EZH2 inhibition suppresses bladder cancer cell growth and metastasis via the JAK2/STAT3 signaling pathway

Chen, Zhiyuan; Du, Yanwei; Liu, Xiuheng; Chen, Hui; Wang, Xiaodong; Guo, Jia; Wang, Min; Wang, Xiao; Wang, Lei

doi:10.3892/ol.2019.10359

Cited by 32 publications

(28 citation statements)

References 45 publications

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“…One of the issues in treatment of patients with BC is the high metastatic capability of BC cells that negatively affects overall survival of patients with this life-threatening disorder, and remarkably reduces efficacy of chemotherapy and radiotherapy, since cancer cells migrate in neighboring and distant tissues, providing problems with their effective eradication [ 26 , 27 , 28 ]. Several molecular pathways such as ZEB1 [ 19 ], EZH2 [ 29 ], PI3K/Akt [ 30 ], and so on have been identified as potential factors involved in metastasis and invasion of BC cells. Epithelial-to-mesenchymal transition (EMT) is one of the most important molecular pathways that enhanced migratory ability of cancer cells [ 31 , 32 ].…”

Section: Introductionmentioning

confidence: 99%

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

et al. 2020

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Bladder cancer (BC) is the 11th most common diagnosed cancer, and a number of factors including environmental and genetic ones participate in BC development. Metastasis of BC cells into neighboring and distant tissues significantly reduces overall survival of patients with this life-threatening disorder. Recently, studies have focused on revealing molecular pathways involved in metastasis of BC cells, and in this review, we focus on microRNAs (miRNAs) and their regulatory effect on epithelial-to-mesenchymal transition (EMT) mechanisms that can regulate metastasis. EMT is a vital process for migration of BC cells, and inhibition of this mechanism restricts invasion of BC cells. MiRNAs are endogenous non-coding RNAs with 19–24 nucleotides capable of regulating different cellular events, and EMT is one of them. In BC cells, miRNAs are able to both induce and/or inhibit EMT. For regulation of EMT, miRNAs affect different molecular pathways such as transforming growth factor-beta (TGF-β), Snail, Slug, ZEB1/2, CD44, NSBP1, which are, discussed in detail this review. Besides, miRNA/EMT axis can also be regulated by upstream mediators such as lncRNAs, circRNAs and targeted by diverse anti-tumor agents. These topics are also discussed here to reveal diverse molecular pathways involved in migration of BC cells and strategies to target them to develop effective therapeutics.

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Section: Introductionmentioning

confidence: 99%

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

et al. 2020

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“…In colorectal cancer, this pathway influences tumor cell activity by regulating the expression of BCL2, E-cadherin, and VEGF, among others,8 while in ovarian cancer, activated STAT3 can promote the occurrence of EMT through the JAK2/STAT3/Snail signaling pathway 9. Furthermore, albumin can induce cell proliferation and transdifferentiation of renal tubular epithelial cells by activating the JAK2/STAT3 signaling pathway 10. However, reports on the correlation between JAK2/STAT3 signaling and EMT in lung adenocarcinoma are limited…”

Section: Introductionmentioning

confidence: 99%

<p>STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway</p>

Guo

Yan

Zhang

et al. 2019

CMAR

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PurposeRecent studies have shown that STIP1 is associated with proliferation and migration in numerous types of tumors; however, the role of STIP1 in lung adenocarcinoma is still poorly understood. Therefore, the aim of this study was to evaluate the role of STIP1 in lung adenocarcinoma, in vitro and in vivo.MethodsThe expression of STIP1 in lung adenocarcinoma was assessed by immunohistochemistry, RT-qPCR, and Western blot. The effects of STIP1 on the proliferation of lung adenocarcinoma cells were detected by the cell counting kit-8 assay; the effect of STIP1 on adhesion of lung adenocarcinoma cells was detected by Giemsa staining, while the cell scratch and Transwell assays were employed to examine the effect of STIP1 on the migratory ability of lung adenocarcinoma cells. Finally, apoptosis was evaluated by Hoechst staining and flow cytometry.ResultsThe expression level of STIP1 in lung adenocarcinoma tissue was significantly higher than that in adjacent normal tissue (P<0.05). Compared with that in nontransfected controls, cell proliferation, adhesion, and migration, as well as vimentin protein expression and levels of phosphorylated JAK2/STAT3, were significantly decreased (P<0.05) in A549 lung adenocarcinoma cells transfected with STIP1 shRNA, whereas E-cadherin protein expression and rates of apoptosis were significantly increased in these cells (P< 0.05).ConclusionElevated expression of STIP1 in lung adenocarcinoma may enhance the proliferative, adhesive, and migratory ability, and reduce the apoptosis of lung adenocarcinoma cells through the JAK2/STAT3 signaling pathway and epithelial-mesenchymal transition (EMT), thereby promoting the recurrence and metastatic potential of this cancer. The results indicate that STIP1 may be an effective therapeutic target for the treatment of lung adenocarcinoma.

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“…On the other hand, previous studies have provided some potential targets of miR-605, such as tumor necrosis factor α-induced protein 3, EN2, enhancer of zeste 2 (EZH2) and forkhead Box P1, which mediate the functional effects of miR-605 in human malignancies ( 18 , 19 , 37 , 38 ). EZH2 is a widely investigated oncogene in several human malignancies, such as non-small cell lung cancer and bladder cancer ( 39 , 40 ). In OS tissues, EZH2 has been found to be upregulated and associated with aggressive tumor behavior and poor prognosis and the knockdown of EZH2 could significantly inhibit OS cell proliferation, migration and invasion ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of microRNA‑605 indicates poor prognosis and promotes the progression of osteosarcoma

2020

Oncol Lett

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Osteosarcoma (OS) is a type of primary bone tumor, which is one of the leading causes of cancer-related death. MicroRNA (miR)-605 has been demonstrated to act as a prognostic biomarker and therapeutic target in various cancers, such as breast cancer and non-small cell lung cancer, but its function in OS remains unclear. The aim of the present study was to investigate the prognostic value of miR-605 in patients with OS by evaluating its expression levels and to explore the biological function of miR-605 in OS progression. For this purpose, tumor tissues and adjacent normal tissues were collected from OS patients, and the expression of miR-605 in the collected tissues and OS MG63, U2OS, HOS, and SAOS-2 cell lines was detected by quantitative real-time PCR. The prognostic value of miR-605 was evaluated by Kaplan-Meier survival curves and Cox regression analysis. The effects of miR-605 on OS cell proliferation, migration and invasion were analyzed by the CCK-8 and transwell assays, respectively. The results of the present study revealed that miR-605 was significantly downregulated in OS tissues compared with adjacent normal tissues, which was associated with the clinical stage and distant metastasis of patients. Additionally, the downregulation of miR-605 predicted the poor prognosis of patients with OS and served as an independent prognostic indicator. The downregulation of miR-605 enhanced cell proliferation, migration, and invasion of OS cells, which suggested that miR-605 may be involved in the progression of OS. The findings of the present study provide a new therapeutic target for the treatment of patients with OS.

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EZH2 inhibition suppresses bladder cancer cell growth and metastasis via the JAK2/STAT3 signaling pathway

Cited by 32 publications

References 45 publications

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

Role of microRNA/Epithelial-to-Mesenchymal Transition Axis in the Metastasis of Bladder Cancer

<p>STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway</p>

Downregulation of microRNA‑605 indicates poor prognosis and promotes the progression of osteosarcoma

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