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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Therapy resistance in cancer leads to patient mortality.
  • Epithelial-to-mesenchymal transition (EMT) is linked to therapy resistance in various cancers.
  • Mechanisms underlying EMT-mediated therapy resistance are not fully understood.

Purpose of the Study:

  • To investigate the role of EMT in mediating resistance to anti-cancer therapies.
  • To identify the molecular mechanisms driving EMT-associated therapy resistance.
  • To explore RHOJ as a potential therapeutic target in resistant cancers.

Main Methods:

  • Utilized a mouse model of skin squamous cell carcinoma with spontaneous EMT.
  • Performed in vivo and in vitro gain and loss of function studies.
  • Conducted genome-wide transcriptomic and proteomic profiling.
  • Investigated RHOJ's interaction with nuclear actin regulatory proteins.

Main Results:

  • EMT tumor cells exhibited high resistance to multiple anti-cancer therapies.
  • RHOJ, a small GTPase highly expressed in EMT cancer cells, was identified as a key regulator of therapy resistance.
  • RHOJ enhances the response to replicative stress and activates DNA damage response pathways, facilitating chemotherapy resistance.
  • Inhibition of actin polymerization sensitized EMT cells to chemotherapy in a RHOJ-dependent manner.

Conclusions:

  • RHOJ is a critical regulator of EMT-associated chemotherapy resistance.
  • RHOJ promotes resistance by enhancing DNA repair mechanisms.
  • Targeting RHOJ or actin polymerization may overcome therapy resistance in EMT-positive cancers.