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βIII-tubulin overexpression in cancer: Causes, consequences, and potential therapies

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ELSEVIER
DOI: 10.1016/j.bbcan.2021.188607

Keywords

Class III beta-tubulin; Microtubule-targeting agents; Drug resistance; Paclitaxel; Vinca alkaloids; Colchicine; Tumor aggressiveness

Funding

  1. Foundation for Women's Cancer Genentech Ovarian Cancer Young Investigator Career Development Award
  2. Wallace and Evelyn Simmers Career Development Award for Ovarian Cancer Research
  3. Mayo Clinic Ovarian Cancer SPORE Developmental Award
  4. Mayo Clinic Ovarian Cancer SPORE Career Enhancement Award
  5. Cancer Society of New Zealand
  6. Wellington Medical Research Foundation

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Understanding the regulation of beta III-tubulin expression and its functions in different cancers is crucial for assessing its prognostic value and developing therapeutic strategies. Targeting tumors overexpressing beta III-tubulin with emerging therapeutic strategies is a key focus of current research.
Class III beta-tubulin (beta III-tubulin) is frequently overexpressed in human tumors and is associated with resistance to microtubule-targeting agents, tumor aggressiveness, and poor patient outcome. Understanding the mechanisms regulating beta III-tubulin expression and the varied functions beta III-tubulin may have in different cancers is vital to assess the prognostic value of this protein and to develop strategies to enhance therapeutic benefits in beta III-tubulin overexpressing tumors. Here we gather all the available evidence regarding the clinical implications of beta III-tubulin overexpression in cancer, describe factors that regulate beta III-tubulin expression, and discuss current understanding of the mechanisms underlying beta III-tubulin-mediated resistance to microtubule-targeting agents and tumor aggressiveness. Finally, we provide an overview of emerging therapeutic strategies to target tumors that overexpress beta III-tubulin.

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