miR-138-5p inhibits the malignant progression of prostate cancer by targeting FOXC1

Zhang, David; Liu, Xiaodong; Zhang, Qingwei; Chen, Xin

doi:10.21203/rs.3.rs-16546/v3

Cited by 11 publications

(14 citation statements)

References 19 publications

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“…33,34 In addition, RGS17 was reported to serve as the downstream target of miR-203 in PCa cells, and knockdown of RGS17 inhibited the tumorigenicity of PCa cells. 35 Consistently, in this study, we found that RGS17 targeted by miR-149-5p was upregulated in PCa, and its expression was inhibited by miR-149-5p overexpression. More specifically, RGS17 enhanced cell viability, proliferation and migration in C4-2 and 22Rv1 cells.…”

Section: Discussionsupporting

confidence: 87%

Hsa-miR-149-5p Suppresses Prostate Carcinoma Malignancy by Suppressing RGS17

Ma¹,

Wei²,

Li³

et al. 2021

CMAR

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Background MicroRNAs (miRNAs) are key players in the progression of human cancers. While several miRNAs have been reported to regulate the development of tumors, the molecular mechanisms and roles of miR-149-5p in prostate carcinoma (PCa) remain unclear. Our aim was to investigate the interaction and functions of miR-149-5p and RGS17 in PCa. Methods Microarray analysis was performed to identify the key miRNA and gene involved in PCa progression. The expression levels of miRNA and mRNA in PCa tissues and cells were verified by qRT-PCR. MTT assay, BrdU proliferation assay and wound-healing assay were applied to assess the effect of miR-149-5p and RGS17 on PCa cells’ viability, proliferation, and migration ability. The association between RGS17 and miR-149-5p was identify using dual-luciferase reporter assay and Western blot assay. Results Data analysis indicated the reduction of miR-149-5p expression in PCa tissues and cells. Experimental investigations also showed that this miRNA suppressed the viability, proliferation and migration ability of PCa cells. RGS17 was found to be the target of miR-149-5p, and the low expression of miR-149-5p upregulated RGS17 in PCa tissues and cells. The results of the cell-function assays showed that RGS17 acted as an oncogene in PCa even though its promotive effect could be reversed by miR-149-5p. Conclusion This research confirmed that by targeting and inhibiting RGS17, miR-149-5p could suppress PCa development.

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Section: Discussionsupporting

confidence: 87%

Hsa-miR-149-5p Suppresses Prostate Carcinoma Malignancy by Suppressing RGS17

Ma¹,

Wei²,

Li³

et al. 2021

CMAR

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“…For example, miR-203 elevation suppressed PC-3 cell proliferation and ADM resistance but promoted apoptosis through inhibiting MEK1 expression (21). 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).…”

Section: Discussionmentioning

confidence: 96%

“…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: 98%

“…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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“…RGS17 has been found to be upregulated in lung cancer and prostate cancer [28,29]. Functionally, overexpression of RGS17 promoted cell proliferation, migration and invasion in hepatocellular carcinoma [30].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA SNHG6 promotes tumorigenesis of nasopharyngeal carcinoma by competitively binding to miR-944 with RGS17

Han¹,

Liu²,

Li³

et al. 2020

Preprint

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Background Previous studies have shown that many long noncoding RNAs (lncRNAs) are involved in the pathogenesis of nasopharyngeal carcinoma (NPC). However, the regulatory mechanism of lncRNA SNHG6 remains unknown. Therefore, this study was design to preliminarily elucidate the role of SNHG6 in NPC. Methods The mRNA expression was detected by RT-qPCR. CCK-8, Transwell and dual luciferase reporter assays were used to investigate the function of SNHG6 in NPC. Results Upregulation of SNHG6 and downregulation of miR-944 were identified in NPC and were associated with TNM stage and distant metastasis in NPC patients. Additionally, SNHG6 acts as a molecular sponge of miR-944. More importantly, SNHG6 promoted NPC cell proliferation, migration and invasion by downregulating miR-944. Further, RGS17 was confirmed to be a direct target of miR-944. MiR-944 restrained NPC progression by targeting RGS17. Besides that, knockdown of RGS17 was found to block NPC progression. Upregulation of SNHG6 weakened the suppressive effect of RGS17 knockdown in NPC. Conclusion LncRNA SNHG6 promotes tumorigenesis of NPC by competitively binding to miR-944 with RGS17.

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miR-138-5p inhibits the malignant progression of prostate cancer by targeting FOXC1

Cited by 11 publications

References 19 publications

Hsa-miR-149-5p Suppresses Prostate Carcinoma Malignancy by Suppressing RGS17

Hsa-miR-149-5p Suppresses Prostate Carcinoma Malignancy by Suppressing RGS17

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 SNHG6 promotes tumorigenesis of nasopharyngeal carcinoma by competitively binding to miR-944 with RGS17

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