MicroRNA-155 promotes bladder cancer growth by repressing the tumor suppressor DMTF1

Peng, Yang; Dong, Wen; Lin, Tianxin; Zhong, Guangzheng; Liao, Bei; Wang, Bo; Gu, Peng; Huang, Li; Xie, Yun; Lu, Fuding; Chen, Zhanghua; Xie, Weibin; Wang, He; Wu, Shaoxu; Huang, Jian

doi:10.18632/oncotarget.3755

Cited by 52 publications

(33 citation statements)

References 48 publications

(54 reference statements)

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“…Elevated expression of miR-155 has been described in multiple cancers, reflecting tumor staging, progression and treatment outcomes (61)(62)(63)(64). In accordance with expectations, miR-155 acts as a vital oncogene in GBCs, as was reported by Kono et al (43).…”

Section: Mir-21supporting

confidence: 72%

The role of microRNAs in gallbladder cancer

Yang

Zhang

et al. 2016

Molecular and Clinical Oncology

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Abstract. MicroRNAs (also referred to as miRNAs or miRs) play a crucial role in post-transcriptional gene regulation and serve as negative gene regulators by controlling a variety of target genes and regulating diverse biological processes, such as cell proliferation, invasion, migration and apoptosis. Aberrant expression of miRNAs is associated with the development and progression of cancer. Recent studies have reported that miRNAs may repress or promote the expression of cancer-related genes via several different signaling pathways in gallbladder cancer (GBC) patients and may function as tumor suppressors or oncogenes, thus providing a promising tool for the diagnosis and therapeutics of GBCs. In this review, we summarize the role of dysregulawted miRNA expression in the signaling pathways implicated in GBC and discuss the significant role of circulating miRNAs in GBC. Therefore, miRNAs may serve as novel therapeutic targets as well as diagnostic or prognostic markers in GBC.

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Section: Mir-21supporting

confidence: 72%

The role of microRNAs in gallbladder cancer

Yang

Zhang

et al. 2016

Molecular and Clinical Oncology

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“…Under hypoxic conditions, upregulated miR-155-5p was demonstrated to induce autophagy by regulating the expression of several autophagy-related genes [23]. In tumor cells, miR-155-5p functions as a promotor of proliferation in oral squamous cell carcinoma [24] and bladder cancer cells [25]. In addition, researchers have found that miR-155-5p mediates T lymphocyte differentiation [26] and inhibits cell apoptosis [27].…”

Section: Introductionmentioning

confidence: 99%

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

Wang

et al. 2019

Epigenetics

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A previous study reported that miR-155-5p knockout mice were more resistant to herpes simplex virus type I (HSV-1) infection. However, the exact underlying molecular mechanism remains to be elucidated. Here, we demonstrated that HSV-1 infection upregulates miR-155-5p expression. By binding to the promoter of serine/arginine-rich splicing factor 2 (SRSF2), which is an important transcriptional activator of HSV-1 genes that was previously reported by our group, and altering the histone modification located near the transcription start site (TSS) of the SRSF2 gene, miR-155-5p promotes the transcription of the SRSF2 gene, ultimately increasing viral replication and viral gene expression. Our results provide insight for an understanding of the roles and molecular mechanism of miR-155-5p in HSV-1 replication and the epigenetic control of SRSF2 gene expression.

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“…Elevated levels of p14 ARF cause cell cycle arrest and cell death in a p53-dependent manner [14]. ARF is an alternative reading frame product of the INK4a/ARF locus and is inactivated in many human cancers.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, studies have found that tumors can occur in mice without p53 mutations or ARF deletions, further illustrating the importance of DMTF1 in the p53 pathway [12]. In cancers such as bladder cancer [14], colorectal cancer [15] and breast cancer [16], it has been reported that overexpression or knockdown of DMTF1 can inhibit or promote cancer progression. In the present study, it was confirmed that miR-6838-5p inhibits the expression of DMTF1 to promote proliferation and invasion of RCC cells by targeting DMTF1.…”

Section: Introductionmentioning

confidence: 99%

MiR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway

Zhai¹,

Wu²,

Zhang³

et al. 2020

Preprint

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Backgroud: Renal cell carcinoma (RCC) is one of the most common renal malignancies in the urinary system. Numerous studies have demonstrated that miRNAs can regulate tumorigenesis and progression, while the underlying molecular mechanism for miR-6838-5p involved in RCC development is still largely unknown.Methods: The relative expression of miR-6838-5p in RCC tissues, RCC cell lines, adjacent normal tissues and normal renal epithelial cells was detected by reverse transcription polymerase chain reaction (RT-qPCR). In vitro studies, cell proliferation and invasion in human RCC cell lines ACHN and 786-O were evaluated by CCK-8 assay, Transwell assay, Colony formation assay and Flow cytometry.Bioinformatics analysis, luciferase report analysis and Western blot assay were proved that Cyclin D binding myb-like transcription factor 1 (DMTF1) is the target of miR-6838-5p.Results: Our study confirmed that miR-6838-5p was upregulated in RCC tissues (30/42, 77.43%, P < 0.01) and RCC cell lines (P < 0.05) compared to adjacent normal tissues and normal renal epithelial cells. In vitro studies demonstrated that overexpression of miR-6838-5p significantly increased cell proliferation and invasion in human RCC cell lines ACHN and 786-O (P < 0.05), whereas inhibition of miR-6838-5p inhibited cell proliferation and invasion (P < 0.05). Furthermore, we found that miR-6838-5p binds to the wild-type DMTF1 3'UTR. In addition, we found that DMTF1 was downregulation in RCC tissues and cell lines. Meanwhile, it was demonstrated in ACHN cells that overexpression of miR-6838-5p inhibited the expression of DMTF1. Finally, we also confirmed that the interaction of miR-6838-5p overexpression and DMTF1 overexpression might rescue the inhibitory effects of overexpression of miR-6838-5p on the expression of phosphatase and tensin homolog (PTEN), p53, Murine double minute 2 (MDM2) and alternative reading frame (ARF) in the DMTF1-mediated ARF-p53 downstream pathway.Conclusions: Our research shows that miR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway, which suggest that miR-6838-5pcan be used as a marker for the diagnosis of RCC.

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MicroRNA-155 promotes bladder cancer growth by repressing the tumor suppressor DMTF1

Cited by 52 publications

References 48 publications

The role of microRNAs in gallbladder cancer

The role of microRNAs in gallbladder cancer

MiR-155-5p modulates HSV-1 replication via the epigenetic regulation of SRSF2 gene expression

MiR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway

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