NF-κB suppresses apoptosis and promotes bladder cancer cell proliferation by upregulating survivin expression in vitro and in vivo

Cui, Xiaolu; Shen, Danfeng; Kong, Chuize; Zhang, Zhe; Zeng, Yu; Lin, Xu‐Yong; Liu, Xiankui

doi:10.1038/srep40723

Cited by 76 publications

(64 citation statements)

References 49 publications

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“…Constitutive NF‐κB activation was observed in high grade bladder cancer . Many studies indicated inhibition of NF‐κB activation suppresses tumor growth, anti‐apoptosis, angiogenesis, and metastatic potential in bladder cancer in vitro and in vivo . In our results demonstrated NF‐κB activation and expression of tumor progression‐associated proteins were significantly decreased by QNZ (NF‐κB inhibitor) in TSGH‐8301 cells.…”

Section: Discussionsupporting

confidence: 56%

“…31 Many studies indicated inhibition of NF-κB activation suppresses tumor growth, anti-apoptosis, angiogenesis, and metastatic potential in bladder cancer in vitro and in vivo. 32,33 In our results 34 NF-κB activation may be regulated by AKT or MAPKs cascades. 11 We used NF-κB reporter gene assay to evaluate effect of AKT or MAPK inhibitors on NF-κB activation in TSGH 8301 cells.…”

Section: Discussionmentioning

confidence: 58%

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Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

Chiang

Chung

Hsu

2019

Environmental Toxicology

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The aim of the present study is to investigate anticancer effect and mechanism of regorafenib in bladder cancer in vitro and in vivo . Human bladder cancer TSGH 8301 cells were treated with regorafenib, NF‐κB, AKT, or mitogen‐activated protein kinase (MAPK) inhibitors for different time. The changes of cell viability, NF‐κB activation, apoptotic signaling transduction, and expression of tumor progression‐associated proteins were evaluated with MTT, NF‐κB reporter gene assay, flow cytometry, and Western blotting assay. TSGH 8301 tumor bearing mice were established and treated with vehicle (140 μL of 0.1% DMSO) or regorafenib (10 mg/kg/day by gavage) for 15 days. The changes of tumor volume, body weight, NF‐κB activation, MAPK activation, and tumor progression‐associated proteins (MMP‐9, XIAP, VEGF, and Cyclin‐D1) after regorafenib treatment were evaluated with digital caliper, digital weight, and ex vivo Western blotting assay. Our results demonstrated NF‐κB activation and protein levels of MMP‐9, XIAP, VEGF, and Cyclin‐D1 were significantly reduced by NF‐κB (QNZ), ERK (PD98059), and P38 (SB203580) inhibitors. Regorafenib also significantly induced extrinsic and intrinsic apoptotic signaling transduction in bladder cancer in vitro . In addition, regorafenib significantly inhibited tumor growth, NF‐κB, p38, ERK activation and expression of tumor progression‐associated proteins in bladder cancer in vitro and in vivo . Taken together, these results proved that regorafenib not only induced apoptosis through extrinsic and intrinsic pathways and but suppressed MAPK/ NF‐κB‐modulated tumor progression in bladder cancer.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 58%

Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

Chiang

Chung

Hsu

2019

Environmental Toxicology

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“…Cell lines of human BC, T24 and 5637, were obtained from the Typical Culture Preservation Commission Cell Bank of the Chinese Academy of Sciences (Shanghai, China). Cell lines were cultured in RPMI-1640 medium supplemented with 1% penicillin/streptomycin and 10% FBS (all from HyClone; GE Healthcare Life Sciences, Logan, UT, USA) and under a humidified atmosphere of 5% CO 2 at 37˚C (15).…”

