TRIM28 protects CARM1 from proteasome-mediated degradation to prevent colorectal cancer metastasis
Science Bulletin, ISSN: 2095-9273, Vol: 64, Issue: 14, Page: 986-997
2019
- 16Citations
- 11Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations16
- Citation Indexes16
- 16
- CrossRef3
- Captures11
- Readers11
- 11
- Mentions1
- News Mentions1
- News1
Most Recent News
Exploring the Mechanisms, Biomarkers, and Therapeutic Targets of TRIM Family in Gastrointestinal Cancer
Introduction Approximately 10 million individuals succumb to malignant tumors annually worldwide, with gastrointestinal cancer standing out as a prevalent malignancy within the digestive system.1 Common
Article Description
TRIM28 (Tripartite motif-containing protein 28), a member of TRIM family, is aberrantly expressed and reportedly has different functions in many types of human cancer. However, the biological roles of TRIM28 and related mechanism in colorectal cancer (CRC) remain unclear. Here, we showed that TRIM28 was downregulated in colorectal cancer compared with normal mucosa, especially at advanced stages, and acted as an independent prognostic factor of favorable outcome. Functional studies demonstrated that TRIM28 restrained CRC migration and invasion in vitro and in vivo. Mechanistically, we reported that CARM1 (co-activator-associated arginine methyltransferase1) was a critical player downstream of TRIM28. TRIM28 interacted with CARM1, and protected CARM1 from proteasome-mediated degradation through physical protein-protein interaction to suppress CRC metastasis. Further, TRIM28 suppressed the migration and invasion of CRC cells through inhibiting WNT/β-catenin signaling in a CARM1-dependent manner, but independent of CARM1′s methyltransferase activity. The protein expression of CARM1 was positively correlated with TRIM28 in CRC tissues. Patients with high levels of TRIM28 and CARM1 had improved prognosis, whereas patients with low TRIM28 and CARM1 expression had the poor outcomes. Thus, our study reveals an inhibitory role of TRIM28 in CRC metastasis, which was achieved through a TRIM28-CARM1-WNT/β-catenin axis. This work provides potential prognostic and therapeutic targets for CRC treatment.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2095927319303184; http://dx.doi.org/10.1016/j.scib.2019.05.024; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85067185710&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36659810; https://linkinghub.elsevier.com/retrieve/pii/S2095927319303184; https://dx.doi.org/10.1016/j.scib.2019.05.024; http://sciencechina.cn/gw.jsp?action=cited_outline.jsp&type=1&id=6579966&internal_id=6579966&from=elsevier
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