Transcriptomic and functional studies reveal miR-431-5p as a tumour suppressor in pancreatic ductal adenocarcinoma cells

Haugen, Øyvind Pernell; Khuu, Cuong; Weidemann, Hanne M; Utheim, Tor Paaske; Bergersen, Linda Hildegard

doi:10.1016/j.gene.2022.146346

Cited by 2 publications

(1 citation statement)

References 44 publications

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“…Myosin-1b (MYO1B) promotes cancer by targeting HIF1a and SNAI2/cyclinD1 60 , 61 . ATP6V0E1 encodes the E subunit of the vacuolar ATPase that is important for cancer cell survival in pancreatic cancer 62 . Lastly, Fibronectin 1 (FN1) can have positive or negative effects on cancer growth depending on the tissue 63 .…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of RNA splicing in early non-alcoholic fatty liver disease through hepatocellular carcinoma

Webster,

Kumar,

2024

Sci Rep

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While changes in RNA splicing have been extensively studied in hepatocellular carcinoma (HCC), no studies have systematically investigated changes in RNA splicing during earlier liver disease. Mouse studies have shown that disruption of RNA splicing can trigger liver disease and we have shown that the splicing factor SRSF3 is decreased in the diseased human liver, so we profiled RNA splicing in liver samples from twenty-nine individuals with no-history of liver disease or varying degrees of non-alcoholic fatty liver disease (NAFLD). We compared our results with three publicly available transcriptome datasets that we re-analyzed for splicing events (SEs). We found many changes in SEs occurred during early liver disease, with fewer events occurring with the onset of inflammation and fibrosis. Many of these early SEs were enriched for SRSF3-dependent events and were associated with SRSF3 binding sites. Mapping the early and late changes to gene ontologies and pathways showed that the genes harboring these early SEs were involved in normal liver metabolism, whereas those harboring late SEs were involved in inflammation, fibrosis and proliferation. We compared the SEs with HCC data from the TCGA and observed that many of these early disease SEs are found in HCC samples and, furthermore, are correlated with disease survival. Changes in splicing factor expression are also observed, which may be associated with distinct subsets of the SEs. The maintenance of these SEs through the multi-year oncogenic process suggests that they may be causative. Understanding the role of these splice variants in metabolic liver disease progression may shed light on the triggers of liver disease progression and the pathogenesis of HCC.

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Section: Discussionmentioning

confidence: 99%

Dysregulation of RNA splicing in early non-alcoholic fatty liver disease through hepatocellular carcinoma

Webster,

Kumar,

2024

Sci Rep

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Metabolic reprogramming and epigenetic modifications in cancer: from the impacts and mechanisms to the treatment potential

Qiu

Jiang

et al. 2023

Exp Mol Med

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Metabolic reprogramming and epigenetic modifications are hallmarks of cancer cells. In cancer cells, metabolic pathway activity varies during tumorigenesis and cancer progression, indicating regulated metabolic plasticity. Metabolic changes are often closely related to epigenetic changes, such as alterations in the expression or activity of epigenetically modified enzymes, which may exert a direct or an indirect influence on cellular metabolism. Therefore, exploring the mechanisms underlying epigenetic modifications regulating the reprogramming of tumor cell metabolism is important for further understanding tumor pathogenesis. Here, we mainly focus on the latest studies on epigenetic modifications related to cancer cell metabolism regulations, including changes in glucose, lipid and amino acid metabolism in the cancer context, and then emphasize the mechanisms related to tumor cell epigenetic modifications. Specifically, we discuss the role played by DNA methylation, chromatin remodeling, noncoding RNAs and histone lactylation in tumor growth and progression. Finally, we summarize the prospects of potential cancer therapeutic strategies based on metabolic reprogramming and epigenetic changes in tumor cells.

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Transcriptomic and functional studies reveal miR-431-5p as a tumour suppressor in pancreatic ductal adenocarcinoma cells

Cited by 2 publications

References 44 publications

Dysregulation of RNA splicing in early non-alcoholic fatty liver disease through hepatocellular carcinoma

Dysregulation of RNA splicing in early non-alcoholic fatty liver disease through hepatocellular carcinoma

Metabolic reprogramming and epigenetic modifications in cancer: from the impacts and mechanisms to the treatment potential

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