TRIP13 promotes the proliferation and invasion of lung cancer cells via the Wnt signaling pathway and epithelial–mesenchymal transition

Li, Zhi-Han; Lei, Lei; Fei, Liangru; Huang, Wenjing; Zheng, Yiwen; Yang, Mingyong; Wang, Zhao; Liu, Chenchen; Xu, Hong‐Tao

doi:10.1007/s10735-020-09919-z

Cited by 21 publications

(16 citation statements)

References 32 publications

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“…Previous studies have shown that over‐expression of TRIP13 contributes to the accumulation of β‐catenin in cancer cells, 10,24,25 indicating a potential role of TRIP13 in Wnt/β‐catenin signaling. Indeed, TRIP13 has been demonstrated to contribute to the activation of Wnt/β‐catenin signaling in colorectal and lung cancers 40,41 . Our data showed that over‐expression of TRIP13 upregulated the levels of active β‐catenin in this study and increased the transcriptional activity of TCF/LEF in cervical cancer cells.…”

Section: Discussionsupporting

confidence: 59%

TRIP13 exerts a cancer‐promoting role in cervical cancer by enhancing Wnt/β‐catenin signaling via ACTN4

Liu

Shen

Zhang

2021

Environmental Toxicology

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Increasing evidence has indicated that thyroid hormone receptor interacting protein 13 (TRIP13) exerts a cancer‐promoting role in a broad spectrum of cancers. However, the detailed relevance and function of TRIP13 in cervical cancer remain undefined. The goal of this work was to evaluate the functional significance and mechanism of TRIP13 in cervical cancer. Our data demonstrated that TRIP13 expression was markedly increased in cervical cancer tissue, and high expression of TRIP13 predicted a low survival rate in cervical cancer patients. Knockdown of TRIP13 caused a significant reduction in the proliferation and invasion of cervical cancer cells. By contrast, over‐expression of TRIP13 accelerated the proliferation and invasion of cervical cancer cells. Further data revealed that TRIP13 enhanced the activation of Wnt/β‐catenin signaling associated with modulation of α‐Actinin‐4 (ACTN4). Knockdown of ACTN4 markedly reversed TRIP13‐mediated activation of Wnt/β‐catenin signaling. In addition, inhibition of Wnt/β‐catenin signaling reversed TRIP13‐induced cancer‐promoting effects in cervical cancer cells. Knockdown of TRIP13 markedly retarded the tumor formation and growth of cervical cells in vivo in nude mice. Taken together, the data of this work indicate that TRIP13 accelerates the proliferation and invasion of cervical cancer by enhancing Wnt/β‐catenin signaling via regulation of ACTN4. These findings underscore a relevance of the TRIP13/ACTN4/Wnt/β‐catenin signaling axis in the progression of cervical cancer and suggest TRIP13 as a potential target for treatment of cervical cancer.

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Section: Discussionsupporting

confidence: 59%

TRIP13 exerts a cancer‐promoting role in cervical cancer by enhancing Wnt/β‐catenin signaling via ACTN4

Liu

Shen

Zhang

2021

Environmental Toxicology

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“…Furthermore, it was demonstrated that TRIP13 overexpression reactivated the Wnt/β-catenin signaling pathway, previously being inactivated due to KIF18B knockdown. The TRIP13-mediated activation of the Wnt/β-catenin signaling pathway has also been reported in lung, colorectal and cervical cancer (27)(28)(29). It was therefore suggested that the activation of the Wnt/β-catenin signaling pathway in BC might be also caused by TRIP13.…”

Section: Discussionmentioning

confidence: 88%

KIF18B promotes breast cancer cell proliferation, migration and invasion by targeting TRIP13 and activating the Wnt/β‑catenin signaling pathway

