MicroRNA-488 inhibits proliferation and motility of tumor cells via downregulating FSCN1, modulated by Notch3 in breast carcinomas

Wu, Yang; Yuan, Ming-Heng; Wu, Haijian; Chen, Wen-Jia; Zhang, Manli; Ye, Qianqian; Liu, Jing; Zhang, Guojun

doi:10.1038/s41419-020-03121-5

Cited by 17 publications

(14 citation statements)

References 24 publications

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“…To elucidate the role of Fascin in TNBC, we performed loss-of-function assays in HS578T and MDAMB231 cell lines. As expected, the wound-healing, transwell migration, and matrigel invasion assays confirmed that the knockdown of Fascin significantly suppressed TNBC cells migration and invasion, which was consistent with the findings of previous studies [18,26] (Fig. 1F, G).…”

Section: Fascin Is Highly Expressed In Tnbc and Enhances Cells Metast...supporting

confidence: 92%

“…Mechanistically, we observed that Fascin can downregulate xCT at the posttranscriptional level in TNBC. The results of previous studies indicated that Fascin is a downstream effector protein that is regulated by a number of other factors, such as transcription factors [34,35], microRNAs [26,36], and long-noncoding RNAs [15,37]. However, accumulating evidence has demonstrated that Fascin can also regulate other factors.…”

Section: Discussionmentioning

confidence: 99%

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Fascin enhances the vulnerability of breast cancer to erastin-induced ferroptosis

Chen

Xie

et al. 2022

Cell Death Dis

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Ferroptosis, which is characterized by intracellular iron accumulation and lipid peroxidation, is a newly described form of regulated cell death that may play a key role in tumour suppression. In the present study, we investigated the expression profiles and biological effects of fascin actin-bundling protein 1 (Fascin, gene name FSCN1) in breast cancer. In addition, bioinformatics analysis of the TCGA cancer database and gain- and loss-of-function studies showed that Fascin enhances sensitivity to erastin-induced ferroptosis. Mechanistically, Fascin directly interacts with cysteine/glutamate transporter (xCT, gene name SLC7A11) and decreases its stability via the ubiquitin-mediated proteasome degradation pathway. Furthermore, we observed that Fascin is substantially upregulated in tamoxifen-resistant breast cancer cell lines, and drug-resistant cells were also more vulnerable to erastin-induced ferroptosis. Taken together, our findings reveal a previously unidentified role of Fascin in ferroptosis by regulating xCT. Thus, ferroptosis activation in breast cancer with high Fascin level may serve as a potential treatment.

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Section: Fascin Is Highly Expressed In Tnbc and Enhances Cells Metast...supporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Fascin enhances the vulnerability of breast cancer to erastin-induced ferroptosis

Chen

Xie

et al. 2022

Cell Death Dis

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“…Then, a 200 μL yellow pipette tip was used to scratch a gap on the cellular monolayers, and cells were then washed with phosphate buffer (PBS) to remove the suspended cells, followed by the incubation in serum-free DMEM medium for additional 24 h. Images were captured using an optical microscope and the gap sized was recorded. To determine the invasive capacity of osteosarcoma cells, transwell experiment was performed as previously described [42][43][44].…”

Section: Cellmentioning

confidence: 99%

MicroRNA-181a-5p Promotes Osteosarcoma Progression via PTEN/AKT Pathway

Sun

Chen

et al. 2022

Analytical Cellular Pathology

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Osteosarcoma is the most common primary malignant bone tumor in children and adolescents with poor prognosis. MicroRNA-181a-5p (miR-181a-5p) is involved in the progression of various tumors; however, its role and underlying mechanism in osteosarcoma remains unclear. In this study, we found that miR-181a-5p was upregulated in human osteosarcoma cells and tissues. miR-181a-5p mimic significantly promoted, while miR-181a-5p inhibitor blocked the proliferation, colony formation, migration, invasion, and cell cycle progression of osteosarcoma cells. Mechanistically, miR-181a-5p bound to the 3 ′ -untranslational region of phosphatase and tensin homolog (PTEN) and reduced its protein expression, thereby activating protein kinase B (PKB/AKT) pathway. Either PTEN overexpression or AKT inhibition notably blocked the tumor-promoting effects of miR-181a-5p. Moreover, we observed that miR-181a-5p mimic further inhibited growth of human osteosarcoma cells in the presence of adriamycin or cisplatin. Overall, miR-181a-5p promotes osteosarcoma progression via PTEN/AKT pathway and it is a promising therapeutic target to treat osteosarcoma.

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“…Plasmids carrying the human miR-128-3p mimic (miR-128-3p mimic) or miRNA negative control mimic (NC), a lentiviral vector containing the human miR-128-3p inhibitor (LV-miR-128-3p-inhibitor), and the corresponding control (LV-NC) were purchased from GenePharma (Shanghai, China). HGC-27 cells were transfected using Lipofectamine 3000 (Thermo Fisher Scientific, Waltham, MA, USA), and GES-1 cells were infected with LV-miR-128-3p-inhibitor or LV-NC [ 17 , 18 ]. At 48 h posttransfection or 72 h after lentivirus infection, according to the manufacturer’s instructions, the culture media were collected, filtered, and stored in a refrigerator at 4°C.…”

Section: Methodsmentioning

confidence: 99%

microRNA-128-3p inhibits CD4+ regulatory T cells enrichment by targeting interleukin 16 in gastric cancer

et al. 2021

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Previous studies have confirmed that microRNA (miR)-128-3p is expressed at low levels in gastric cancer (GC), and low miR-128-3p expression promotes the growth of GC cells. However, whether the dysregulation of miR-128-3p expression affects tumor-infiltrating lymphocytes (TILs) and leads to immune escape remains unclear. In the present study, predictive bioinformatics approaches showed that miR-128-3p expression was inversely correlated with tumor-infiltrating lymphocyte enrichment. When CD4 + T cells and regulatory T cells (Tregs) were enriched, lower miR-128-3p expression was associated with worse overall survival. However, when numbers of CD8 + T cells were decreased, the upregulation of miR-128-3p expression had a favorable effect on GC prognosis. Dual-luciferase reporter assays and cell biology experiments revealed that interleukin 16 (IL16) was the target of miR-128-3p and was negatively regulated by miR-128-3p. In addition, GC cells were cocultured with T lymphocytes, and the subsequent flow cytometric analysis showed that overexpression of miR-128-3p in tumor cells decreased the percentages of CD4+ CD25+ Foxp3+ Tregs by downregulating IL16 expression in GC, whereas miR-128-3p inhibition had the opposite effect. Moreover, the recombinant IL16 reversed the effects of miR-128-3p overexpression, and a competitive antibody against the IL16 receptor CD4 also reversed the effects of miR-128-3p knockdown. These studies identified the mechanism by which the miR-128-3p/IL16 axis promotes the infiltration of CD4+ Tregs in GC, and this mechanism will be a promising therapeutic target in GC immunotherapy.

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MicroRNA-488 inhibits proliferation and motility of tumor cells via downregulating FSCN1, modulated by Notch3 in breast carcinomas

Cited by 17 publications

References 24 publications

Fascin enhances the vulnerability of breast cancer to erastin-induced ferroptosis

Fascin enhances the vulnerability of breast cancer to erastin-induced ferroptosis

MicroRNA-181a-5p Promotes Osteosarcoma Progression via PTEN/AKT Pathway

microRNA-128-3p inhibits CD4+ regulatory T cells enrichment by targeting interleukin 16 in gastric cancer

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