The effects of STAT3 and Survivin silencing on the growth of human bladder carcinoma cells

Zhang, Baogang; Lu, Zhihua; Hou, Yuchuan; Hu, Jinghai; Chun-xi, Wang

doi:10.1007/s13277-014-1704-8

Cited by 22 publications

(13 citation statements)

References 19 publications

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“…Many studies have shown that Survivin could serve as a molecular target for bladder cancer therapy [33–35]. Knockdown of Survivin by using siRNA could dramatically suppress the proliferation and invasion of bladder cancer cells.…”

Section: Discussionmentioning

confidence: 99%

miR-138-5p contributes to cell proliferation and invasion by targeting Survivin in bladder cancer cells

et al. 2016

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BackgroundSurvivin (encoded by the gene BIRC5) plays an important role in the carcinogenesis of bladder cancer. Identifying miRNAs that target Survivin in the setting of bladder cancer will help to develop Survivin-based therapies for bladder cancer.MethodsThe expression levels of miR-138-5p and Survivin protein were measured in 12 resected bladder cancer specimens. The correlation between miR-138-5p and Survivin was further examined by evaluating Survivin expression in human bladder cancer cell lines that either overexpressed or knocked down miR-138-5p. A luciferase reporter assay was performed to test the direct binding of miR-138-5p to the target gene BIRC5. We also investigated the biological role of miR-138-5p targeting to Survivin in bladder cancer cell lines both in vivo and in vitro.ResultsIn this study, we found that the Survivin protein was either absent or weakly expressed in normal adjacent tissues and consistently up-regulated in bladder cancer tissues; however, the mRNA levels did not vary as much, suggesting that a post-transcriptional mechanism was involved. Because microRNAs are powerful post-transcriptional regulators of gene expression, we used bioinformatic analyses to search for microRNAs that could potentially target BIRC5 in the setting of bladder cancer. We identified 2 specific targeting sites for miR-138-5p in the 3′ untranslated region (3′-UTR) of BIRC5. We further identified an inverse correlation between miR-138-5p and Survivin protein levels in bladder cancer tissue samples. By overexpressing or knocking down miR-138-5p in bladder cancer cells, we experimentally confirmed that miR-138-5p directly recognizes the 3′-UTR of the BIRC5 transcript and regulates Survivin expression. Furthermore, the biological consequences of the targeting of BIRC5 by miR-138-5p were examined in vitro via cell proliferation and invasion assays and in vivo using a mouse xenograft tumor model. We demonstrated that BIRC5 repression by miR-138-5p suppressed the proliferative and invasive characteristics of bladder cancer cells and that miR-138-5p exerted an anti-tumor effect by negatively regulating BIRC5 in a xenograft mouse model.ConclusionsTaken together, our findings provide the first clues regarding the role of miR-138-5p as a tumor suppressor in bladder cancer by inhibiting BIRC5 translation.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-016-0569-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

miR-138-5p contributes to cell proliferation and invasion by targeting Survivin in bladder cancer cells

et al. 2016

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“…The (a) tumor diameter and the (b) shortest track were measured using a vernier caliper every five days. The tumor volume (in cubic millimeter) was calculated according to the formula V=ab 2 /2 (15). On day 20, the tumors were removed and weighed.…”

Section: Methodsmentioning

confidence: 99%

Knockdown of TRAF4 expression suppresses osteosarcoma cell growth in vitro and in vivo

Yao

Wang

Cai

et al. 2014

International Journal of Molecular Medicine

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Tumor necrosis factor (TNF) receptor-associated factor 4 (TRAF4) is an adapter molecule that is overexpressed in certain cancers. TRAF4 is overexpressed in osteosarcoma tissues and osteosarcoma cells. Using the technique of RNA interference, the expression of TRAF4 in the human osteosarcoma Saos-2 cell line was shown to be downregulated. The proliferation, cell cycle arrest and apoptosis ability of Saos‑2 cells were examined, as was tumor development in a xenograft mouse model. The results showed that the TRAF4 knockdown exerts inhibitory effects on the proliferation ability of Saos-2 cells and tumor development in a xenograft mouse model. Simultaneously, it was found that TRAF4 knockdown led to cell cycle arrest in the G1 phase and promoted Saos-2 cell apoptosis. Following TNF-α treatment, the expression of nuclear factor κB was significantly reduced in the TRAF4‑small interfering RNA group. These results indicate that TRAF4 regulated osteosarcoma cell growth in vitro and in vivo, and offers a candidate molecular target for osteosarcoma prevention and therapy.

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“…In this study, the downregulation of STAT3 or Survivin, an inhibitor of apoptosis, suppressed the proliferation of BC cells. Moreover, no additive effects were recorded by the STAT3 and Survivin joined knockdown, suggesting that they both belong to the same pathway in T24 cells [75]. …”

Section: Role Of Stat3 Signaling In Bladder Cancermentioning

confidence: 99%

Role of STAT3 pathway in genitourinary tumors

Santoni

Conti²,

Piva

et al. 2015

Future Sci. OA

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The STAT3 is often dysregulated in genitourinary tumors. In prostate cancer, STAT3 activation correlates with Gleason score and pathological stage and modulates cancer stem cells and epithelial-mesenchymal transition. In addition, STAT3 promotes the progression from carcinoma in situ to invasive bladder cancer and modulates renal cell carcinoma angiogenesis by increasing the expression of HIF1α and VEGF. STAT3 is also involved in the response to tyrosine kinase inhibitors sunitinib and axitinib, in patients with metastatic renal cell carcinoma, and to second-generation androgen receptor inhibitor enzalutamide in patients with advanced prostate cancer. In this review, we describe the role of STAT3 in genitourinary tumors, thus describing its potential for future therapeutic strategies.Regulation of the protein STAT3 is often dysfunctional in genitourinary tumors, including prostate, bladder and kidney cancer. STAT3 is involved in the generation of these tumors and has an effect in their response to treatments. In this review, we describe its role in genitourinary tumors and discuss its potential for use in future therapies.

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The effects of STAT3 and Survivin silencing on the growth of human bladder carcinoma cells

Cited by 22 publications

References 19 publications

miR-138-5p contributes to cell proliferation and invasion by targeting Survivin in bladder cancer cells

miR-138-5p contributes to cell proliferation and invasion by targeting Survivin in bladder cancer cells

Knockdown of TRAF4 expression suppresses osteosarcoma cell growth in vitro and in vivo

Role of STAT3 pathway in genitourinary tumors

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