Silencing TRIP13 inhibits cell growth and metastasis of hepatocellular carcinoma by activating of TGF-β1/smad3

Yao, Jianning; Zhang, Xuexiu; Zhang, Yingbo; Zhao, Dan; Gao, Bing; Zhou, Haining; Gao, Shilin; Zhang, Lianfeng

doi:10.1186/s12935-018-0704-y

Cited by 40 publications

(45 citation statements)

References 51 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…*P < 0.05, **P < 0.01, ***P < 0.001 ACTN4 expression in HCC cells. Additionally, different with our result, an earlier research reported that TRIP13 facilitates HCC cell growth and metastasis through activating of TGF-β1/smad3 signaling [28].…”

Section: Discussioncontrasting

confidence: 99%

Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of hepatocellular carcinoma via interacting with ACTN4

Zhu

Wei

Zhang

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Background: ATPase associated with a variety of cellular activities (AAA ATPase) family members are closely linked to tumor formation and progression. However, their roles in hepatocellular carcinoma (HCC) largely remain unclear. Methods: Bioinformatic analyses of public databases were used to excavate the potential AAA ATPases that may contribute to HCC, and thyroid hormone receptor interactor 13 (TRIP13) was selected to following researches because of its most prominently differential expression. Western blot, qRT-PCR and immunohistochemistry were used to detect the expression of TRIP13 in HCC tissues, and then the relationship between TRIP13 expression and clinicopathological parameters were evaluated. Finally, its functions and potential mechanisms were investigated through a series gain-and loss-of-function strategies both in vitro and in vivo. Results: TRIP13 was significantly overexpressed in HCC tissues and high level of TRIP13 was closely correlated with a worse clinical outcome. Functionally, elevated TRIP13 facilitated cell proliferation, migration, invasion, and promoted cellular epithelial-mesenchymal transition (EMT) in vitro, while promote tumor growth and lung metastasis in vivo. Mechanistically, TRIP13 interacted with ACTN4 and positively regulated its expression, thus activating the AKT/mTOR pathway to drive tumor progression. Moreover, miR-192-5p served as an upstream regulator of TRIP13 by directly binding to TRIP13 mRNA 3′ UTR, which may partially explain the high expression of TRIP13 in HCC. Conclusion: Our findings identified TRIP13 as a promising candidate oncogene in HCC, and TRIP13 induced cell migration, invasion and metastasis of HCC through the AKT/mTOR signaling via interacting with ACTN4.

show abstract

Section: Discussioncontrasting

confidence: 99%

Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of hepatocellular carcinoma via interacting with ACTN4

Zhu

Wei

Zhang

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

show abstract

“…Silencing TRIP13 could act as a tumor suppressor for liver cancer, which inhibited cell growth and metastasis in vivo and in vitro experiments (18). Overexpression of TRIP13 abrogated mitotic spindle checkpoint and induced proteasome-mediated degradation of MAD2 in multiple myeloma mainly through the Akt pathway.…”

Section: Discussionmentioning

confidence: 96%

Identification of Energy Metabolism Genes for the Prediction of Survival in Hepatocellular Carcinoma

Chen

Gao

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) samples were clustered into three energy metabolism-related molecular subtypes (C1, C2, and C3) with different prognosis using the gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). HCC energy metabolism-related molecular subtype analysis was conducted based on the 594 energy metabolism genes. Differential expression analysis yielded 576 differentially expressed genes (DEGs) among the three subtypes, which were closely related to HCC progression. Six genes were finally selected from the 576 DEGs through LASSO-Cox regression and used in constructing a six-gene signature-associated prognostic risk model, which was validated using the TCGA internal and three GEO external validation cohorts. The risk model showed that high ANLN, ENTPD2, TRIP13, PLAC8, and G6PD expression levels were associated with bad prognosis, and high expression of ADH1C was associated with a good prognosis. The validation results showed that our risk model had a high distinguishing ability of prognosis in HCC patients. The four enriched pathways of the risk model were obtained by gene set enrichment analysis (GSEA) and found to be associated with the tumorigenesis and development of HCC, including the cell cycle, Wnt signaling pathway, drug metabolism cytochrome P450, and primary bile acid biosynthesis. The risk score calculated from the established risk model in 204 samples and other clinical characteristics were used in building a nomogram with a good prognostic prediction ability (C-index = 0.746, 95% CI = 0.714-0.777). The area under the curves (AUCs) of the nomogram model in 1-, 2-, and 3-years were 0.82, 0.77, and 0.79, respectively. Then, qRT-PCR and immunohistochemistry were used to validate the mRNA expression levels of the six genes, and significant differences in mRNA and gene expression were observed among the tumor and adjacent tissues. Overall, our study divided HCC patients into three energy metabolism-related molecular subtypes with different prognosis. Then, a risk model with a good performance in prognostic prediction was built using the TCGA dataset. This model can be used as an independent prognostic evaluation index for HCC patients.

show abstract

“…The overexpression of KIF2C has been significantly associated with poor prognosis of HCC (Chen et al, 2017). TRIP13 is overexpressed in HCC tissues and can induce progression and invasion of HCC (Yao et al, 2018; FIGURE 11 | Kaplan-Meier survival and receiver operating characteristic (ROC) curves in training and validation datasets. Kaplan-Meier survival curves of overall survival for hepatocellular varcinoma (HCC) patients in the International Cancer Genome Consortium (ICGC) (A) and The Cancer Genome Atlas (TCGA) (B) set.…”

Section: Discussionmentioning

confidence: 99%

Identification of Crucial Genes Associated With Immune Cell Infiltration in Hepatocellular Carcinoma by Weighted Gene Co-expression Network Analysis

Wang

Liu

et al. 2020

Front. Genet.

View full text Add to dashboard Cite

Silencing TRIP13 inhibits cell growth and metastasis of hepatocellular carcinoma by activating of TGF-β1/smad3

Cited by 40 publications

References 51 publications

Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of hepatocellular carcinoma via interacting with ACTN4

Elevated TRIP13 drives the AKT/mTOR pathway to induce the progression of hepatocellular carcinoma via interacting with ACTN4

Identification of Energy Metabolism Genes for the Prediction of Survival in Hepatocellular Carcinoma

Identification of Crucial Genes Associated With Immune Cell Infiltration in Hepatocellular Carcinoma by Weighted Gene Co-expression Network Analysis

Contact Info

Product

Resources

About