TRIM26 functions as a novel tumor suppressor of hepatocellular carcinoma and its downregulation contributes to worse prognosis

Journal Article · Fri Jul 31 04:00:00 EDT 2015 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2015.05.117· OSTI ID:22462128

Wang, Yi ^[1]; He, Du ^[2]; Yang, Liang ^[3]; Wen, Bo ^[4]; Dai, Jinfen ^[5]; Zhang, Qian ^[6]; Kang, Jian ^[5]; He, Weiyang ^[6]; Ding, Qianshan ^[5]; He, De ^[1]

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1. Department of General Surgery, The Affiliated Baoan Hospital of Southern Medical University, Shenzhen, Guangdong, 518101 (China)
2. Department of Oncology, The Central Hospital of Enshi Autonomous of Prefecture, Enshi Clinical College of Wuhan University, Enshi, Hubei, 445000 (China)
3. Department of Oncology, Qianjiang Central Hospital, Qianjiang, Hubei, 433100 (China)
4. Department of Urology, The Affiliated Baoan Hospital of Southern Medical University, Shenzhen, Guangdong, 518101 (China)
5. Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060 (China)
6. Department of Immunology, School of Basic Medicine, Wuhan University, Wuhan, Hubei, 430071 (China)

Hepatocellular carcinoma (HCC) is the one of the most common malignancies worldwide and its prognosis is extremely poor. Tripartite motif (TRIM) proteins play crucial roles in cancer cell biology but the function of tripartite motif 26 (TRIM26) has not been investigated. We demonstrated that low expression level of TRIM26 in tumor samples was significantly correlated with worse prognosis in HCC patients. We also demonstrated its expression level was associated with several clinicopathologic features such as AFP level and T stage of HCC patients. Furthermore, we validated that TRIM26 was significantly downregulated in HCC tissue compared with normal liver tissue. To further clarify the functional role of TRIM26 in HCC, We confirmed that TRIM26 silencing can promote cancer cell proliferation, colony forming, migration and invasion in vitro with HCC cell lines HepG2 and Bel-7402. Then we utilized bioinformatic tool to predict gene influenced by TRIM26, showing TRIM26 could modulate gene sets about cancer cell metabolism. In conclusion, we proved that TRIM26 is a novel tumor suppressor modulating multiple metabolism-related pathways in HCC. To our best knowledge, this is the first study to investigate the function of TRIM26 in cancer biology. Our findings provide useful insight into the mechanism of HCC origin and progression. Moreover, TRIM26 may represent a novel therapeutic target for HCC. - Highlights: • TRIM26 is down-regulated in liver cancer samples and functions as a novel tumor suppressor. • Down-regulation of TRIM26 is associated with worse prognosis of hepatocellular carcinoma (HCC). • Knockdown of TRIM26 promotes the proliferation and metastasis of HCC cells. • TRIM26 may function in abnormal metabolic progress of HCC.

• OSTI ID: 22462128
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 3 Vol. 463; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANIMAL TISSUES
BIOLOGY
CELL PROLIFERATION
COMPARATIVE EVALUATIONS
GENES
HEPATOMAS
IN VITRO
LIVER
METABOLISM
METASTASES
PATIENTS
PROTEINS