Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rottlerin has been reported to exert its anti-tumor activity in various types of human cancers. However, the underlying molecular mechanism has not been fully elucidated. In the current study, we explored whether rottlerin exhibits its tumor suppressive function in hepatocellular carcinoma cells. Our MTT assay results showed that rottlerin inhibited cell growth in hepatocellular carcinoma cells. Moreover, we found that rottlerin induced cell apoptosis and caused cell cycle arrest at G1 phase. Furthermore, our wound healing assay result demonstrated that rottlerin retarded cell migration in hepatocellular carcinoma cells. Additionally, rottlerin suppressed cell migration and invasion. Notably, we found that rottlerin upregulated DDX3 expression and subsequently downregulated Cyclin D1 expression and increased p21 level. Importantly, down-regulation of DDX3 abrogated the rottlerin-mediated tumor suppressive function, whereas overexpression of DDX3 promoted the anti-tumor activity of rottlerin. Our study suggests that rottlerin exhibits its anti-cancer activity partly due to upregulation of DDX3 in hepatocellular carcinoma cells.
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PMID:Rottlerin upregulates DDX3 expression in hepatocellular carcinoma. 2920 43

YEATS domain containing 4 (YEATS4) is usually amplified and functions as an oncogene in several malignancies, such as colorectum, ovarian, breast and lung. However, the biological role of YEATS4 in hepatocellular carcinoma (HCC) has not yet been discussed. Herein, we found that YEATS4 was significantly upregulated in HCC compared to para-cancerous tissues, and was associated with poor prognosis, large tumor size, poor differentiation and distant metastasis. In addition, YEATS4 promoted HCC cell proliferation and colony formation by binding to and increasing the transcriptional activity of the TCEA1 promoter. Concurrently, upregulation of TCEA1 increased the stability of the DDX3 protein, a member of the DEAD box RNA helicase family, and augmented the proliferative and colony forming ability of HCC cells. Furthermore, YEATS4 accelerated tumor growth in vivo in a xenograft HCC model. Taken together, our study provides evidence for the first time on the potential role of the YEATS4/TCEA1/DDX3 axis in regulating HCC progression, and presents YEATS4 as a promising therapeutic target and prognosis maker for HCC.
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PMID:Abnormal expression of YEATS4 associates with poor prognosis and promotes cell proliferation of hepatic carcinoma cell by regulation the TCEA1/DDX3 axis. 3041 57


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