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PLIN2 has been found to be dysregulated in several human malignancies, which influences cancer progression. However, the roles of PLIN2 in regulating hepatocellular carcinoma (HCC) progression are still unclear. Here, we revealed that PLIN2 was frequently upregulated in HCC cells and tissues, and increased PLIN2 expression was associated with poor prognosis outcomes in HCC. In HCC cells, overexpressing PLIN2 promoted cell proliferation, PLIN2-deficiency inhibited cell vitality. Mechanistically, silencing of PLIN2 expression downregulated hypoxia inducible factor 1-α (HIF1α) expression and this downregulation in turn inhibited the targeting genes of HIF1α. Furthermore, we found that PLIN2 stabilized and retarded the degradation of the HIF1α through autophagy-lysosomal pathway by inhibiting AMPK/ULK1. Collectively, we clarified the carcinogenic role of PLIN2 in HCC and suggested a prognostic biomarker for diagnosis and clinical therapy in the future.
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http://dx.doi.org/10.1016/j.yexcr.2022.113244 | DOI Listing |
Clin J Gastroenterol
September 2025
Department of Hepatobiliary and Pancreatic Oncology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 541-8567, Japan.
Hepatic reactive lymphoid hyperplasia (RLH), also known as hepatic pseudolymphoma, is a rare benign condition that predominantly affects middle-aged-to-elderly women and is often associated with autoimmune disorders. The imaging features of hepatic RLH frequently mimic those of malignant hepatic tumors, such as hepatocellular carcinoma (HCC), cholangiocarcinoma, or metastatic liver tumors, making its diagnosis based solely on imaging modalities challenging, often leading to unnecessary surgical resection. However, the optimal diagnostic strategy for hepatic RLH remains controversial.
View Article and Find Full Text PDFTransl Oncol
September 2025
Department of General Surgery, Affiliated Zhangjiagang Hospital of Soochow University. Electronic address:
Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. Although mitochondrial metabolism contributes to tumorigenesis, the specific roles of individual mitochondrial components remain unclear.NADH:ubiquinone oxidoreductase core subunit S8 (NDUFS8), a key subunit of mitochondrial complex I, has been implicated in non-hepatic malignancies, but its functional relevance in HCC is unknown.
View Article and Find Full Text PDFJ Cell Mol Med
September 2025
School of Life Science, Institute of Biochemistry and Molecular Biology, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Hepatocellular carcinoma (HCC) is one of the leading cancers worldwide, and its development is strongly associated with the tumour microenvironment, particularly fibrosis and chronic inflammation. This study aims to investigate the role of the Hedgehog (Hh) pathway, a key signalling pathway in HCC progression, in the interaction between HCC cells and monocytes, which are central players in inflammation. Using a transwell migration assay, GLI1, the downstream transcriptional effector of the Hh pathway in HCC cells, was found to promote the migration of THP-1 monocyte cells.
View Article and Find Full Text PDFGut
September 2025
Department of Gastroenterology and Hepatology, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Eur J Pharmacol
September 2025
Department of Emergency Medicine, Shuang-Ho Hospital, Taipei Medical University, New Taipei City, Taiwan; Department of Emergency Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan. Electronic address:
Background: This study seeks to provide preclinical evidence demonstrating the potential of Antrocinol, a derivative of antrocin derived from the active compound of Antrodia cinnamomea, as a promising small-molecule drug candidate for overcoming drug-resistant hepatocellular carcinoma (HCC).
Methods: We developed Lenvatinib-resistant Huh-7 and HepG cell lines (Huh-7/LR, HepG2/LR) to evaluate their viability and apoptotic response to Antrocinol. Autophagy-dependent cell death was assessed in Huh-7/LR cells using Z-VAD-FMK and shATG5 transfection.