Effects of microRNA-135a on the epithelial–mesenchymal transition, migration and invasion of bladder cancer cells by targeting GSK3β through the Wnt/β-catenin signaling pathway

Mao, Xia-Wa; Xiao, Jiaquan; Li, Zhongyi; Zheng, Yian; Zhang, Nan

doi:10.1038/emm.2017.239

Cited by 46 publications

(44 citation statements)

References 42 publications

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“…The invasion ability shown by means of the transwell analysis declined dramatically too. 22,23 Taking all the above results together, we demonstrated here that NSCs/NPCs had inhibitory effects on the growth and invasion of U87 glioma in vitro might do so via affecting the growth and invasion of U87 stemlike cells. And possibly, this effect was executed through the PI3K/AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 56%

Neural stem cell‐derived factors inhibit the growth and invasion of U87 stem‐like cells in vitro

Tan

et al. 2018

J of Cellular Biochemistry

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Glioma is one of the most common and aggressive tumors in the brain. Significant attention has been paid to the potential use of neural stem/progenitor cells (NSCs/NPCs) as delivery vehicles to cure gliomas. However, whether the NSCs/NPCs or the factors they produced could make a contribution still remains to be seen. In this study, we focused on the inhibitory effects of the factors produced by NSCs/NPCs on the biological behavior of the glioma stem‐like cell in vitro. The human glioma cell line U87 was selected and the U87 stem‐like cells were addressed. After being cultured in the NSC condition medium (NSC‐CM), the viability and proliferation of U87 stem‐like cells were significantly reduced. The invasion of U87 stem‐like cells and the migration of U87 cells were also significantly decreased. However, no significant change was observed in regard to the astrocytic differentiation of U87 stem‐like cells. These indicated that NSCs/NPCs produced some factors and had an inhibitory effect on the growth and invasion but not the terminal differentiation of U87 stem‐like cells. It is worth paying attention to NSCs/NPCs as a high‐potential candidate for glioma treatment.

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Section: Discussionmentioning

confidence: 56%

Neural stem cell‐derived factors inhibit the growth and invasion of U87 stem‐like cells in vitro

Tan

et al. 2018

J of Cellular Biochemistry

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“…In colon adenocarcinoma, miR‐135a was suggested to be a "sponge" of lncRNA FOXD3‐AS1 to regulate cell proliferation, migration, invasion, and apoptosis by targeting SIRT1 . In addition, several studies have also revealed that the positive effects of miR‐135a on BC cell proliferation, epithelial‐mesenchymal transition, migration and invasion . However, whether miR‐135a participated in the regulation of MBNL1‐AS1 in BC progression remains unclear.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

et al. 2019

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LncRNAs have been shown to play essential roles in bladder cancer (BC) progress.Our microarrays of clinical samples firstly screened that lncRNA muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) was poorly expressed in BC tissues. However, its biological function in BC remains not well understood. Here we examined the clinical correlations with MBNL1-AS1 in BC patients. Then, 5673 and T24 cell lines were employed to investigate the role of MBNL1-AS1 in the proliferation and apoptosis of BC cells in vitro and in vivo. Furthermore, miR-135a-5p (miR-135a)/PHLPP2/FOXO1 axis was focused to explore its regulatory mechanism in BC.The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. The apoptotic cells and the cleavages of caspase-3/9 were reduced in MBNL1-AS1-silenced BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO1 axis, providing a novel insight for BC diagnosis and treatment. K E Y W O R D S bladder cancer, FOXO1, MBNL1-AS1, miR-135a-5p, PHLPP2 | 725 WEI Et al.

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“…It has been widely reported that the expression levels of Wnt factors are significantly upregulated in bladder cancer (30,31), and the Wnt/β-catenin signalling is important in the malignant progression of bladder cancer (32,33). For example, Shen et al showed that the levels of β-catenin in human bladder cancer tissues were upregulated with increasing grade of malignancy (30).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA SNHG20 promotes bladder cancer via activating the Wnt/β-catenin signalling pathway

Zhao

Gao

et al. 2018

Int J Mol Med

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The long non‑coding RNA, small nucleolar RNA host gene 20 (SNHG20), is involved in promoting several common types of human cancer, however, the exact function of SNHG20 in the pathogenesis of bladder cancer remains to be elucidated. The present study aimed to examine the regulatory mechanism of SNHG20 underlying the malignant progression of bladder cancer. Reverse transcription‑quantitative polymerase chain reaction and western blotting were used to examine mRNA and protein expression. Cell survival, proliferation, apoptosis, colony formation, migration and invasion were also studied. The resulting data indicated that SNHG20 was significantly upregulated in bladder cancer tissues and cell lines, compared with its expression in adjacent non‑tumour tissues and the SV‑HUC‑1 normal urinary tract epithelial cell line, respectively. In addition, the high expression of SNHG20 was associated with advanced clinical stage, lymph node metastasis, and reduced patient survival rate. The knockdown of SNHG20 caused a significant reduction in cancer cell survival, proliferation, colony formation, migration and invasion, and induced cell apoptosis. Additionally, the inhibition of SNHG20 reduced tumour growth in vivo. Investigations into the mechanism revealed that the inhibition of SNHG20 suppressed the activation of Wnt/β‑catenin signalling and the expression of certain key genes in bladder cancer cells. Taken together, these results indicated that SNHG20 is involved in promoting bladder cancer and may be used as a potential therapeutic target for the treatment of this disease.

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Effects of microRNA-135a on the epithelial–mesenchymal transition, migration and invasion of bladder cancer cells by targeting GSK3β through the Wnt/β-catenin signaling pathway

Cited by 46 publications

References 42 publications

Neural stem cell‐derived factors inhibit the growth and invasion of U87 stem‐like cells in vitro

Neural stem cell‐derived factors inhibit the growth and invasion of U87 stem‐like cells in vitro

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

Long non-coding RNA SNHG20 promotes bladder cancer via activating the Wnt/β-catenin signalling pathway

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