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Identification of HIF-dependent alternative splicing in gastrointestinal cancers and characterization of a long, coding isoform of SLC35A3. | LitMetric

AI Article Synopsis

  • * This study focuses on identifying HIF-dependent alternative splicing events in pancreatic cancer cells under hypoxic conditions and correlating these findings with data from various cancer patient cohorts to pinpoint relevant splice events for further research.
  • * The research successfully validates specific HIF-dependent splicing events in human gastrointestinal cancer cell lines and patient-derived pancreatic cancer organoids, culminating in the discovery of a mechanism producing a hypoxia-dependent isoform of the SLC35A3 transporter.

Article Abstract

Intra-tumor hypoxia is a common feature in many solid cancers. Although transcriptional targets of hypoxia-inducible factors (HIFs) have been well characterized, alternative splicing or processing of pre-mRNA transcripts which occurs during hypoxia and subsequent HIF stabilization is much less understood. Here, we identify many HIF-dependent alternative splicing events after whole transcriptome sequencing in pancreatic cancer cells exposed to hypoxia with and without downregulation of the aryl hydrocarbon receptor nuclear translocator (ARNT), a protein required for HIFs to form a transcriptionally active dimer. We correlate the discovered hypoxia-driven events with available sequencing data from pan-cancer TCGA patient cohorts to select a narrow set of putative biologically relevant splice events for experimental validation. We validate a small set of candidate HIF-dependent alternative splicing events in multiple human gastrointestinal cancer cell lines as well as patient-derived human pancreatic cancer organoids. Lastly, we report the discovery of a HIF-dependent mechanism to produce a hypoxia-dependent, long and coding isoform of the UDP-N-acetylglucosamine transporter SLC35A3.

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Source
http://dx.doi.org/10.1016/j.ygeno.2020.12.039DOI Listing

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