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Updated: Sep 5, 2025

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EV-Mediated Chemoresistance in the Tumor Microenvironment: Is NF-κB a Player?

Mauro Di Vito Nolfi1, Davide Vecchiotti1, Irene Flati1

  • 1Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L'Aquila, L'Aquila, Italy.

Frontiers in Oncology
|July 11, 2022
PubMed

Insights

Chemotherapy resistance in cancer is driven by communication between tumor cells and their environment. The NF-κB pathway and extracellular vesicles (EVs) create a cycle that promotes inflammation and drug resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Drug resistance is a primary cause of cancer therapy failure.
  • Chemotherapy can induce a defensive response in the tumor microenvironment (TME).
  • Cell-to-cell communication via extracellular vesicles (EVs) in the TME promotes tumor progression and therapy resistance.

Purpose of the Study:

  • To review the interplay between NF-κB signaling and EVs in sustaining chemoresistance within the TME.
  • To elucidate the molecular mechanisms driving inflammation, EVs release, and acquired drug resistance.

Main Methods:

  • Literature review focusing on NF-κB signaling.
  • Analysis of extracellular vesicle (EV) function in the tumor microenvironment (TME).
  • Examination of molecular pathways linking inflammation, EVs, and drug resistance.

Main Results:

  • NF-κB activation is implicated in both the release and response to EVs.
  • EVs carry factors that activate survival pathways and immune escape mechanisms.
  • The NF-κB/EVs axis contributes to sustained tumor progression and chemoresistance.

Conclusions:

  • The NF-κB and EVs interplay is a critical mechanism promoting chemoresistance in the TME.
  • Targeting this axis may offer novel therapeutic strategies against drug-resistant cancers.
  • Understanding these molecular mechanisms is key to overcoming treatment failure.
Keywords:
NF-κBdrug resistanceextracellular vesiclesinflammasometumor microenvironment

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