miR‑202 suppresses prostate cancer growth and metastasis by targeting PIK3CA

Zhang, Shengping; Cai, Jiarong; Xie, Weihao; Luo, Hui; Yang, Fei

doi:10.3892/etm.2018.6296

Cited by 20 publications

(18 citation statements)

References 32 publications

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“…In particular, miR-202 was found to inhibit cell proliferation via inhibiting the expression of ARL5A in human colorectal carcinoma [26]. Similarly, miR-202 suppressed cell growth and metastasis in prostate cancer [27]. In the present study, the same inhibitory effect of miR-202 on cell migration and invasion was also identified in EC.…”

Section: Discussionsupporting

confidence: 76%

MicroRNA-202 inhibits cell migration and invasion through targeting FGF2 and inactivating Wnt/β-catenin signaling in endometrial carcinoma

Chen

Xing

et al. 2019

Bioscience Reports

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Recently, many mircroRNAs (miRNAs) involved in the development and progression of cancer have been reported to regulate cell growth and metastasis, including microRNA-202 (miR-202). The purpose of the present study was to elucidate the effect of miR-202 on endometrial carcinoma (EC) cell migration and invasion. First, qRT-PCR showed that miR-202 was down-regulated in EC tissues, which was associated with poor prognosis in EC patients. Functionally, transwell assay indicated that miR-202 inhibited cell migration and invasion in EC cells. In addition, miR-202 also blocked epithelial–mesenchymal transition (EMT) through suppressing N-cadherin and Vimentin expressions and promoting E-cadherin expression. Moreover, the dual-luciferase reporter assay showed that fibroblast growth factor 2 (FGF2) is a direct target gene for miR-202 in EC cells. Furthermore, up-regulation of FGF2 attenuated the inhibitory effect of miR-202 on cell migration and invasion in EC. Besides that, miR-202 inactivated the Wnt/β-catenin signaling by suppressing β-catenin expression in EC. In conclusion, miR-202 inhibited cell migration and invasion by targeting FGF2 and inactivating the Wnt/β-catenin signaling in EC.

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Section: Discussionsupporting

confidence: 76%

MicroRNA-202 inhibits cell migration and invasion through targeting FGF2 and inactivating Wnt/β-catenin signaling in endometrial carcinoma

Chen

Xing

et al. 2019

Bioscience Reports

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“…miR-202 is located within a chromosomal fragile site in the 10q26 locus that has been previously found to modulate the pathological processes of several malignancies, with marked effects on tumor cell proliferation, invasion and migration ( 17 , 18 ). Meng et al ( 19 ) found that miR-202 significantly inhibited cell migration and invasion in esophageal squamous cell carcinoma (ESCC) cell lines by targeting laminin α1.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

et al. 2020

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The enhanced migratory ability of endometrial stromal cells (ESCs) is a key factor in the formation of functional endometrium-like tissues outside the uterine cavity during endometriosis (EMS). Although accumulating evidence has suggested the importance of microRNAs (miRNAs) in the pathogenesis of EMS, the role of particular miRNAs in the invasiveness of ESCs remain poorly understood. In the present study, the function of miRNAs in the invasiveness of ESCs, along with the associated underlying mechanism involved, were investigated. Initially, the expression patterns of miRNAs in the ectopic and eutopic endometrium isolated from patients with EMS were analyzed using microarray. MicroRNA-202-5p (miR-202) was selected for further study due to its previously reported suppressive effects on the invasion in various types of cancers. The expression of miR-202 and K-Ras in eutopic and ectopic endometrioma tissues were detected using reverse transcription-quantitative PCR, immunohistochemistry and western blotting. The migration and invasion ability of ESCs was determined using wound healing and Transwell invasion assays, respectively. Compared with that from healthy individuals, miR-202 expression was demonstrated to be lower in the eutopic endometrium from patients with EMS, which was even lower in ectopic endometrium. Functional experiments in primary ESCs revealed that enhanced miR-202 expression suppressed the cell invasion and migration abilities, which was also accompanied with increased E-cadherin and reduced N-cadherin expression in ESCs, suggesting its potentially suppressive role in epithelial-mesenchymal transition. K-Ras is a well-known regulator of the ERK signaling pathway that was shown to be directly targeted and negatively regulated by miR-202. In addition, K-Ras expression was found to be upregulated in the ectopic endometrium, where it correlated negatively with that of miR-202. Knocking down K-Ras expression mimicked the anti-invasive effects of miR-202 overexpression on ESCs, whilst K-Ras overexpression attenuated the inhibitory role of miR-202 overexpression in ESC invasion. The K-Ras/Raf1/MEK/ERK signaling pathway was also blocked by miR-202 overexpression. These findings suggested that miR-202 inhibited ESC migration and invasion by inhibiting the K-Ras/Raf1/MEK/ERK signaling pathway, rendering miR-202 a candidate for being a therapeutic target for EMS.

