SOX2 in cancer stemness: tumor malignancy and therapeutic potentials.

Abstract

Cancer stem cells (CSCs), a minor subpopulation of tumor bulks with self-renewal and seeding capacity to generate new tumors, posit a significant challenge to develop effective and long-lasting anti-cancer therapies. The emergence of drug resistance appears upon failure of chemo-/radiation therapy to eradicate the CSCs, thereby leading to CSC-mediated clinical relapse. Accumulating evidence suggests that transcription factor SOX2, a master regulator of embryonic and induced pluripotent stem cells, drives cancer stemness, fuels tumor initiation, and contributes to tumor aggressiveness through major drug resistance mechanisms like epithelial-to-mesenchymal transition, ATP-binding cassette drug transporters, anti-apoptotic and/or pro-survival signaling, lineage plasticity, and evasion of immune surveillance. Gaining a better insight and comprehensive interrogation into the mechanistic basis of SOX2-mediated generation of CSCs and treatment failure might therefore lead to new therapeutic targets involving CSC-specific anti-cancer strategies.

• Authors: Mahfuz Al Mamun, Kaiissar Mannoor, Jun Cao, Firdausi Qadri, Xiaoyuan Song
• Journal: Journal of molecular cell biology (J Mol Cell Biol) Vol. 12 Issue 2 Pg. 85-98 (02 20 2020) ISSN: 1759-4685 [Electronic] United States
• PMID: 30517668 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © The Author(s) (2019). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS.

Chemical References

• Antineoplastic Agents
• SOX2 protein, human
• SOXB1 Transcription Factors

Topics

• Antineoplastic Agents (pharmacology)
• Drug Resistance, Neoplasm
• Epithelial-Mesenchymal Transition
• Gene Expression Regulation, Neoplastic
• Humans
• Molecular Targeted Therapy (methods)
• Neoplasms (drug therapy, genetics, metabolism)
• Neoplastic Stem Cells (metabolism)
• SOXB1 Transcription Factors (antagonists & inhibitors, genetics, metabolism)
• Signal Transduction
• Tumor Escape