ArticleMolecular therapy. Nucleic acids2021
TRIM29 alters bioenergetics of pancreatic cancer cells via cooperation of miR-2355-3p and DDX3X recruitment to AK4 transcript.
Article in Molecular therapy. Nucleic acids, 2021. 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, 16 citations in OpenAlex.
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- Deficiency ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- O-GlcNAcylation of TRIM29 and OGT translation forms a feedback loop to promote adaptive response of PDAC cells to glucose deficiency.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- DDX3X interacts with SIRT7 to promote PD-L1 expression to facilitate PDAC progression.Oncogenesis · 2024Article
- Article
- From slides to insights: Harnessing deep learning for prognostic survival prediction in human colorectal cancer histology.Open life sciences · 2023Article
- TRIM29 knockdown prevented the colon cancer progression through decreasing the ubiquitination levels of KRT5.Open life sciences · 2023Article
- Article
- Article
- TRIM29 in Cutaneous Squamous Cell Carcinoma.Frontiers in medicine · 2021Review
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
TRIM29 is dysregulated in pancreatic cancer and implicated in maintenance of stem-cell-like characters of pancreatic cancer cells. However, the exact mechanisms underlying oncogenic function of TRIM29 in pancreatic cancer cells remain largely unclarified. Using a global screening procedure, the current study found that adenylate kinase 4 (AK4) was profoundly reduced by TRIM29 knockdown. In addition, our data demonstrated that TRIM29 knockdown altered bioenergetics and suppressed proliferation and invasion of pancreatic cancer cells via downregulation of AK4 at the posttranscriptional level. The current study demonstrated that upregulation of microRNA-2355-3p (miR-2355-3p) upregulated AK4 expression via facilitating DDX3X recruitment to the AK4 transcript, and TRIM29 knockdown thereby destabilized the AK4 transcript via miR-2355-3p downregulation. Collectively, our study uncovers posttranscriptional stabilization of the AK4 transcript by miR-2355-3p interaction to facilitate DDX3X recruitment. Regulation of AK4 by TRIM29 via miR-2355-3p thereby provides additional information for further identification of attractive targets for therapy with pancreatic cancer.
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