Increased expression of TRIP13 drives the tumorigenesis of bladder cancer in association with the EGFR signaling pathway

Gao, Yanjun; Liu, Shanhui; Guo, Qi; Zhang, Su; Zhao, Yuhao; Wang, Hanzhang; Li, Tianbao; Gong, Yang; Wang, Yuhan; Zhang, Tao; Dong, Zhilong; Bacich, Dean J.; Chowdhury, Wasim H.; Rodríguez, Ronald; Wang, Zhiping

doi:10.7150/ijbs.32718

Cited by 26 publications

(25 citation statements)

References 34 publications

(38 reference statements)

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“…The suppression of EGFR phosphorylation is independent of the RAS mutation status, as HCT116 p53-wt,MSI and SW480 p53mut,MSS cells exhibited mutations in KRAS at the G13D and G12V codons, respectively, and both cell lines showed lower EGFR phosphorylation after TRIP13 knockdown. A prior study demonstrates that TRIP13 binds EGFR and activates its signaling pathway [42]. However, the present study did not find, in CRC cells, a direct interaction between TRIP13 and EGFR.…”

Section: Discussioncontrasting

confidence: 95%

“…This indicates that TRIP13 is involved in the EGFR/ Akt signaling pathway. Since a prior study shows TRIP13 interaction with EGFR [42], we performed an immunoprecipitation assay to demonstrate the interaction between TRIP13 and EGFR using CRC cells, SW480 p53-mut,MSS and HT29 p53-mut,MSS . The results showed that there was no direct interaction between EGFR and TRIP13 (Fig.…”

Section: The Trip13-fgfr4 Interaction Is Involved In the Egfr-akt Sigmentioning

confidence: 99%

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TRIP13 promotes metastasis of colorectal cancer regardless of p53 and microsatellite instability status

et al. 2020

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This study demonstrates overexpression of TRIP13 in colorectal cancers is independent of patient's gender, age, race/ethnicity, pathologic stage (primary and liver metastatic lesions), and p53 and microsatellite instability status. Furthermore, it establishes role of TRIP13 in colorectal cancer metastasis and identifies COL6A3, TREM2, SHC3, and KLK7 as its downstream targets. Additionally, TRIP13 activates EGFR‐AKT pathway via its interaction with FGFR4.

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Section: Discussioncontrasting

confidence: 95%

Section: The Trip13-fgfr4 Interaction Is Involved In the Egfr-akt Sigmentioning

confidence: 99%

TRIP13 promotes metastasis of colorectal cancer regardless of p53 and microsatellite instability status

et al. 2020

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“…Mutations in this gene are correlated with gastric, breast, colorectal, and ovarian cancer. CAMK2G could support cancers through activating transcription factors such as AKT1, CREB, and CDK1/2 [ 27 , 28 ]. Chai et al reported CAMK2G was related to lung tumor by affecting stem-like traits and suggested these were mediated through NF- κ B activation.…”

Section: Discussionmentioning

confidence: 99%

Potential Drug Prediction of Glioblastoma Based on Drug Perturbation-Induced Gene Expression Signatures

Zhu

Mao

Man

2021

BioMed Research International

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Objectives. Glioblastoma (GBM) is a malignant brain tumor which is the most common and aggressive type of central nervous system cancer, with high morbidity and mortality. Despite lots of systematic studies on the molecular mechanism of glioblastoma, the pathogenesis is still unclear, and effective therapies are relatively rare with surgical resection as the frequently therapeutic intervention. Identification of fundamental molecules and gene networks associated with initiation is critical in glioblastoma drug discovery. In this study, an approach for the prediction of potential drug was developed based on perturbation-induced gene expression signatures. Methods. We first collected RNA-seq data of 12 pairs of glioblastoma samples and adjacent normal samples from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified by DESeq2, and coexpression networks were analyzed with weighted gene correlation network analysis (WGCNA). Furthermore, key driver genes were detected based on the differentially expressed genes and potential chemotherapeutic drugs and targeted drugs were found by correlating the gene expression profiles with drug perturbation database. Finally, RNA-seq data of glioblastoma from The Cancer Genome Atlas (TCGA) dataset was collected as an independent validation dataset to verify our findings. Results. We identified 1771 significantly DEGs with 446 upregulated genes and 1325 downregulated genes. A total of 24 key drivers were found in the upregulated gene set, and 81 key drivers were found in the downregulated gene set. We screened the Crowd Extracted Expression of Differential Signatures (CREEDS) database to identify drug perturbations that could reverse the key factors of glioblastoma, and a total of 354 drugs were obtained with p value < 10-10. Finally, 7 drugs that could turn down the expression of upregulated factors and 3 drugs that could reverse the expression of downregulated key factors were selected as potential glioblastoma drugs. In addition, similar results were obtained through the analysis of TCGA as independent dataset. Conclusions. In this study, we provided a framework of workflow for potential therapeutic drug discovery and predicted 10 potential drugs for glioblastoma therapy.

