ArticleNature communications2021
LINC00842 inactivates transcription co-regulator PGC-1α to promote pancreatic cancer malignancy through metabolic remodelling.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 66 citations in OpenAlex.
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- MULGONET: An interpretable neural network framework to integrate multi-omics data for cancer recurrence prediction and biomarker discovery.Fundamental research · 2026Article
- LINC-EPS Protects Against Neurodegeneration by Driving a PGC-1α-Mediated Anti-Ferroptosis Program in Parkinson's Disease.International journal of biological sciences · 2026Article
- Lithium exposure causes ferroptosis to induce unexplained miscarriage through non-canonical MBOAT1 pathway.Nature communications · 2025Article
- Post-Translational Modifications: Key "Regulators" of Pancreatic Cancer Malignant Phenotype-Advances in Mechanisms and Targeted Therapies.Biomedicines · 2025Review
- Recent advances in hydrogel-based delivery systems for the treatment of pancreatic cancer.Materials today. Bio · 2025Review
- SLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation in pancreatic cancer.British journal of cancer · 2025Article
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- Role of noncoding RNA and protein interaction in pancreatic cancer.Chinese medical journal · 2025Review
- Targeted mitochondrial therapy for pancreatic cancer.Translational oncology · 2025Review
- mCommunications biology · 2025Article
- Role of PGC-1α in the proliferation and metastasis of malignant tumors.Journal of molecular histology · 2025Review
- Targeting protein modification: a new direction for immunotherapy of pancreatic cancer.International journal of biological sciences · 2025Review
- Integrated multi-omics analysis identifies features that predict human pluripotent stem cell-derived progenitor differentiation to cardiomyocytes.Journal of molecular and cellular cardiology · 2024Article
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Authors and funding
24 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanism underlying pancreatic ductal adenocarcinoma (PDAC) malignancy remains unclear. Here, we characterize a long intergenic non-coding RNA LINC00842 that plays a role in PDAC progression. LINC00842 expression is upregulated in PDAC and induced by high concentration of glucose via transcription factor YY1. LINC00842 binds to and prevents acetylated PGC-1α from deacetylation by deacetylase SIRT1 to form PGC-1α, an important transcription co-factor in regulating cellular metabolism. LINC00842 overexpression causes metabolic switch from mitochondrial oxidative catabolic process to fatty acid synthesis, enhancing the malignant phenotypes of PDAC cells. High LINC00842 levels are correlated with elevated acetylated- PGC-1α levels in PDAC and poor patient survival. Decreasing LINC00842 level and inhibiting fatty acid synthase activity significantly repress PDAC growth and invasiveness in mouse pancreatic xenograft or patient-derived xenograft models. These results demonstrate that LINC00842 plays a role in promoting PDAC malignancy and thus might serve as a druggable target.
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