Tumor microenvironment-driven non-cell-autonomous resistance to antineoplastic treatment

Yidi Qu, Bo Dou, Horyue Tan, Yibin Feng*, Ning Wang*, Di Wang*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

71 Citations (Scopus)

Abstract

Drug resistance is of great concern in cancer treatment because most effective drugs are limited by the development of resistance following some periods of therapeutic administration. The tumor microenvironment (TME), which includes various types of cells and extracellular components, mediates tumor progression and affects treatment efficacy. TME-mediated drug resistance is associated with tumor cells and their pericellular matrix. Noninherent-adaptive drug resistance refers to a non-cell-autonomous mechanism in which the resistance lies in the treatment process rather than genetic or epigenetic changes, and this mechanism is closely related to the TME. A new concept is therefore proposed in which tumor cell resistance to targeted therapy may be due to non-cell-autonomous mechanisms. However, knowledge of non-cell-autonomous mechanisms of resistance to different treatments is not comprehensive. In this review, we outlined TME factors and molecular events involved in the regulation of non-cell-autonomous resistance of cancer, summarized how the TME contributes to non-cell-autonomous drug resistance in different types of antineoplastic treatment, and discussed the novel strategies to investigate and overcome the non-cell-autonomous mechanism of cancer non-cell-autonomous resistance.

Original languageEnglish
Article number69
Number of pages16
JournalMolecular Cancer
Volume18
DOIs
Publication statusPublished - 30 Mar 2019

Scopus Subject Areas

  • Molecular Medicine
  • Oncology
  • Cancer Research

User-Defined Keywords

  • Tumor
  • Non-cell-autonomous drug resistance
  • Tumor microenvironment
  • Drug resistance

Fingerprint

Dive into the research topics of 'Tumor microenvironment-driven non-cell-autonomous resistance to antineoplastic treatment'. Together they form a unique fingerprint.

Cite this