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“…The results showed that these lncRNAs were involved in various immune responses, antigen processing and presentation, T cell receptor signaling pathway, epidermal growth factor receptor signaling pathway, ERBB signaling pathway, ECM receptor interaction, focal adhesion, and primary immunode ciency. Epidermal growth factor was reported to activate the androgen receptor and increase the expression of TRIP13 to promote bladder cancer progression [27,28]. Notably, ECM modi cation could not only promote tumor cells to escape, but also help generate and maintain the cancer stem cell niche [29].…”

Section: Discussionmentioning

confidence: 99%

Development and verification of immune-related long non-coding RNA prognostic signature in bladder cancer

Lai¹,

Wu²,

Li³

et al. 2020

Preprint

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Background: Bladder cancer is the second most common malignant tumor in urogenital system. The research aimed to investigate the prognostic role of immune-related long non-coding RNA (lncRNA) in bladder cancer. Methods: We extracted 411 bladder cancer samples from The Cancer Genome Atlas database. Single-sample gene set enrichment analysis was employed to assess the immune cell infiltration of these samples. We recognized differentially expressed lncRNAs between tumors and paracancerous tissues, and differentially expressed lncRNAs between the high and low immune cell infiltration groups. Venn diagram analysis detected differentially expressed lncRNAs that intersected the above groups. LncRNAs with prognostic significance were identified by regression analysis and survival analysis. Multivariate Cox analysis was used to establish the risk score model. The nomogram was established and evaluated by receiver operating characteristic (ROC) curve analysis, concordance index (C-index) analysis, calibration chart, and decision curve analysis (DCA). Additionally, we performed gene set enrichment analysis to explore the potential functions of the screened lncRNAs in tumor pathogenesis.Results: Three hundred and twenty differentially expressed lncRNAs were recognized. We randomly divided patients into the training data set and the testing data set at a 2: 1 ratio. In the training data set, 9 immune-related lncRNAs with prognostic significance were identified. The risk score model was constructed to classify patients as high- and low-risk cohorts. Patients in the low-risk cohort had better survival outcomes than those in the high-risk cohort. The nomogram was established based on the indicators including age, gender, TNM stage, and risk score. The model’s predictive performance was confirmed by ROC curve analysis, C-index analysis, calibration chart, and DCA. The testing data set also achieved similar results. Bioinformatics analysis suggested that the 9-lncRNA signature was involved in modulation of various immune responses, antigen processing and presentation, and T cell receptor signaling pathway.Conclusions: The immune-related lncRNAs have the potential to predict the prognosis of bladder cancer and may play a key role in bladder cancer biology.Trial registration: It was a retrospective study and the gene expression data were obtained from the TCGA database. Trial registration was not needed.

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Increased expression of TRIP13 drives the tumorigenesis of bladder cancer in association with the EGFR signaling pathway

Cited by 26 publications

References 34 publications

TRIP13 promotes metastasis of colorectal cancer regardless of p53 and microsatellite instability status

TRIP13 promotes metastasis of colorectal cancer regardless of p53 and microsatellite instability status

Potential Drug Prediction of Glioblastoma Based on Drug Perturbation-Induced Gene Expression Signatures

Development and verification of immune-related long non-coding RNA prognostic signature in bladder cancer

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