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. 2021 Oct 22;11:761379. doi: 10.3389/fonc.2021.761379

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Copyright © 2021 Cheng, Li, Gao, Zhi and Ren

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TME and cisplatin resistance in OSCC. TME is typically characterized by hypoxia and immunosuppression. Hypoxia induces HIF-1α-mediated signaling cascades, including induction of VEGF expression to promote tumor angiogenesis in hypoxic conditions and inhibition of apoptosis by regulating the expression of Bcl-2 anti-apoptotic family. In addition, a large number of cellular factors released by cancer cells and various bystander cells cause immune evasion by regulating the production and function of immune cells. Overall, the above pathways contribute to the cisplatin resistance of OSCC.