ArticleCell death discovery2025
NDR2 regulates non-small cell lung cancer cell migration under starvation by supporting autophagosome biogenesis through LC3 and ATG9A regulation.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Integrative multi-omics analysis identifies LIPA as a prognostic hub and ferroptosis regulator in lung adenocarcinoma.Molecular and cellular biochemistry · 2026Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is characterized by the deregulation of the Hippo kinase NDR2 and high basal autophagic activity. NDR2 promotes autophagy-driven tumor growth in some cancers, but evidence in lung cancer is lacking. Human bronchial epithelial tumor cell (HBEC) lines H2030, H2030-BrM3, and H1299, with or without NDR2 depletion via siRNA or shRNA, were cultured for up to 24 h in the presence or absence of serum, and with or without the autophagosome-lysosome fusion inhibitor chloroquine (CQ). Autophagosome biogenesis, migration and Golgi apparatus functionality were analyzed. Serum deprivation of HBECs silences the expression of NDR1 but not NDR2. As shown by the increased expression of the autophagosome marker LC3-II, NDR2 participates to the formation and distribution of phagophores/autophagosomes in HBECs in an ATG9A-dependent manner. NDR2 is required for cargos degradation since its depletion disrupts lysosomal trafficking and/or fusion with autophagosomes. Finally, NDR2 silencing inhibits filopodia formation and cell polarization during HBEC migration under serum deprivation by disrupting Golgi repositioning to the leading edge, a process essential for cell migration. These data highlight NDR2's role in Golgi- and autophagy-regulated migration during starvation. Unlike NDR1, NDR2 is stabilized under starvation and promotes autophagy by regulating LC3 and ATG9A, thereby supporting NSCLC cell proliferation and migration. Routine staining for NDR2 and/or ATG9 could aid in diagnosing NSCLC with high migratory potential.
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Registered trials
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