Skip to main content

microRNAs-Mediated Regulation of Voltage Gated Anion Channel 1, a Major Player in ROS Generation and Cancer Progression

  • Living reference work entry
  • First Online:
Handbook of Oxidative Stress in Cancer: Therapeutic Aspects
  • 21 Accesses

Abstract

Cancer cells show elevated level of mitochondrial reactive species (mROS) generation. Voltage-dependent anion channel 1(VDAC1), an outer mitochondrial membrane (OMM) protein plays significant role in mitochondrial energy production as well as in metabolism. VDAC1 has been shown to influence the metastatic potential of cancer cells via production of mROS. Therefore, the regulation of VDAC1 expression seems an attractive area of research in cancer biology. Recent researches show that microRNA plays important roles in cancer metastasis by regulating expression of different proteins. In this context regulation of VDAC1 by microRNAs could be an attractive strategy as a therapeutic approach in cancer biology. Therefore, herein, we discuss the tumor suppressor role of several microRNAs in controlling the cancer progression network by targeting VDAC1 expression.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Institutional subscriptions

Similar content being viewed by others

References

  • Bargaje R, Gupta S, Sarkeshik A, Park R, Xu T, Sarkar M, Halimani M, Sinha S, Roy J, Yates J, Pillai B (2012) Identification of novel targets for miR-29a using miRNA proteomics. PLoS One 7(8):e43243

    Article  CAS  Google Scholar 

  • Caterino M, Ruoppolo M, Mandola A, Costanzo M, Orrù S, Imperlini E (2017) Protein-protein interaction networks as a new perspective to evaluate distinct functional roles of voltage-dependent anion channel isoforms. Mol BioSyst 13(12):2466–2476

    Article  CAS  Google Scholar 

  • Chaudhuri AD, Choi DC, Kabaria S, Tran A, Junn E (2016) MicroRNA-7 regulates the function of mitochondrial permeability transition pore by targeting VDAC1 expression. J Biol Chem 291(12):6483–6493

    Article  CAS  Google Scholar 

  • DeHart DN, Fang D, Heslop K, Li L, Lemasters JJ, Maldonado EN (2018) Opening of voltage dependent anion channels promotes reactive oxygen species generation, mitochondrial dysfunction and cell death in cancer cells. Biochem Pharmacol 148:155–162

    Article  CAS  Google Scholar 

  • Ghildiyal M, Zamore PD (2009) Small silencing RNAs: an expanding universe. Nat Rev Genet 10:94–108

    Article  CAS  Google Scholar 

  • Grills C, Jithesh PV, Blayney J, Zhang S-D, Fennell DA (2011) Gene expression meta-analysis identifies VDAC1 as a predictor of poor outcome in early stage non-small cell lung cancer. PLoS One 6(1):e14635

    Article  CAS  Google Scholar 

  • Huang Q, Ma B, Su Y, Chan K, Qu H, Huang J, Wang D, Qiu J, Liu H, Yang X, Wang Z (2020) miR-197-3p represses the proliferation of prostate cancer by regulating the VDAC1/AKT/β-catenin signaling axis. Int J Biol Sci 16(8):1417–1426

    Article  CAS  Google Scholar 

  • Huntzinger E, Izaurralde E (2011) Gene silencing by microRNAs: contributions of translational repression and mRNA decay. Nat Rev Genet 12:99–110

    Article  CAS  Google Scholar 

  • Ishizu H, Siomi H, Siomi MC (2012) Biology of PIWI-interacting RNAs: new insights into biogenesis and function inside and outside of germlines. Genes Dev 26:2361–2373

    Article  CAS  Google Scholar 

  • Kasinski AL, Slack FJ (2011) MicroRNAs en route to the clinic: progress in validating and targeting microRNAs for cancer therapy. Nat Rev Cancer 11:849–864

    Article  CAS  Google Scholar 

  • Li QQ, Zhang L, Wan HY, Liu M, Li X, Tang H (2015) CREB1-driven expression of miR-320a promotes mitophagy by down-regulating VDAC1 expression during serum starvation in cervical cancer cells. Oncotarget 6(33):34924–34940

    Article  Google Scholar 

  • Lin S, Gregory RI (2015) MicroRNA biogenesis pathways in cancer. Nat Rev Cancer 15:321–333

    Article  CAS  Google Scholar 

  • Liu X, He B, Xu T, Pan Y, Hu X, Chen X, Wang S (2018) MiR-490-3p functions as a tumor suppressor by inhibiting oncogene VDAC1 expression in colorectal cancer. J Cancer 9(7):1218–1230

