The mi<scp>R</scp>‐203/<scp>SNAI</scp>2 axis regulates prostate tumor growth, migration, angiogenesis and stemness potentially by modulating <scp>GSK</scp>‐3<i>β</i>/<i>β</i>‐<scp>CATENIN</scp> signal pathway

Tian, Xinxin; Tao, Fangfang; Zhang, Baotong; Dong, Jin‐Tang; Zhang, Zhiqian

doi:10.1002/iub.1720

Cited by 37 publications

(29 citation statements)

References 42 publications

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“…Tian et al indicated that SNAI2 regained the inhibitory impacts of miR-203 on the growth, metastasis and angiogenesis of prostate cancer cells [34], which was consistent with our findings.…”

Section: Discussionsupporting

confidence: 93%

miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

Zhang¹,

Yang²

2020

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MicroRNAs have been verified as critical regulators in the development of melanoma. MiR-33a-5p was significantly downregulated in melanoma. However, the specific role and regulatory mechanism of miR-33a-5p in melanoma were still unclear. The present study identified that miR-33a-5p was downregulated in melanoma tissues and cells, while SNAI2 was upregulated. MiR-33a-5p directly targeted SNAI2 and negatively regulated its expression in melanoma cells. Overexpression of miR-33a-5p repressed proliferation, migration, invasion, EMT and promoted apoptosis of melanoma cell in vitro, these effects were partially reversed by SNAI2 overexpression. In addition, miR-33a-5p impaired melanoma growth in vivo by inhibiting SNAI2. Mechanistically, miR-33a-5p repressed activation of the PI3K/AKT/mTOR pathway by targeting SNAI2. In conclusion, miR-33a-5p repressed the progression of melanoma by targeting SNAI2 via inactivation of the PI3K/AKT/mTOR signaling pathway, providing a potential molecular mechanism for the treatment of melanoma.

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Section: Discussionsupporting

confidence: 93%

miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

Zhang¹,

Yang²

2020

neo

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“…miR-203 plays the role of tumor suppressor gene and regulate RGS17 expression then affect the malignant behavior of PC cells (22). It also has been reported that miR-203/SNAI2 axis had important function in angiogenesis, tumorigenesis, metastasis, stemness in PC (23). Such results indicate that miR-203 is a suppressor in tumors, which is consistent with our results.…”

Section: Discussionsupporting

confidence: 91%

“…The results showed that knockdown of CAR10 could inhibit viability but promote apoptosis, and promoted cleaved-caspase3 expression, but reduced pro-caspase3 expression through regulating miR-203 expression in PC cells. Previous study has demonstrated the antiproliferative and apoptosis-inducing effects of miR-203 in prostate cancer (21)(22)(23). However, the role of miR-203 in apoptosis and its target genes in PC still need further research.…”

Section: Discussionmentioning

confidence: 99%

“…miR-203 is one of the important members of the miRNAs family, and located on human chromosome 14 q32, 33-site (17). Studies have shown that miR-203 is abnormally expressed in a variety of tumor tissues including esophageal carcinoma (down-regulation), osteosarcoma (down-regulation), ovarian cancer (upregulation), and prostate cancer (down-regulation), and is closely related to tumor cell growth, metastasis and invasion (18)(19)(20)(21)(22)(23). A recent study reported that miRNA-203 restrains epithelial-mesenchymal transition, invasion and migration of papillary thyroid cancer via downregulating AKT3 expression (24).…”

Section: Introductionmentioning

confidence: 99%

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The Inhibition of Long Non-Coding RNA CAR10 and The Regulation of miR-203 Expression Suppresses Cell Viability and Induces Cell Apoptosis in Prostate Cancer

