MiR-182 Is Associated with Growth, Migration and Invasion in Prostate Cancer via Suppression of FOXO1

Wallis, Christopher J.D.; Gordanpour, Aida; Bendavid, Jessica Stojcic; Sugar, Linda; Nam, Robert K.; Seth, Arun

doi:10.7150/jca.13176

Cited by 53 publications

(55 citation statements)

References 20 publications

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“…Previous studies have revealed that decreased transcriptional expressions and activities of FOXO1 and FOXO3a were correlated with increasing tumor grade and associated with cancer progression . In addition, both FOXO1 and FOXO3a are involved in the regulation of cell apoptosis, proliferation and invasion in PCa . However, the precise molecular mechanism of the abnormal expression of FOXO remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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β‐arrestin1‐medieated inhibition of FOXO3a contributes to prostate cancer cell growth in vitro and in vivo

et al. 2018

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Recently, β‐arrestin1 has been indicated as a prostate cancer promoter through promoting cell proliferation and epithelial to mesenchymal transition, but its underlying mechanism remains unclear. Here, our data revealed that β‐arrestin1 could promote cell growth through inhibiting the transcriptional activity and expression of FOXO3a in prostate cancer cells in vitro and in vivo. We found that β‐arrestin1 could promote the cell and tumor growth of prostate cancer, and β‐arrestin1 expression represented a negative correlation with FOXO3a expression but not FOXO1 expression in prostate cancer cell lines and tissues. In addition, forced expression of β‐arrestin1 induced a significant decrease of FOXO3a expression but had no clear effect on FOXO1 expression. Mechanistically, β‐arrestin1 could interact with FOXO3a and MDM2, respectively, and promote the interaction between FOXO3a and MDM2, whereas it had no obvious interaction with FOXO1. Furthermore, β‐arrestin1 could inhibit the transcriptional activity of FOXO3a via Akt and ERK1/2 pathways. Together, our results revealed a novel mechanism for β‐arrestin1 in the regulation of the prostate cancer procession through inhibiting FOXO3a.

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Section: Introductionmentioning

confidence: 99%

“…[10][11][12][13] In addition, both FOXO1 and FOXO3a are involved in the regulation of cell apoptosis, proliferation and invasion in PCa. 9,[14][15][16][17][18][19][20] However, the precise molecular mechanism of the abnormal expression of FOXO remains unclear.…”

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confidence: 99%

β‐arrestin1‐medieated inhibition of FOXO3a contributes to prostate cancer cell growth in vitro and in vivo

et al. 2018

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“…It has been found that miR‐182 is upregulated in various cancers, including prostate cancer (Wallis et al, ; Yan et al, ), glioblastoma (Kouri et al, ), hepatocellular carcinoma (Du et al, ). Moreover, miR‐182 is capable of promoting cellular differentiation by regulating the expression of snail family transcriptional repressor 2 ( SNAI2 ), thereby inducing the mesenchymal‐to‐epithelial transition (Qu et al, ).…”

Section: Discussionmentioning

confidence: 99%

Testin was regulated by circRNA3175‐miR182 and inhibited endometrial epithelial cell apoptosis in pre‐receptive endometrium of dairy goats

Zhang

Liu

et al. 2018

Journal Cellular Physiology

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Circular RNAs (circRNAs) in various tissues and cell types from mammalian sources have been studied. However, present knowledge on circRNAs in the development of pre-receptive endometrium (PE) in dairy goats is limited. In the pre-receptive endometrium of dairy goats, higher circRNA3175 (ciR3175) levels, lower miR-182 levels and higher Testin (TES) levels were detected. And ciR3175 could decreased the miR-182 levels by acting as a miRNA sponge, and miR-182 could down-regulated the expression level of TES via the predicted target site in endometrial epithelial cells (EECs) in vitro. Via this way, ciR3175 functioned as a competing endogenous RNAs (ceRNA) that sequestered miR-182, thereby protecting TES transcripts from miR-182-mediated suppression in EECs in vitro. Further, TES inhibited EECs apoptosis by decreasing the expression level of BCL-2/BAX via the MAPK pathway. Thus, a ciR3175-miR182-TES pathway in the endometrium was identified in EECs, and the modulation of which could emerge as a potential target in regulating the pre-receptive endometrium development in dairy goats.

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“…The interaction between miR‐182 and FOXO1 had been studied in many physiological processes and diseases. For instance, miR‐182 could act to increase prostate cancer proliferation, migration, and invasion through suppression of FOXO1 (Wallis et al, ), whereas the miR‐182/ FOXO1 pathway induced cell apoptosis and inhibited osteoblast proliferation and differentiation (Kim et al, ), which might be a valuable axis in the development of further therapeutic interventions. The effect of FOXO1 in hepatic fibrosis has also been investigated in previous studies, and it has been confirmed that FOXO1 could regulate proliferation and transdifferentiation of HSCs (Adachi et al, ).…”

Section: Introductionmentioning

confidence: 99%

Effect of miR‐182 on hepatic fibrosis induced by Schistosomiasis japonica by targeting FOXO1 through PI3K/AKT signaling pathway

Huang

Fan

Tao

et al. 2018

Journal Cellular Physiology

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The study aimed to investigate the impact of miR-182 and FOXO1 on S. japonica-induced hepatic fibrosis. Microarray analysis was performed to screen out differential expressed miRNAs and mRNAs. Rat hepatic fibrosis model and human hepatocellular cell line LX-2 were used to study the effect of miR-182 and FOXO1. qRT-PCR and Western blot were used to detect the expression of miR-182, FOXO1 or other fibrosis markers. The targeting relationship between FOXO1 and miR-182 was verified by luciferase reporter assay. Immunohistochemistry or immunofluorescence staining was conducted to detect FOXO1 or α-SMA in rat hepatic tissues. Cell viability and apoptosis were detected by MTT assay and flow cytometry. The expression of PI3K/AKT pathway-related proteins was detected by Western blot. miR-182 was highly expressed in liver fibrosis samples, and FOXO1 expression was negatively correlated with miR-182 expression. After transfection of miR-182, FOXO1 expression was down-regulated, with the results of LX-2 cells proliferation inhibition and apoptosis induction, as well as the aggravation of rat hepatic fibrosis. The expression of p-AKT/AKT and p-S6/S6 was increased, meaning that the PI3K/AKT signal pathway was activated. The results were reversed when treated with Wortmannin (PI3K inhibitor). After transfection of miR-182 inhibitor, FOXO1 expression was up-regulated, LX-2 cell proliferation was inhibited, and apoptosis rate was increased. High-expressed miR-182 and low-expressed FOXO1 promoted proliferation and inhibiting apoptosis on liver fibrosis cells, stimulating the development of S. japonica-induced hepatic fibrosis through feeding back to PI3K/AKT signaling pathway.

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MiR-182 Is Associated with Growth, Migration and Invasion in Prostate Cancer via Suppression of FOXO1

Cited by 53 publications

References 20 publications

β‐arrestin1‐medieated inhibition of FOXO3a contributes to prostate cancer cell growth in vitro and in vivo

β‐arrestin1‐medieated inhibition of FOXO3a contributes to prostate cancer cell growth in vitro and in vivo

Testin was regulated by circRNA3175‐miR182 and inhibited endometrial epithelial cell apoptosis in pre‐receptive endometrium of dairy goats

Effect of miR‐182 on hepatic fibrosis induced by Schistosomiasis japonica by targeting FOXO1 through PI3K/AKT signaling pathway

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