miR-148a Suppresses estrogen-induced viability and migration of breast cancer cells via inhibition of estrogen receptor α expression

Ma, Fengwang; Feng, Yeqian; Li, Weihui; Li, Zexuan; Liu, Tiebang; Li, Lingjiang

doi:10.3892/etm.2017.4255

Cited by 9 publications

(6 citation statements)

References 38 publications

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“…On the other hand, it was found that miR-148a can be regulated via estrogen receptors, i.e. GPER and ERα 44,45 . In turn, expression changes observed in the case of miR-592 seem to be directly related with a decrease of nuclear estrogen receptors level.…”

Section: Discussionmentioning

confidence: 99%

G protein-coupled estrogen receptor mediates anti-inflammatory action in Crohn’s disease

Jacenik

Zielińska

Mokrowiecka

et al. 2019

Sci Rep

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Estrogens exert immunomodulatory action in many autoimmune diseases. Accumulating evidence highlights the meaningful impact of estrogen receptors in physiology and pathophysiology of the colon. However, the significance of G protein-coupled estrogen receptor (GPER) on Crohn’s disease (CD), one of the inflammatory bowel disease (IBD) types, is still elusive. Our study revealed GPER overexpression at the mRNA and protein levels in patients with CD. To evaluate the effects of GPER activation/inhibition on colitis development, a murine 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced model of CD was used. We showed that activation of GPER reduces mortality, improves macroscopic and microscopic scores and lowers C-reactive protein (CRP) level. The impact of estrogen signaling on the suppression of the intestinal inflammation was proved by immunohistochemistry. It was demonstrated that GPER activation is accompanied by modulation of extracellular-signal regulated kinase (ERK) signaling pathway and expression level of genes involved in signal transmission and immune response as well as the expression of some microRNAs (miR-145, miR-148-5p and miR-592). Our study revealed that the membrane-bound estrogen receptor GPER mediates anti-inflammatory action and seems to be a potent therapeutic target in maintaining remission in CD.

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Section: Discussionmentioning

confidence: 99%

G protein-coupled estrogen receptor mediates anti-inflammatory action in Crohn’s disease

Jacenik

Zielińska

Mokrowiecka

et al. 2019

Sci Rep

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“…A recent systematic review of observational studies investigated the prognostic significance of miR-148a in various cancers and reported a correlation between low miR-148a levels and poor overall survival in patients with cancer (6). miR-148a has been found to be dysregulated in several cancers, including ovarian cancer (7), breast cancer (8,9), colorectal cancer (10), gastrointestinal cancer (11), prostate cancer (12), hepatocellular carcinoma (13), papillary thyroid carcinoma (14) and renal cancer (15). In ovarian cancer, miR-148a is decreased in the plasma of patients compared with healthy controls and its expression level is positively associated with survival time (16).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‑148a inhibits viability and invasion of ovarian cancer OVCAR3 cells by targeting FOXO3

et al. 2019

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Decreased expression of microRNA (miR)-148a is associated with poor prognosis in ovarian cancer. The aim of the present study was to investigate the impact of miR-148a on tumor cell viability and invasion via targeting forkhead box protein O3 (FOXO3). Expression of miR-148a was detected in paired tumor and adjacent normal tissues. OVCAR3 cells were transfected with miR-148a mimic and inhibitor. Cell viability, apoptosis and invasion were determined. A luciferase reporter assay was used to study the association between miR-148a and FOXO3. In addition, the influence of miR-148a on tumor cell growth was investigated by performing xenograft assays in nude mice. RT-qPCR showed that miR-148a was downregulated in ovarian cancer tissues. Overexpression of miR-148a in OVCAR3 cells inhibited cell viability, suppressed invasion and promoted cellular apoptosis. The dual-luciferase assay indicated that miR-148a directly regulated the expression of FOXO3, a transcription factor of caspase-3. Western blotting confirmed that the expression of caspase-3 was regulated by the modulation of miR-148a expression. In vivo assays revealed that miR-148a overexpression inhibited the growth of OVCAR3 ×enograft tumors in nude mice. miR-148a is a tumor suppressor in ovarian cancer OVCAR3 cells and in nude mice. The suppressive effect is due to inhibiting cell viability and invasion as well as promoting apoptosis. These results may provide theoretical basis for targeting miR-148a in the treatment of ovarian cancer.

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“…The present in vitro study revealed that overexpression of microRNA-148a reduced ERα, PI3K and p-AKT protein expression levels in osteoblasts in vitro. Ma et al previously reported that microRNA-148a suppresses estrogen induced viability and migration through ERα expression in breast cancer cells (23). Zhang et al suggested that microRNA-148a promotes cancer cell growth by targeting PI3K/Akt protein expression in osteosarcoma (24).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑148a inhibition protects against ovariectomy‑induced osteoporosis through PI3K/AKT signaling by estrogen receptor α

Xiao

2018

Mol Med Report

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The present study aimed to investigate the effect of microRNA‑148a downregulation on osteoporosis by using an ovariectomized rat model. Reverse transcription‑quantitative polymerase chain reaction was used to analyze microRNA‑148a expression levels, MTT and flow cytometry assays were used to examine cytotoxicity and apoptosis, respectively. The gap‑associated proteins were quantified using western blotting. The expression of microRNA‑148a was significantly increased in osteoporosis rat following ovariectomy. Overexpression of microRNA‑148a significantly promoted apoptosis and inhibited cell growth, whereas downregulation of microRNA‑148a significantly reduced apoptosis and increased cell growth. Overexpression of microRNA‑148a significantly reduced estrogen receptor a (ERα) protein expression and suppressed phosphoinositide‑3‑kinase regulatory subunit 1 (PI3K) and phosphorylated‑protein kinase B (AKT) protein expression in osteoblasts in vitro. The inhibition of ERα increased the microRNA‑148a effect on apoptosis in osteoblasts in vitro. Subsequently, LY294002, an PI3K inhibitor, significantly increased the effect of microRNA‑148a on apoptosis in osteoblasts in vitro. The findings of the present study revealed that anti‑microRNA‑148a protected cells against ovariectomy‑induced osteoporosis through ERα by PI3K/AKT signaling.

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miR-148a Suppresses estrogen-induced viability and migration of breast cancer cells via inhibition of estrogen receptor α expression

Cited by 9 publications

References 38 publications

G protein-coupled estrogen receptor mediates anti-inflammatory action in Crohn’s disease

G protein-coupled estrogen receptor mediates anti-inflammatory action in Crohn’s disease

Overexpression of miR‑148a inhibits viability and invasion of ovarian cancer OVCAR3 cells by targeting FOXO3

MicroRNA‑148a inhibition protects against ovariectomy‑induced osteoporosis through PI3K/AKT signaling by estrogen receptor α

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