NDFIP1 limits cellular TAZ accumulation via exosomal sorting to inhibit NSCLC proliferation

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Yirui Cheng1, Xin Lu1, Fan Li1

  • 1State Key Laboratory of Oncogenes and Related Genes, Ren Ji Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.

Protein & Cell
|March 17, 2023
PubMed

Insights

NDFIP1 acts as a tumor suppressor in non-small cell lung cancer (NSCLC) by regulating the oncogenic protein TAZ. NDFIP1 promotes TAZ exosome secretion, inhibiting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • NDFIP1 is a known tumor suppressor, but its role in non-small cell lung cancer (NSCLC) is unclear.
  • NDFIP1 interacts with WW domain-containing proteins, facilitating their exosome loading.
  • The function of WWTR1 (TAZ) in NSCLC and its regulation by NDFIP1 via exosomes remain uninvestigated.

Purpose of the Study:

  • To investigate the role of NDFIP1 in NSCLC.
  • To elucidate the mechanism by which NDFIP1 regulates the oncogenic protein TAZ.
  • To determine if NDFIP1-mediated TAZ exosome secretion affects tumor development.

Main Methods:

  • Quantitative analysis of NDFIP1 expression in NSCLC samples and cell lines.
  • Co-immunoprecipitation to confirm TAZ-NDFIP1 interaction.
  • Exosome isolation and analysis of TAZ presence.
  • CRISPR-Cas9 knockout of NDFIP1.
  • In vitro and in vivo proliferation assays.
  • Western blotting to assess protein levels and degradation.
  • Correlation analysis in xenograft models and clinical samples.

Main Results:

  • NDFIP1 expression is downregulated in NSCLC and correlates with shorter overall survival (OS).
  • NDFIP1 interacts with TAZ, and NDFIP1 is required for TAZ packaging into exosomes.
  • NDFIP1 knockout causes TAZ accumulation without affecting mRNA levels or degradation rate.
  • Exosome secretion influences cellular TAZ levels.
  • NDFIP1 inhibits NSCLC proliferation in vitro and in vivo.
  • Silencing TAZ rescues the proliferation increase caused by NDFIP1 knockout.
  • TAZ is negatively correlated with NDFIP1 in tumors, and serum exosomal TAZ is lower in NSCLC patients.

Conclusions:

  • NDFIP1 functions as a tumor suppressor in NSCLC.
  • NDFIP1 regulates TAZ stability and promotes its secretion via exosomes.
  • This NDFIP1-mediated exosome pathway represents a novel regulatory mechanism for TAZ in NSCLC progression.
Keywords:
NDFIP1NSCLCTAZcargo sortingexosome

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