ArticleCancer gene therapy2024
LAMC2 mitigates ER stress by enhancing ER-mitochondria interaction via binding to MYH9 and MYH10.
Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- ACOT9, a mitochondrial metabolism-related gene, promotes ROS-associated epithelial remodeling in laryngeal squamous cell carcinoma.Journal of translational medicine · 2026Article
- RNF126 mediates fetal growth restriction via ubiquitination-dependent degradation of the MYH9/MYH10 complex.iScience · 2026Article
- Plasma membrane mediated GLUT10 mitochondrial targeting regulates intracellular ascorbic acid homeostasis.iScience · 2026Article
- Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders.Nature reviews. Neuroscience · 2026Review
- Prognostic significance of genes associated with disulfidptosis in lung squamous cell carcinoma.Journal of cardiothoracic surgery · 2026Article
- Molecular mechanism of Danshen injection in treating endometrial fibrosis induced by intrauterine adhesions via the LAMC2-CD44-TGF-β1-SMAD2/3 signaling pathway.Frontiers in physiology · 2026Article
- Application of the Mass Spectrometry-High-Throughput Technique Over the Immunohistochemical Analysis for Human Brain Tumor Diagnosis and Prognosis: Insights Into Biomarkers' Identification for the Case Study of Grade IV Astrocytomas and Meningiomas.Biomedical chromatography : BMC · 2025Article
- Reduced NRF2/Mfn2 activity promotes endoplasmic reticulum stress and senescence in adipose-derived mesenchymal stem cells in hypertrophic obese mice.World journal of stem cells · 2025Article
- A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Exploring the dual role of endoplasmic reticulum stress in urological cancers: Implications for tumor progression and cell death interactions.Journal of cell communication and signaling · 2024Review
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Authors and funding
9 authors.
Funding
Abstract
Highly proliferative and metastatic tumors are constantly exposed to both intrinsic and extrinsic factors that induce adaptation to stressful conditions. Chronic adaptation to endoplasmic reticulum (ER) ER stress is common to many different types of cancers, and poses a major challenge for acquired drug resistance. Here we report that LAMC2, an extracellular matrix protein upregulated in many types of cancers, is localized in the ER of lung, breast, and liver cancer cells. Under tunicamycin-induced ER stress, protein level of LAMC2 is upregulated. Transfection of cancer cells with LAMC2 resulted in the attenuation of ER stress phenotype, accompanied by elevation in mitochondrial membrane potential as well as reduction in reactive oxygen species (ROS) levels and apoptosis. In addition, LAMC2 forms protein complexes with MYH9 and MYH10 to promote mitochondrial aggregation and increased ER-mitochondria interaction at the perinuclear region. Moreover, overexpression of LAMC2 counteracts the effects of ER stress and promotes tumor growth in vivo. Taken together, our results revealed that in complex with MYH9 and MYH10, LAMC2 is essential for promoting ER-mitochondria interaction to alleviate ER stress and allow cancer cells to adapt and proliferate under stressful conditions. This study provides new insights and highlights the promising potential of LAMC2 as a therapeutic target for cancer treatment.
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