ArticleOncogene2020
Loss of TRIM29 suppresses cancer stem cell-like characteristics of PDACs via accelerating ISG15 degradation.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- ISGylation-mediated stabilization of CYP4Z1 fuels breast cancer initiation and progression.Experimental & molecular medicine · 2026Article
- The simultaneous targeted Inhibition of ISG15 and HMGCR disrupts cancer stemness through metabolic collapse and induces synthetic lethality in pancreatic ductal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025Review
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- 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
- SIRT1 ISGylation accelerates tumor progression by unleashing SIRT1 from the inactive state to promote its deacetylase activity.Experimental & molecular medicine · 2024Article
- Unveiling the Multifaceted Roles of ISG15: From Immunomodulation to Therapeutic Frontiers.Vaccines · 2024Review
- ISG15 Promotes Progression and Gemcitabine Resistance of Pancreatic Cancer Cells Through ATG7.International journal of biological sciences · 2024Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- TRIM17-mediated ubiquitination and degradation of RBM38 promotes cisplatin resistance in non-small cell lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- ISG15 and ISGylation modulates cancer stem cell-like characteristics in promoting tumor growth of anaplastic thyroid carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- Article
- lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression.Acta biochimica et biophysica Sinica · 2023Article
- The Functional Roles of ISG15/ISGylation in Cancer.Molecules (Basel, Switzerland) · 2023Review
- M2 macrophage-derived exosomal miR-193b-3p promotes progression and glutamine uptake of pancreatic cancer by targeting TRIM62.Biology direct · 2023Article
- TRIM29 knockdown prevented the colon cancer progression through decreasing the ubiquitination levels of KRT5.Open life sciences · 2023Article
- Ubiquitin signaling in pancreatic ductal adenocarcinoma.Frontiers in molecular biosciences · 2023Review
- From slides to insights: Harnessing deep learning for prognostic survival prediction in human colorectal cancer histology.Open life sciences · 2023Article
- Laminin 332 expression levels predict clinical outcomes and chemotherapy response in patients with pancreatic adenocarcinoma.Frontiers in cell and developmental biology · 2023Article
- The diverse repertoire of ISG15: more intricate than initially thought.Experimental & molecular medicine · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRIM family proteins are defined as E3 ubiquitin ligases because of their RING-finger domains. The ubiquitin-like protein interferon-stimulated gene 15 (ISG15) encodes a 15-kDa protein, that is implicated in the posttranslational modification of diverse proteins. Both TRIM29 and ISG15 play both pro-tumoral and anti-tumoral functions in cancer cells derived from different histology. In the current study, we demonstrated that correlation expression of TRIM29 and ISG15 in pancreatic ductal adenocarcinomas (PDACs). The current study demonstrated that TRIM29 knockdown destabilized ISG15 protein via promoting its processing by calpain 3 (CAPN3). Importantly, the current study found that TRIM29 knockdown suppressed cancer stem cell-like features of PDACs, which can be rescued by ISG15 independent of its conjugation function. In addition, the current study demonstrated that extracellular free ISG15 played an important role in maintenance of cancer stem cell-like features of PDACs. Thereby, the current study displayed a novel mechanism by which TRIM29 modulates ISG15 stability via CAPN3-mediated processing, and subsequently extracellular ISG15 maintains the cancer stem cell-like features of PDAC via autocrine mode of action.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.