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“…MiR-202 is an intronic RNA that participates in multiple cellular physiological processes, including cell growth, apoptosis, migration, and invasion [36][37][38]. The expression of miR-202-5p is regulated by SF1 or SRY (Sex-Determining Region Y)-Box 9 (SOX9) during mouse testis differentiation [11].…”

Section: Discussionmentioning

confidence: 99%

Transactivation of miR-202-5p by Steroidogenic Factor 1 (SF1) Induces Apoptosis in Goat Granulosa Cells by Targeting TGFβR2

Ding¹,

Jin²,

Wang

et al. 2020

Cells

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MicroRNAs play key roles during ovary development, with emerging evidence suggesting that miR-202-5p is specifically expressed in female animal gonads. Granulosa cells (GCs) are somatic cells that are closely related to the development of female gametes in mammalian ovaries. However, the biological roles of miR-202-5p in GCs remain unknown. Here, we show that miR-202-5p is specifically expressed in GCs and accumulates in extracellular vesicles (EVs) from large growth follicles in goat ovaries. In vitro assays showed that miR-202-5p induced apoptosis and suppressed the proliferation of goat GCs. We further revealed that miR-202-5p is a functional miRNA that targets the transforming growth factor-beta type II receptor (TGFβR2). MiR-202-5p attenuated TGF-β/SMAD signaling through the degradation of TGFβR2 at both the mRNA and protein level, decreasing p-SMAD3 levels in GCs. Moreover, we verified that steroidogenic factor 1 (SF1) is a transcriptional factor that binds to the promoters of miR-202 and cytochrome P450 family 19 subfamily A member 1 (CYP19A1) through luciferase reporter and chromatin immunoprecipitation (ChIP) assays. That contributed to positive correlation between miR-202-5p and CYP19A1 expression and estradiol (E2) release. Furthermore, SF1 repressed TGFβR2 and p-SMAD3 levels in GCs through the transactivation of miR-202-5p. Taken together, these results suggest a mechanism by which miR-202-5p regulates canonical TGF-β/SMAD signaling through targeting TGFβR2 in GCs. This provides insight into the transcriptional regulation of miR-202 and CYP19A1 during goat ovarian follicular development.

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miR‑202 suppresses prostate cancer growth and metastasis by targeting PIK3CA

Cited by 20 publications

References 32 publications

MicroRNA-202 inhibits cell migration and invasion through targeting FGF2 and inactivating Wnt/β-catenin signaling in endometrial carcinoma

MicroRNA-202 inhibits cell migration and invasion through targeting FGF2 and inactivating Wnt/β-catenin signaling in endometrial carcinoma

MicroRNA‑202 inhibits endometrial stromal cell migration and invasion by suppressing the K‑Ras/Raf1/MEK/ERK signaling pathway

Transactivation of miR-202-5p by Steroidogenic Factor 1 (SF1) Induces Apoptosis in Goat Granulosa Cells by Targeting TGFβR2

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