Disruption of serine/threonine protein phosphatase 5 inhibits tumorigenesis of urinary bladder cancer cells

Chen, Ming; Lv, Jian-Min; Ye, Jian-Qing; Cui, Xingang; Qu, Fajun; Chen, Lu; Liu, Xi; Pan, Xiuwu; Li, Lin; Huang, Hai; Yang, Qiwei; Chen, Jie; Wang, Linhui; Gao, Yi; Xu, Danfeng

doi:10.3892/ijo.2017.3997

Cited by 10 publications

(14 citation statements)

References 32 publications

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“…The current standard treatments for MIBC and NMIBC are transurethral resection of bladder tumor (TURBT) and radical cystectomy, respectively, with or without postoperative cisplatin-based combination chemotherapy 4–7. However, due to high recurrence,8 the cost and curative effect of BCa are still unsatisfactory. Considering early diagnosis and effective treatment, it remains urgent to identify novel cytogenetic molecules for BCa.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway</p>

Zhang¹,

Chang²,

Chen³

et al. 2019

CMAR

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BackgroundHepatoma-derived growth factor (HDGF) is a heparin-binding protein that has been observed to be abnormally expressed in numerous malignancies, but the definite role of HDGF in bladder cancer (BCa) has not been clarified. Here, we conduct the present study to evaluate correlations between HDGF and BCa.MethodsBioinformatics analysis was used to evaluate HDGF expression levels in BCa tissues. The effect of HDGF on cell proliferation, migration, invasion, cell cycle and apoptosis was analyzed utilizing CCK-8, clone formation, Transwell assays and flow cytometry, respectively. In addition, the xenograft tumor model was established.ResultsBased on bioinformatics analysis, we noticed that HDGF was highly expressed in BCa tissues and was positively correlated with poor prognosis in patients. Knockdown of HDGF markedly reduced tumorigenesis in BCa cells. Furthermore, the results of flow cytometry showed that HDGF deletion enhanced apoptosis in T24 and 253J cells and led to cell cycle arrest in G1 phase. In further studies, we found that tumor growth was inhibited in xenograft nude mouse models with HDGF deletion. The results of RNA-seq analysis revealed that the PI3K-AKT signaling pathway-related genes were obviously changed in HDGF-deficient 253J cells, and this result was further confirmed by Western blot analysis.ConclusionIn summary, we suggest that HDGF plays a substantial role in BCa and promotes tumor development and progression by regulating the PI3K-AKT signaling pathway, which provides a promising target for BCa treatment.

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Section: Introductionmentioning

confidence: 99%

<p>Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway</p>

Zhang¹,

Chang²,

Chen³

et al. 2019

CMAR

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“…Then, we conducted GO based on DAVID, which demonstrated that the DEGs were mainly abundant in cell division, mitotic nuclear division, cell proliferation, protein kinase binding and protein serine/threonine kinase activity. Based on these observations, we con rmed their role in BC development (22)(23)(24). Additionally, enrichment of the DEGs in some KEGG pathways, for instance, ECM-receptor interaction and Focal adhesion implicate that they are essential in the pathogenesis of BC.…”

Section: Discussionmentioning

confidence: 62%

Identifying Stage-Associated Hub Genes in Bladder Cancer via Weighted Gene Co-Expression Network and Robust Rank Aggregation Analyses

Feng

Zhong

Jian-hua

et al. 2021

Preprint

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Background Bladder cancer (BC) is among the most frequent cancers globally. Although substantial efforts have been put to understand its pathogenesis, its underlying molecular mechanisms have not been fully elucidated. Methods The Robust Rank Aggregation (RRA) approach was adopted to integrate four eligible bladder urothelial carcinoma (BLCA) microarray datasets from the GEO. Differentially expressed genes (DEGs) sets were identified between tumor samples and equivalent healthy samples. We constructed gene co-expression networks using WGCNA to explore the alleged relationship between BC clinical characteristics and gene sets, as well as to identify hub genes. We also incorporated the WGCNA and RRA to screen DEGs. Results CDH11, COL6A3, EDNRA and SERPINF1 were selected from the key module and validated. Based on the results, significant downregulation of the hub genes occurred during the early stages of BC. Moreover, Receiver operating characteristics (ROC) curves and Kaplan-Meier (KM) plots showed that the genes exhibited favorable diagnostic and prognostic value for BC. Based on GSEA for single hub gene, all the genes were closely linked to BC cell proliferation. Conclusions These results offer unique insight into the pathogenesis of BC and recognize CDH11, COL6A3, EDNRA and SERPINF1 as potential biomarkers with diagnostic and prognostic roles in BC.

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“…Researchers have also found that PPP5C, another serine/threonine protein phosphatase, is highly expressed in bladder cancer tissues compared to normal urothelial tissues, which may be related to the mediation of cell proliferation (Chen et al. ). Increases in Et STP may also be related to drug efflux from the cell, which decreases effective intracellular drug concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…showed that knockdown of PPP5C markedly inhibited cell proliferation and colony formation (Chen et al. ). Studies have also shown that PP2A can facilitate virus replication and control ongoing DNA replication (Perl et al.…”

Section: Discussionmentioning

confidence: 99%

Molecular characterization of serine/threonine protein phosphatase of Eimeria tenella

Zhao

Zhu

et al. 2020

J Eukaryotic Microbiology

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Avian coccidiosis is a widespread and economically significant poultry disease caused by several Eimeria species, including Eimeria tenella. Previously, E. tenella serine/threonine protein phosphatase (EtSTP) was found to be differentially expressed in drug‐sensitive (DS) and drug‐resistant strains using RNA‐seq. In the present study, we found that transcription and translation levels of EtSTP were higher in diclazuril‐resistant (DZR) strains and maduramicin‐resistant (MRR) strains than in DS strains using quantitative real‐time PCR (qPCR) and Western blotting. Enzyme activity results indicated that the catalytic activity of EtSTP was higher in the two drug‐resistant strains than in DS strains. Western blot and qPCR analysis also showed that expression levels of EtSTP were higher in unsporulated oocysts (UO) and second‐generation merozoites (SM). Indirect immunofluorescence localization showed that EtSTP was located in most areas of the parasite with the exception of refractile bodies, and fluorescence intensity was enhanced during development. In vitro inhibition experiments showed that the ability of sporozoites (SZ) to invade cells was significantly decreased after treatment with anti‐rEtSTP antibody. These results indicated that EtSTP acted mainly during the developmental and reproductive stages of the parasite and may be related to the resistance of coccidia to external drug pressure.

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Disruption of serine/threonine protein phosphatase 5 inhibits tumorigenesis of urinary bladder cancer cells

Cited by 10 publications

References 32 publications

<p>Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway</p>

<p>Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway</p>

Identifying Stage-Associated Hub Genes in Bladder Cancer via Weighted Gene Co-Expression Network and Robust Rank Aggregation Analyses

Molecular characterization of serine/threonine protein phosphatase of Eimeria tenella

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