Zhang¹,

Chen²,

Wang³

et al. 2020

Preprint

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Background: Prostate cancer (PC) is one of the most common malignant tumors. Recently, it has been reported that long noncoding RNAs (lncRNAs) play key roles in tumor progression. Studies have revealed that long non-coding RNA CAR10 (CAR10) can regulate tumor cell behaviors through sponging miR-203. In this study, we examined the effects of CAR10 in PC cells. Methods: Firstly, real time-quantitative polymerase chain reaction (qRT-PCR) was used to explore CAR10 expression in tumor tissues, peripheral blood of PC patients, and PC cells. We used the dual-luciferase reporter gene assay to analyze the relationship between CAR10 and miR-203. Moreover, flow cytometry, MTT assay, and western blot assay were used to determine cell apoptosis, cell viability, and apoptosis-related protein expression. Results: The results showed that CAR10 expression was remarkably higher in PC samples compared with that of control, and CAR10 regulated miR-203 negatively in PC cells. The qRT-PCR results also showed that miR-203 expression was significantly decreased in PC samples. Moreover, knockdown of CAR10 inhibited PC cell viability and promoted cleaved caspase-3 expression but induced PC cell apoptosis and, reduced pro-caspase-3 expression; miR-203 inhibitor reversed these effects. Conclusion: Our study found that CAR10 is a potential oncogene in PC and suggests that CAR10 inhibition could inhibit PC cell viability but promote PC cell apoptosis through regulating miR-203 expression. Our results show that CAR10 is a potential target for the treatment of PC.

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“…Additionally, downregulated miR-203 was more frequently detected in groups III and IV compared with groups I and II. Because several reports suggested that low expression of miR-203 promoted angiogenesis [22,29], we hypothesized that miR-203 may be associated with HB pathogenesis and progression. To explore the potential role of miR-203 in HB, MTT, wound healing, and tube formation assays were performed to determine cell viability, in vitro migration capacity, and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA CRNDE Regulates Angiogenesis in Hepatoblastoma by Targeting the MiR-203/VEGFA Axis

Chen

Yuan

et al. 2020

Pathobiology

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Objective: has been shown to participate in multiple malignancies, but the role of miR-203 in hepatoblastoma (HB) remains unclear. The aim of our study was to investigate the effects of miR-203 in HB. Methods: A total of 15 pairs of HB tissues and para-tumour normal tissues were collected for the experiments. RT-qPCR and Western blotting were performed to detect the expression of CRNDE, miR-203, and VEGFA at the mRNA and/or protein levels, respectively. A dual luciferase assay verified the target relationship between miR-203 and the 3′UTR of VEGFA as well as miR-203 and CRNDE. In addition, MTT, wound healing, and tube formation assays were performed to assess the effects of miR-203, VEGFA, and CRNDE on cell proliferation, migration, and angiogenesis, respectively. Results: Our data revealed that miR-203 expression was decreased in HB tissues, while long non-coding RNA (lncRNA) CRNDE expression was increased. The dysregulation of miR-203 and CRNDE was closely related to tumour size and stage. Moreover, overexpression of miR-203 inhibited angiogenesis. A dual luciferase assay verified that VEGFA is a direct target of miR-203 and that CRNDE binds to miR-203. Furthermore, our results showed that miR-203 suppressed cell viability, migration, and angiogenesis by regulating VEGFA expression. Additionally, it was confirmed that CRNDE promoted angiogenesis by negatively regulating miR-203 expression. Conclusion: lncRNA CRNDE targets the miR-203/VEGFA axis and promotes angiogenesis in HB. These results provide insight into the underlying mechanisms of HB and indicate that CRNDE and miR-203 might be potential targets for HB therapy.

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The miR‐203/SNAI2 axis regulates prostate tumor growth, migration, angiogenesis and stemness potentially by modulating GSK‐3β/β‐CATENIN signal pathway

Cited by 37 publications

References 42 publications

miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

miR-33a-5p inhibits the growth and metastasis of melanoma cells by targeting SNAI2

The Inhibition of Long Non-Coding RNA CAR10 and The Regulation of miR-203 Expression Suppresses Cell Viability and Induces Cell Apoptosis in Prostate Cancer

Long Non-Coding RNA CRNDE Regulates Angiogenesis in Hepatoblastoma by Targeting the MiR-203/VEGFA Axis

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