Section: Methodsmentioning

confidence: 99%

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Jiang

et al. 2018

Oncol Rep

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MicroRNA (miR)-26a-5p and miR-26b-5p consistently play an antitumor role in many types of cancers, but the underlying mechanism remains unclear in bladder cancer (BC). In the present study, we found that, in BC tissues, the levels of miR-26a-5p and miR-26b-5p were lower than in paired normal tissues. The upregulation of miR-26-5p significantly inhibited the proliferation of BC cell lines (T24 and 5637). Bioinformatics analysis indicated that Programmed Cell Death 10 (PDCD10) was the downstream target gene of miR-26a-5p/miR-26b-5p, and this was ascertained by western blotting and quantitative real-time reverse transcription PCR (RT-qPCR). In addition, in the 3'-UTR of PDCD10, the binding site was identified using a luciferase reporter assay. We determined that clinical BC tissues presented higher PDCD10 levels than adjacent normal tissues and that PDCD10 promoted proliferation of BC cell lines. Overexpression of miR-26a-5p/miR-26b-5p inhibited the stimulatory effect on proliferation of BC cells induced by PDCD10. In addition, in vivo experiments and clinical data revealed that the prognosis of BC patients with high expression of miR-26a-5p/miR-26b-5p and low expression of PDCD10 was better than that of patients with low miR-26-5p and high PDCD10 expression. These data revealed that miR-26a-5p and miR-26b-5p were pivotal regulators in BC progression by targeting the proliferation-related protein, PDCD10. The miR-26-5p/PDCD10 interaction may provide important insight into the pathway of BC progression and present novel opportunities for future diagnosis and treatment strategies, especially for patients with high levels of PDCD10.

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“…BCa is manifested with highly recurrent multiple tumors [22,23]. Clinical tumor staging, pathological grade, and lymph node metastasis have been proven to be vital predictors of clinical prognosis [24]. Numerous studies have demonstrated that pathological grading and clinical tumor staging play pivotal roles are associated with lymph node metastasis and predict clinical prognosis of patients with BCa in clinical practice.…”

Section: Discussionmentioning

confidence: 99%

Immune Checkpoint Human Endogenous Retrovirus-H Long Terminal Repeat-Associating Protein 2 is Upregulated and Independently Predicts Unfavorable Prognosis in Bladder Urothelial Carcinoma

Lin

Wang

et al. 2019

Nephron

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Background/Aims: human endogenous retrovirus-H long terminal repeat-associating protein 2 (HHLA2) is highly expressed in multiple solid malignant tumors, making it a potential biomarker for tumorigenesis and invasion. However, the expression and clinical significance of HHLA2 in bladder urothelial carcinoma (BUC) have not been extensively studied. This study aimed to investigate the relationship between HHLA2 expression and clinicopathological characteristics of BUC. Methods: A total of 212 patients pathologically diagnosed with BUC were included in this study. HHLA2 expression was analyzed by immunohistochemical staining and qRT-polymerase chain reaction. Correlations of HHLA2 expression and pathological characteristics, including 5-year recurrence-free survival (RFS) and overall survival (OS) were examined, and the diagnostic value of HHLA2 was estimated by using the receiver operating characteristic (ROC) curve. Results: Immunohistochemical staining showed that the expression of HHLA2 was significantly upregulated in BUC tissues compared with normal bladder tissues. In BUC tissues, HHLA2 expression was significantly associated with tumor size, tumor stage, tumor grade, and lymph node metastasis (all p < 0.05). HHLA2 expression was an independent prognostic factor of tumor metastasis (p < 0.05). The Kaplan-Meier survival curve revealed that high HHLA2 expression was significantly correlated with the poor RFS and OS of BUC patients (both p < 0.05), and the ROC curve showed HHLA2 could be a good diagnostic marker. Conclusions: HHLA2 can independently predict unfavorable prognosis in BUC.

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NF-κB suppresses apoptosis and promotes bladder cancer cell proliferation by upregulating survivin expression in vitro and in vivo

Cited by 76 publications

References 49 publications

Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

miRNA‑26a‑5p and miR‑26b‑5p inhibit the proliferation of bladder cancer cells by regulating PDCD10

Immune Checkpoint Human Endogenous Retrovirus-H Long Terminal Repeat-Associating Protein 2 is Upregulated and Independently Predicts Unfavorable Prognosis in Bladder Urothelial Carcinoma

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