RNA       Date:  2022-04-29

2.  GABPB1-AS1 Promotes the Development of Osteosarcoma by Targeting SP1 and Activating the Wnt/β-Catenin Pathway.

Authors:  Jingyang Chen; Meiru Bian; Lingxiao Pan; Chengdong Liu; Hanshi Yang
Journal:  J Oncol       Date:  2022-03-18       Impact factor: 4.375

3.  HOTTIP Mediated Therapy Resistance in Glioma Cells Involves Regulation of EMT-Related miR-10b.

Authors:  Zhang Li; Ming Li; Pengcheng Xia; Zhiming Lu
Journal:  Front Oncol       Date:  2022-03-24       Impact factor: 6.244

4.  Regulation of Let-7a-5p and miR-199a-5p Expression by Akt1 Modulates Prostate Cancer Epithelial-to-Mesenchymal Transition via the Transforming Growth Factor-β Pathway.

Authors:  Abdulrahman Alwhaibi; Varun Parvathagiri; Arti Verma; Sandeep Artham; Mir S Adil; Payaningal R Somanath
Journal:  Cancers (Basel)       Date:  2022-03-23       Impact factor: 6.639

  4 in total

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