    Article  Google Scholar 

  • Liu N, Li Y, Nan W, Zhou W, Huang J, Li R, Zhou L, Hu R (2020) Interaction of TPPP3 with VDAC1 promotes endothelial injury through activation of reactive oxygen species. Oxidative Med Cell Longev 2020:5950195

    Google Scholar 

  • Lujambio A, Lowe SW (2012) The microcosmos of cancer. Nature 482:347–355

    Article  CAS  Google Scholar 

  • Magrì A, Reina S, De Pinto V (2018) VDAC1 as pharmacological target in cancer and neurodegeneration: focus on its role in apoptosis. Front Chem 6:108

    Article  Google Scholar 

  • Messina A, Reina S, Guarino F, De Pinto V (2012) VDAC isoforms in mammals. Biochim Biophys Acts 1818(6):1466–1476

    Article  CAS  Google Scholar 

  • Pittala S, Krelin Y, Shoshan-Barmatz V (2018) Targeting liver cancer and associated pathologies in mice with a mitochondrial VDAC1-based peptide. Neoplasia 20(6):594–609

    Article  CAS  Google Scholar 

  • Price C, Chen J (2014) MicroRNAs in cancer biology and therapy: current status and perspectives. Genes Dis 1:53–63

    Article  Google Scholar 

  • Sampson MJ, Lovell RS, Craigen WJ (1997) The murine voltage-dependent anion channel gene family. Conserved structure and function. J Biol Chem 272(30):18966–18973

    Article  CAS  Google Scholar 

  • Shoshan-Barmatz V, Ben-Hail D (2012) VDAC, a multi-functional mitochondrial protein as a pharmacological target. Mitochondrion 12(1):24–34

    Article  CAS  Google Scholar 

  • Shoshan-Barmatz V, De Pinto V, Zweckstetter M, Raviv Z, Keinan N, Arbel N (2010) VDAC, a multi-functional mitochondrial protein regulating cell life and death. Mol Asp Med 31(3):227–285

    Article  CAS  Google Scholar 

  • Shoshan-Barmatz V, Ben-Hail D, Admoni L, Krelin Y, Tripathi SS (2015) The mitochondrial voltage-dependent anion channel 1 in tumor cells. Biochim Biophys Acta 1848(10 Pt B):2547–2575

    Article  CAS  Google Scholar 

  • Sullivan LB, Chandel NS (2014) Mitochondrial reactive oxygen species and cancer. Cancer Metab 2:17. https://doi.org/10.1186/2049-3002-2-17

    Article  PubMed  PubMed Central  Google Scholar 

  • Wang F, Qiang Y, Zhu L, Jiang Y, Wang Y, Shao X, Yin L, Chen J, Chen Z (2016) MicroRNA-7 downregulates the oncogene VDAC1 to influence hepatocellular carcinoma proliferation and metastasis. Tumour Biol 37(8):10235–10246

    Article  CAS  Google Scholar 

  • Wu C-H, Lin Y-W, Wu T-F, Ko J-L, Wang P-H (2016) Clinical implication of voltage-dependent anion channel 1 in uterine cervical cancer and its action on cervical cancer cells. Oncotarget 7(4):4210–4225

    Article  Google Scholar 

  • Yang G, Zhou D, Li J, Wang W, Zhong W, Fan W, Yu M, Cheng H (2019) VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer. Oncol Lett 18(3):2340–2347

    CAS  PubMed  PubMed Central  Google Scholar 

  • Zhang G, Jiang G, Wang C, Zhong K, Zhang J, Xue Q, Li X, Jin H, Li B (2016) Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression. Oncotarget 7(31):49470–49480

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Kuntal Dey .

Editor information

Editors and Affiliations

Section Editor information

Rights and permissions

Reprints and permissions

Copyright information

© 2022 Springer Nature Singapore Pte Ltd.

About this entry

Check for updates. Verify currency and authenticity via CrossMark

Cite this entry

Dey, K., De, S. (2022). microRNAs-Mediated Regulation of Voltage Gated Anion Channel 1, a Major Player in ROS Generation and Cancer Progression. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-1247-3_72-1

Download citation

  • DOI: https://doi.org/10.1007/978-981-16-1247-3_72-1

  • Received:

  • Accepted:

  • Published:

  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-16-1247-3

  • Online ISBN: 978-981-16-1247-3

  • eBook Packages: Springer Reference Biomedicine and Life SciencesReference Module Biomedical and Life Sciences

Publish with us

Policies and ethics