[Corrigendum] Mutation of TGF‑β receptor II facilitates human bladder cancer progression through altered TGF‑β1 signaling pathway

This study investigated the effects of Golgi membrane protein 73 (GP73) on the epithelial–mesenchymal transition (EMT) and on bladder cancer cell invasion and metastasis through the TGF‐β1/Smad2 signalling pathway. Paired bladder cancer and adjacent tissue samples (102) and normal bladder tissue samples (106) were obtained. Bladder cancer cell lines (T24, 5637, RT4, 253J and J82) were selected and assigned to blank, negative control (NC), TGF‐β, thrombospondin‐1 (TSP‐1), TGF‐β1+ TSP‐1, GP73‐siRNA‐1, GP73‐siRNA‐2, GP73‐siRNA‐1+ TSP‐1, GP73‐siRNA‐1+ pcDNA‐GP73, WT1‐siRNA and WT1‐siRNA + GP73‐siRNA‐1 groups. Expressions of GP73, TGF‐β1, Smad2, p‐Smad2, E‐cadherin and vimentin were detected using RT‐qPCR and Western blotting. Cell proliferation, migration and invasion were determined using MTT assay, scratch testing and Transwell assay, respectively. Compared with the blank and NC groups, levels of GP73, TGF‐β1, Smad2, p‐Smad2, N‐cadherin and vimentin decreased, and levels of WT1 and E‐cadherin increased in the GP73‐siRNA‐1 and GP73‐siRNA‐2 groups, while the opposite results were observed in the WT1 siRNA, TGF‐β, TSP‐1 and TGF‐β + TSP‐1 groups. Cell proliferation, migration and invasion notably decreased in the GP73‐siRNA‐1 and GP73‐siRNA‐2 groups in comparison with the blank and NC groups, while in the WT1 siRNA, TGF‐β, TSP‐1 and TGF‐β + TSP‐1 groups, cell migration, invasion and proliferation showed the reduction after the EMT. These results suggest that GP73 promotes bladder cancer invasion and metastasis by inducing the EMT through down‐regulating WT1 levels and activating the TGF‐β1/Smad2 signalling pathway.

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GP73 promotes invasion and metastasis of bladder cancer by regulating the epithelial–mesenchymal transition through the TGF‐β1/Smad2 signalling pathway

Yang

Liu

et al. 2018

J Cellular Molecular Medi

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Tumor exome sequencing and copy number alterations reveal potential predictors of intrinsic resistance to multi-targeted tyrosine kinase inhibitors

et al. 2017

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Multi-targeted tyrosine kinase inhibitors (TKIs) have broad efficacy and similar FDA-approved indications, suggesting shared molecular drug targets across cancer types. Irrespective of tumor type, 20-30% of patients treated with multi-targeted TKIs demonstrate intrinsic resistance, with progressive disease as a best response. We conducted a retrospective cohort study to identify tumor (somatic) point mutations, insertion/deletions, and copy number alterations (CNA) associated with intrinsic resistance to multi-targeted TKIs. Using a candidate gene approach (n=243), tumor next-generation sequencing and CNA data was associated with resistant and non-resistant outcomes. Resistant individuals (n=11) more commonly harbored somatic point mutations in NTRK1, KDR, TGFBR2, and PTPN11 and CNA in CDK4, CDKN2B, and ERBB2 compared to non-resistant (n=26, p<0.01). Using a random forest classification model for variable reduction and a decision tree classification model, we were able to differentiate intrinsically resistant from non-resistant patients. CNA in CDK4 and CDKN2B were the most important analytical features, implicating the cyclin D pathway as a potentially important factor in resistance to multi-targeted TKIs. Replication of these results in a larger, independent patient cohort has potential to inform personalized prescribing of these widely utilized agents.

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Tumor microenvironment and epithelial-mesenchymal transition in bladder cancer: Cytokines in the game?

Martins‐Lima

Chianese

Altucci

et al. 2023

Front. Mol. Biosci.

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Bladder cancer (BlCa) is a highly immunogenic cancer. Bacillus Calmette-Guérin (BCG) is the standard treatment for non-muscle invasive bladder cancer (NMIBC) patients and, recently, second-line immunotherapies have arisen to treat metastatic BlCa patients. Understanding the interactions between tumor cells, immune cells and soluble factors in bladder tumor microenvironment (TME) is crucial. Cytokines and chemokines released in the TME have a dual role, since they can exhibit both a pro-inflammatory and anti-inflammatory potential, driving infiltration and inflammation, and also promoting evasion of immune system and pro-tumoral effects. In BlCa disease, 70–80% are non-muscle invasive bladder cancer, while 20–30% are muscle-invasive bladder cancer (MIBC) at the time of diagnosis. However, during the follow up, about half of treated NMIBC patients recur once or more, with 5–25% progressing to muscle-invasive bladder cancer, which represents a significant concern to the clinic. Epithelial-mesenchymal transition (EMT) is one biological process associated with tumor progression. Specific cytokines present in bladder TME have been related with signaling pathways activation and EMT-related molecules regulation. In this review, we summarized the immune landscape in BlCa TME, along with the most relevant cytokines and their putative role in driving EMT processes, tumor progression, invasion, migration and metastasis formation.

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[Corrigendum] Mutation of TGF‑β receptor II facilitates human bladder cancer progression through altered TGF‑β1 signaling pathway

Cited by 5 publications

References 38 publications

GP73 promotes invasion and metastasis of bladder cancer by regulating the epithelial–mesenchymal transition through the TGF‐β1/Smad2 signalling pathway

GP73 promotes invasion and metastasis of bladder cancer by regulating the epithelial–mesenchymal transition through the TGF‐β1/Smad2 signalling pathway

Tumor exome sequencing and copy number alterations reveal potential predictors of intrinsic resistance to multi-targeted tyrosine kinase inhibitors

Tumor microenvironment and epithelial-mesenchymal transition in bladder cancer: Cytokines in the game?

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