MicroRNA-146b Overexpression Promotes Human Bladder Cancer Invasion via Enhancing ETS2-Mediated mmp2 mRNA Transcription

Zhu, Junlan; Xu, Changshui; Ruan, Li-Ming; Wu, Jianping; Li, Yang; Zhang, Xingguo

doi:10.1016/j.omtn.2019.04.007

Cited by 20 publications

(17 citation statements)

References 56 publications

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“…The results showed that knockdown of MMP2 decreased the invasion of U5637(SNHG1) cells compared with that noted in scramble nonsense transfectants, while it did not affect U5637(SNHG1) migration under the same experimental conditions ( Figures 2 F and 2G). Given that many previous studies, from us 21 , 22 as well as from others, 23 , 24 showing that MMP2 is able to specifically promote invasion, rather than migration, in many cancer cells, and that MMP2 is a well-known proteinase essential for the breakdown of the extracellular matrix (EMC) in cancer cell invasion, our results reveal that MMP2 is at least a SNHG1 downstream effector specifically responsible for the promotion of human basal MIBC-invasive activities.…”

Section: Resultssupporting

confidence: 54%

lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

Yang

Hua

et al. 2020

Molecular Therapy - Nucleic Acids

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Although basal muscle-invasive bladder cancers (MIBCs) are predominant, are more aggressive, and have bad prognoses, molecular mechanisms underlying how basal MIBC formation/progression have been barely explored. In the present study, SNHG1, a long non-coding RNA, was shown to be expressed at higher levels in basal MIBC cells than in other types of bladder BC cells, and its presence could promote basal MIBC cell invasion. The results revealed that SNHG1 specifically induced MMP2 expression via increasing its transcription and mRNA stability. In one mechanism, SNHG1 directly bound with PP2A catalytic subunit (PP2A-c) to inhibit interactions of PP2A-c with c-Jun and then promoted c-Jun phosphorylation that, in turn, mediated MMP2 transcription. In another mechanism, SNHG1 markedly induced autophagy in the cells via induction of increases in the abundance of autophagy-related proteins. The latter initiated autophagy and further abolished miR-34a stability, which reduced overall miR-34a binding directly to the 3′ UTR of MMP2 mRNA, thereby promoting MMP2 mRNA stabilization. These results provided novel insight into understanding the specific functions of SNHG1 in basal MIBC. Such findings may ultimately prove highly significant for the design/synthesis of new SNHG1-based compounds for the treatment of basal MIBC patients.

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Section: Resultssupporting

confidence: 54%

lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

Yang

Hua

et al. 2020

Molecular Therapy - Nucleic Acids

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“…miR‐328‐3p was also demonstrated to be downregulated in bladder cancer, which predicted poor prognosis; miR‐328‐3p overexpression caused apparent repression in cell proliferation, migration and invasion, and EMT . miR‐146b was reported to be overexpressed in bladder cancer tissues, and silence of miR‐146b resulted in significant inhibitory effects on cell invasion and migration . The above reports indicate that miRNA can function as an oncogene or a tumor suppressive gene in the progression of bladder cancer.…”

Section: Discussionmentioning

confidence: 94%

MicroRNA‐769‐5p suppresses cell growth and migration via targeting NUSAP1 in bladder cancer

Chen

Zhang

Kadier

et al. 2020

Clinical Laboratory Analysis

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Background Nucleolar and spindle‐associated protein 1 (NUSAP1) has been identified to be strongly implicated in the carcinogenesis of cervical carcinoma, breast cancer, and liver cancer, and shows a high expression level in bladder cancer, indicating that NUSAP1 might be a potent target for cancer treatment. Using bioinformatics methods, we found that NUSAP1 was a putative target of miR‐769‐5p. Here, we aimed to explore whether miR‐769‐5p is involved in bladder cancer progression via targeting NUSAP1. Methods MiR‐769‐5p expression patterns in bladder cancer tissues and cells were detected by RT‐PCR. Kaplan‐Meier was used to determine the clinical effects of miR‐769‐5p expression levels on the overall survival of bladder cancer patients. Bioinformatics methods were used to predict the binding sites between miR‐769‐5p and NUSAP1, which was verified by the luciferase gene reporter assay. CCK‐8, flow cytometry, wound healing and transwell chamber experiments were performed to test cell growth, apoptosis, migration and invasion capacities. Results miR‐769‐5p was lowly expressed in bladder cancer tissues and cells, which was closely associated with poor prognosis. Overexpression of miR‐769‐5p induced significant repressions in cell growth, migration, and invasion and caused an obvious increase in cell apoptosis, whereas these tendencies were reversed when NUSAP1 was upregulated. Conclusion This study demonstrates that miR‐769‐5p functions as a tumor suppressor in bladder cancer via targeting NUSAP1.

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“…miRNAs work as crucial regulators of genes by pairing with the 3= untranslated region (3=-UTR) in target mRNAs to degrade mRNA or repress protein translation (17,18). Accumulating evidence has shown that miRNAs play critical roles in the development of numerous cancers, including ccRCC (19)(20)(21). The tumor suppressor function of miRNA 224-5p (miR-224-5p) has been justified by recent research.…”

mentioning

confidence: 99%

FOXM1-Activated LINC01094 Promotes Clear Cell Renal Cell Carcinoma Development via MicroRNA 224-5p/CHSY1

Jiang

Zhang

et al. 2020

Molecular and Cellular Biology

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Clear cell renal cell carcinoma (ccRCC) is regarded as the most aggressive subtype of RCC, with high rates of metastasis and recurrence. An extensive body of studies had proved long noncoding RNAs (lncRNAs) play pivotal parts in the development and evolution of diverse malignant tumors. However, the potential of LINC01094 in ccRCC tumorigenesis is still unexplored. In the present research, with the aid of the TCGA database, we found that LINC01094 was highly expressed in ccRCC tissues. Upregulation of LINC01094 was also confirmed in ccRCC cell lines, and functional experiments delineated that LINC01094 knockdown led to inhibition on ccRCC cell growth and metastasis. Moreover, LINC01094 was activated by FOXM1 at the transcriptional level. Further assay demonstrated that LINC01094 worked as a sponge of microRNA 224-5p (miR-224-5p) and CHSY1 was a miR-224-5p-targeted mRNA. Further, we verified that LINC01094 acted as a competing endogenous RNA in ccRCC to regulate CHSY1 expression via competitively bind to miR-224-5p. Lastly, our results expounded that LINC01094 exerted its tumor-promoting performance in ccRCC development through miR-224-5p/CHSY1 regulatory axis, which shed light on the molecular mechanism underlying LINC01094 in ccRCC and opened a new prospective for the treatment of ccRCC.

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MicroRNA-146b Overexpression Promotes Human Bladder Cancer Invasion via Enhancing ETS2-Mediated mmp2 mRNA Transcription

Cited by 20 publications

References 56 publications

lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

MicroRNA‐769‐5p suppresses cell growth and migration via targeting NUSAP1 in bladder cancer

FOXM1-Activated LINC01094 Promotes Clear Cell Renal Cell Carcinoma Development via MicroRNA 224-5p/CHSY1

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