Tripartite motif-containing 67 promotes progression of hepatocellular carcinoma by regulating MAPK signaling pathway
- Hepatobiliary Pancreat Dis Int. 2026 Apr 27:S1499-3872(26)00053-6. doi: 10.1016/j.hbpd.2026.04.007.
- 1. Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
- 2. Department of Hepatobiliary Pancreatic Tumor Center, Chongqing University Cancer Hospital, Chongqing 400030, China.
- 3. Department of Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
- 4. Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Electronic address: [email protected].
Background: Hepatocellular carcinoma (HCC) remains a significant health concern, given its rising incidence and the increasing complexity associated with its management. The exploration of novel intervention approaches, particularly in the realm of specific biological target therapy, underscores the imperative to identify new biological targets associated with HCC.
Methods: Based on high-throughput Sequencing results from Gene Expression Omnibus (GEO) database, tripartite motif-containing 67 (TRIM67) was identified as a potential biological target for HCC. Five pairs of Cancer and adjacent tissues were obtained from HCC patients at our hospital. Moreover, we used Cell Culture and nude mice to evaluate the role and mechanisms of TRIM67 on HCC. After sample collection, immunofluorescence, immunohistochemistry, and Western blot were employed to validate the expression of TRIM67 and Bad in HCC patients. Migration levels were assessed using scratch and transwell assays, while cell proliferation was evaluated through plate cloning, EdU and CCK-8 assays. Apoptosis levels were analyzed via flow cytometry and Western blot. Finally, proteins associated with the MAPK/ERK1/2 signaling pathway were identified using Western blot and immunofluorescence.
Results: TRIM67 expression was increased in Cancer tissues compared with adjacent tissues. In addition, the increased expression of TRIM67 in HCC cell lines (MHCC97-H and HUH7) was elucidated. Up-regulation of TRIM67 can significantly activate MAPK/ERK1/2 and promote tumor proliferation and migration, and inhibit cell Apoptosis.
Conclusions: Taken together, TRIM67 promoted HCC progression via the activation of MAPK/ERK1/2. Furthermore, TRIM67 may be a biological target for HCC treatment.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: LPL ReceptorResearch Areas: Neurological Disease