Language

English

Publication Date

7-1-2025

Journal

Oncogene

DOI

10.1038/s41388-025-03360-w

PMID

40189704

PMCID

PMC12167707

PubMedCentral® Posted Date

4-6-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Lung cancer continues to be the leading cause of cancer-related deaths globally. Unraveling the regulators behind lung cancer growth and its metastatic spread, along with understanding the underlying mechanisms, is crucial for developing novel and effective therapeutic strategies. While much research has focused on identifying potential oncogenes or tumor suppressors, the roles of certain genes can vary depending on the context and may even exhibit contradictory effects. In this study, we demonstrate that acyl-CoA binding domain containing 3 (ACBD3), a Golgi resident protein, promotes primary lung cancer growth by recruiting phosphatidylinositol (PI)-4-kinase IIIβ (PI4KB) to the Golgi, thereby enhancing oncogenic secretion in chromosome 1q-amplified lung cancer cells. Conversely, in chromosome 1q-diploid lung cancer cells, ACBD3 acts as a suppressor of lung cancer metastasis by inhibiting the NOTCH signaling pathway and reducing cancer cell motility. This highlights the intricacy of cancer progression and cautions against simplistic approaches targeting individual oncogenes for cancer therapy.

Keywords

Humans, Lung Neoplasms, Carcinoma, Non-Small-Cell Lung, Neoplasm Metastasis, Cell Proliferation, Cell Movement, Animals, Cell Line, Tumor, Membrane Proteins, Signal Transduction, Mice, Adaptor Proteins, Signal Transducing, Receptors, Notch, Golgi Apparatus

Published Open-Access

yes

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