Research progress on bladder cancer molecular genetics

Kang, Zhengjun; Li, Yuhui; Yu, Yang; Guo, Zhan

doi:10.4103/0973-1482.145792

Cited by 10 publications

(8 citation statements)

References 69 publications

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“…which was statistically significant compared to control group (P = 0.019). Furthermore, most of the mutations either deletion or duplication were found in exon 1, which was statistically significant (P = 0.001) compared to control group, followed by exons 6,8,9,12,11,7,5,4,3, and 2.…”

Section: R Bazrafshani Et Al Deletion/duplication Mutation Screementioning

confidence: 81%

Deletion/duplication mutation screening of TP53 gene in patients with transitional cell carcinoma of urinary bladder using multiplex ligation‐dependent probe amplification

et al. 2015

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Bladder cancer is a molecular disease driven by the accumulation of genetic, epigenetic, and environmental factors. The aim of this study was to detect the deletions/duplication mutations in TP53 gene exons using multiplex ligation‐dependent probe amplification (MLPA) method in the patients with transitional cell carcinoma (TCC). The achieved formalin‐fixed paraffin‐embedded tissues from 60 patients with TCC of bladder were screened for exonal deletions or duplications of every 12 TP53 gene exons using MLPA. The pathological sections were examined by three pathologists and categorized according to the WHO scoring guideline as 18 (30%) grade I, 22 (37%) grade II, 13 (22%) grade III, and 7 (11%) grade IV cases of TCC. None mutation changes of TP53 gene were detected in 24 (40%) of the patients. Furthermore, mutation changes including, 15 (25%) deletion, 17 (28%) duplication, and 4 (7%) both deletion and duplication cases were observed among 60 samples. From 12 exons of TP53 gene, exon 1 was more subjected to exonal deletion. Deletion of exon 1 of TP53 gene has occurred in 11 (35.4%) patients with TCC. In general, most mutations of TP53, either deletion or duplication, were found in exon 1, which was statistically significant. In addition, no relation between the TCC tumor grade and any type of mutation were observed in this research. MLPA is a simple and efficient method to analyze genomic deletions and duplications of all 12 exons of TP53 gene. The finding of this report that most of the mutations of TP53 occur in exon 1 is in contrast to that of the other reports suggesting that exons 5–8 are the most (frequently) mutated exons of TP53 gene. The mutations of exon 1 of TP53 gene may play an important role in the tumorogenesis of TCC.

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Section: R Bazrafshani Et Al Deletion/duplication Mutation Screementioning

confidence: 81%

Deletion/duplication mutation screening of TP53 gene in patients with transitional cell carcinoma of urinary bladder using multiplex ligation‐dependent probe amplification

et al. 2015

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“…The highly metastatic and invasive characteristics of BC reduce the effectiveness of treatments; therefore, these characteristics have become a focus of research (4,5). In addition, numerous clinicians emphasize that management, prevention and diagnosis are also of importance to effective control of BC (6)(7)(8). Therefore, it is necessary to elucidate the underlying molecular mechanisms of BC.…”

Section: Introductionmentioning

confidence: 99%

microRNA‑145 modulates migration and invasion of bladder cancer cells by targeting N‑cadherin

Zhang

Chang

et al. 2018

Mol Med Report

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MicroRNA (miRNA)‑145 has been demonstrated to serve a role in several types of tumors, however, the potential molecular mechanism of action of miRNA‑145 in bladder cancer metastasis remains to be elucidated. This study aimed to investigate the potential modulation of miRNA‑145 in bladder carcinoma and elucidate the underlying molecular mechanism. The expression of miRNA‑145 in bladder adenocarcinoma tissues and bladder cancer cells was measured by reverse transcription‑quantitative polymerase chain reaction. miRNA‑145 mimics and inhibitor were transfected into bladder cancer (BC) cells to determine the role of miRNA‑145 on cell motility and invasion measured by wound healing and transwell assays. Luciferase assay was performed to confirm whether N‑cadherin was the direct target of miRNA‑145. Subsequently, expression of N‑cadherin and matrix metalloproteinase‑9 (MMP9) in BC cells were detected by western blot analysis. miRNA‑145 was significantly downregulated cells and tissues from patients with BC, compared with healthy controls. miRNA‑145 markedly inhibited the ability of BC cells to migrate and invade. Furthermore, N‑cadherin was identified as a target of miRNA‑145 in BC cells. MMP9, acting downstream of N‑cadherin, was downregulated in BC cells by miRNA‑145. In the present study, miRNA‑145 suppressed the migration and invasion of BC cells by regulating N‑cadherin. The results of the present study indicated that miRNA‑145 may function as a tumor suppressor and may have a potential to be a diagnostic and predictive biomarker, and a therapeutic target for treatment of BC.

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“…The occurrence and development of bladder cancer is a multi-factor and multi-step process 11 . Current studies have con rmed that multiple oncogenes and tumor suppressor genes play very important roles in this process 12 . The abnormally high expression of oncogenes such as MDM2 13 and CCND1 14 , and abnormal deletion or mutation of tumor suppressor genes such as TP53 15 and PTEN 16 have been revealed.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of ZNF280A Inhibits Cell Proliferation and Promotes Cell Apoptosis of Bladder Cancer

Lin

Wang

Chen

et al. 2020

Preprint

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Background: ZNF280A is a member of zinc finger protein family, whose role in human cancers is little known and rarely reported. This study aimed to investigate the role of ZNF280A in bladder cancer. Methods: Immunohistochemical analysis was performed to detect the expression of ZNF280A in clinical samples. ZNF280A knockdown cell models were constructed by transfection of shRNA-expressing lentivirus. MTT assay and flow cytometry were performed for detecting cell proliferation, apoptosis and cycle. Wound healing and Transwell assays were operated to detect cell migration. Western blotting and Human Apoptosis Antibody Microarray were used to measure expression of related proteins. Mice xenograft model was constructed for in vivo study.Results: Our study demonstrated that ZNF280A was up-regulated in bladder cancer tissues compared with normal tissues, whose high expression was significantly correlated with advanced malignant grade. Knockdown of ZNF280A inhibited cell proliferation and cell migration, promoted cell apoptosis and G1/G2 phase arrest. The tumor growth in vivo was also proved to be inhibited by ZNF280A. Moreover, ZNF280A may promote bladder cancer through regulation of MAPK9, Cyclin D1 and PIK3CA. Conclusions: In this study, ZNF280A was shown as a potential tumor promotor and prognosis indicator for bladder cancer. Targeting ZNF280A may be a promising strategy for the development of novel bladder cancer treatment.

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Research progress on bladder cancer molecular genetics

Cited by 10 publications

References 69 publications

Deletion/duplication mutation screening of TP53 gene in patients with transitional cell carcinoma of urinary bladder using multiplex ligation‐dependent probe amplification

Deletion/duplication mutation screening of TP53 gene in patients with transitional cell carcinoma of urinary bladder using multiplex ligation‐dependent probe amplification

microRNA‑145 modulates migration and invasion of bladder cancer cells by targeting N‑cadherin

Knockdown of ZNF280A Inhibits Cell Proliferation and Promotes Cell Apoptosis of Bladder Cancer

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