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  1. Home
  2. Cancer-associated Fibroblast-derived Exosomal Fam83f Regulates Kif23 Expression To Promote The Malignant Progression And Reduce Radiosensitivity In Non-small Cell Lung Cancer.
  1. Home
  2. Cancer-associated Fibroblast-derived Exosomal Fam83f Regulates Kif23 Expression To Promote The Malignant Progression And Reduce Radiosensitivity In Non-small Cell Lung Cancer.

Related Experiment Video

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
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Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

863

Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression

Yi Li1, Mingming Zhou2, Xiaogang Hu2

  • 1Department of Thoracic Surgery, Suining Central Hospital, Suining, 629099 China.

Cytotechnology
|January 27, 2025

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
Cancer-associated fibroblastsExosomesFAM83FKIF23NSCLC

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Cancer-associated fibroblasts (CAFs) promote non-small cell lung cancer (NSCLC) progression and radioresistance via exosomal transfer of FAM83F. Depleting FAM83F in CAF exosomes inhibits NSCLC growth and sensitizes tumors to radiotherapy.

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Cancer-associated fibroblasts (CAFs) are key players in the tumor microenvironment.
  • Exosomes mediate intercellular communication, influencing cancer progression.
  • CAF-derived exosomes' role in non-small cell lung cancer (NSCLC) requires further investigation.

Purpose of the Study:

  • To elucidate the mechanisms by which CAF-derived exosomes regulate NSCLC.
  • To investigate the role of FAM83F in CAF-mediated NSCLC progression and radioresistance.

Main Methods:

  • Analysis of FAM83F expression in NSCLC cells and CAF-conditioned medium.
  • Investigation of FAM83F transfer via CAF-derived exosomes.
  • Assessment of exosome function in vitro (proliferation, invasion, migration, radiosensitivity) and in vivo (tumor formation).
  • Exploration of FAM83F-KIF23 interaction in NSCLC cells.
  • Main Results:

    • CAFs promote NSCLC proliferation, invasion, migration, and radioresistance.
    • CAF-derived exosomes transfer FAM83F to NSCLC cells, enhancing malignancy.
    • FAM83F-deficient CAF exosomes inhibit NSCLC progression and sensitize cells to radiotherapy.
    • FAM83F interacts with KIF23, influencing exosome-induced effects.
    • FAM83F-deficient CAF exosomes suppressed tumor growth in vivo.

    Conclusions:

    • CAF-derived exosomal FAM83F is a critical driver of NSCLC progression and radioresistance.
    • Targeting the CAF exosome-FAM83F-KIF23 axis presents a potential therapeutic strategy for NSCLC.
    • Modulating CAF exosome content offers a novel approach to overcome NSCLC treatment resistance.