et al. 2022

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Kinesin superfamily member 18B (KIF18B) has previously been reported to be upregulated in breast cancer (BC) and is involved in BC tumorigenesis. Therefore, the present study aimed to investigate the effects and underlying mechanisms of KIF18B in BC. Comprehensive bioinformatics analysis was performed, using data from The Cancer Genome Atlas. KIF18B knockdown and thyroid hormone receptor-interacting protein 13 (TRIP13) overexpression in BC cells were induced via transfection, by using the short hairpin RNA-KIF18B and overexpression-TRIP13 vectors, respectively. Cellular processes, including proliferation, migration and invasion were assessed using colony formation, wound healing and Transwell assays, respectively. mRNA and protein expression levels were determined using reverse transcription-quantitative PCR and western blot analysis, respectively. Protein-protein interactions were determined using co-immunoprecipitation. The results demonstrated that the KIF18B expression levels were upregulated in BC, particularly in triple-negative BC (TNBC) tissues and cell lines. KIF18B knockdown inhibited the proliferation, migration and invasion of HCC-1937 TNBC cells. Furthermore, MMP12 and MMP9 protein expression levels were decreased by KIF18B knockdown. TRIP13 expression was also demonstrated to be upregulated in BC, particularly in TNBC tissues and cell lines. TRIP13 expression levels positively correlated with those of KIF18B in BC tissues and cells, and further analysis verified that TRIP13 and KIF14B were able to directly bind to each other. However, TRIP13 overexpression abolished the effects of KIF18B knockdown on HCC-1937 cells. Furthermore, KIF18B knockdown decreased β-catenin, c-Myc and cyclin D1 protein expression levels; however, TRIP13 overexpression resulted in the recovery of all respective protein expression levels. On the whole, the present study demonstrates that KIF18B promotes BC malignant events, including the proliferation, migration and invasion of TNBC cells. These results indicate that KIF18B may play an oncogenic role in BC by upregulating TRIP13 expression, thereby activating the Wnt/β-catenin signaling pathway.

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“…TRIP13 may be overexpressed in cancer cells in various forms, affecting the mitotic process of cells, leading to tumorigenesis and promoting the malignant transformation of cancer cells [33][34]. TTK, on the other hand, is considered as a potential therapeutic target and biological marker for lung cancer, and upregulation of TTK protein expression implies a more advanced lung cancer stage as well as poorer survival [35][36].…”

Section: Discussionmentioning

confidence: 99%

Identification of pivotal genes with prognostic evaluation value in lung adenocarcinoma by bioinformatics analysis

Wang

Zhao

Wang

et al. 2022

Preprint

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Lung cancer remains the leading cause of cancer morbidity and mortality worldwide, and over diagnosis causes various unnecessary losses in patients' lives and health. How to more effectively screen lung cancer patients and their potential prognostic risk become the focus of our current study. By analyzing the LUAD expression profile in The Cancer Genome Atlas (TCGA), we constructed a weighted gene co-expression network using differentially expressed genes (DEGs) to find the key modules and pivotal genes. A COX proportional risk regression model based on the least absolute shrinkage and selection operator (LASSO) was used to assess the predictive value of the model for the prognosis of LUAD patients. A total of 4107 up-regulated DEGs and 2022 down-regulated DEGs were identified in this study, and enrichment analysis showed that these analyzes were associated with the extracellular matrix of cells and adhesion. Ten gene markers consisting of LDHA, TOP2A, UBE2C, TYMS, TRIP13, EXO1, TTK, TPX2, ZWINT, and UHRF1 were established by extracting the central genes in the key modules, and the upregulation of these genes was accompanied by an increased prognostic risk of patients. Among them, high expression of LDHA, TRIP13, TTK in LUAD was associated with shorter overall survival and could be used as independent prognostic factors to participate in metabolic processes such as tumor NAD. The present study provides a powerful molecular target for the study of LUAD prognosis and provides a theoretical basis for the diagnosis and treatment of LUAD and the development of targeted inhibitors.

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TRIP13 promotes the proliferation and invasion of lung cancer cells via the Wnt signaling pathway and epithelial–mesenchymal transition

Cited by 21 publications

References 32 publications

TRIP13 exerts a cancer‐promoting role in cervical cancer by enhancing Wnt/β‐catenin signaling via ACTN4

TRIP13 exerts a cancer‐promoting role in cervical cancer by enhancing Wnt/β‐catenin signaling via ACTN4

KIF18B promotes breast cancer cell proliferation, migration and invasion by targeting TRIP13 and activating the Wnt/β‑catenin signaling pathway

Identification of pivotal genes with prognostic evaluation value in lung adenocarcinoma by bioinformatics analysis

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