MiR-128-3p suppresses breast cancer cellular progression via targeting LIMK1

Zhao, Jie; Li, Dengfeng; Fang, Lin

doi:10.1016/j.biopha.2019.108947

Cited by 58 publications

(42 citation statements)

References 41 publications

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“…Several previous studies showed that miR-128-3P played an inhibitory role in various cancer cases. For example, it was reported that miR-128-3p suppressed breast cancer progression by targeting LIM domain kinase 1(LIMK1) [68]. Furthermore, miR-128-3p was demonstrated to inhibit glioma cell proliferation and differentiation through the IRS-1/PI3K/AKT signaling pathway [69].…”

Section: Discussionmentioning

confidence: 99%

Exosomal miRNA-128-3p from mesenchymal stem cells of aged rats regulates osteogenesis and bone fracture healing by targeting Smad5

Xu¹,

Luo²,

Wang³

et al. 2020

J Nanobiotechnol

106

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Transplantation of mesenchymal stem cells (MSCs) has been considered an effective therapeutic treatment for a variety of diseases including bone fracture. However, there are associated complications along with MSCs transplantation. There is evidence to show that exosomes (Exos) derived from MSCs exert a similar paracrine function. In addition, repair capabilities of MSCs decline with age. Hence, this study aims to confirm whether the Exos protective function on osteogenic differentiation and fracture healing from aged MSCs was attenuated. This information was used in order to investigate the underlying mechanism. MSCs were successfully isolated and identified from young and aged rats, and Exos were then obtained. Aged-Exos exhibited significantly attenuated effects on MSCs osteogenic differentiation in vitro and facture healing in vivo. Using miRNA array analysis, it was shown that miR-128-3p was markedly upregulated in Aged-Exos. In vitro experiments confirmed that Smad5 is a direct downstream target of miR-128-3p, and was inhibited by overexpressed miR-128-3p. A series gain-and loss-function experiment indicated that miR-128-3P serves a suppressor role in the process of fracture healing. Furthermore, effects caused by miR-128-3P mimic/ inhibitor were reversed by the application of Smad5/siSmad5. Taken together, these results suggest that the therapeutic effects of MSCs-derived Exos may vary according to differential expression of miRNAs. Exosomal miR-128-3P antagomir may act as a promising therapeutic strategy for bone fracture healing, especially for the elderly.

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Section: Discussionmentioning

confidence: 99%

Exosomal miRNA-128-3p from mesenchymal stem cells of aged rats regulates osteogenesis and bone fracture healing by targeting Smad5

Xu¹,

Luo²,

Wang³

et al. 2020

J Nanobiotechnol

106

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“…Selenium could mitigate lPS-induced myocardial inflammation by modulating the mir-128-3p/p38MaPK-nF-κB pathway (31). mir-128-3p also functions as a tumor suppressor in human breast cancer (32), glioma (33) and hepatocellular carcinoma (34). in the present study, mir-128-3p interference aggravated lPS-mediated damage in HMec-1 cells, and abolished the Hulc knockdown-mediated reduction of apoptosis and expression levels of proinflammatory cytokines in LPS-treated HMEC-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

et al. 2020

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Sepsis is a serious clinical condition characterized by systemic inflammation. The long noncoding rna (lncrna) highly upregulated in liver cancer (Hulc) was validated to partake in the development of sepsis. The present study aimed to investigate the potential mechanism of Hulc in lipopolysaccharide (lPS)-induced sepsis. reverse transcription-quantitative polymerase chain reaction (rT-qPcr) and western blot analysis was employed to examine the expression of Hulc, microrna (mir)-128-3p, rac family small GTPase 1 (RAC1) and pro-inflammatory factors [IL-6, TnF-α, intercellular adhesion molecule (icaM1) and vascular cell adhesion molecule (VcaM1)] in the serum of patients with sepsis or lPS-induced human dermal microvascular endothelial cells (HMec-1). Flow cytometry and western blot assays were performed to detect cell apoptosis. The targeted relationship among HULC, miR-128-3p and RAC1 was confirmed by a dual-luciferase reporter assay, rna binding protein immunoprecipitation (riP) assay and rna pull-down assay. Hulc and rac1 were found to be upregulated, and mir-128-3p was downregulated in the serum of patients with sepsis and lPS-stimulated HMec-1 cells. lPS promoted apoptosis and inflammation, which were decreased by silencing of HULC. Hulc targeted mir-128-3p and negatively regulated its expression. Hulc knockdown protected HMec-1 cells from lPS-induced injury by upregulating mir-128-3p. rac1 was a target of mir-128-3p, and gain of rac1 also relieved the silencing of Hulc-mediated suppressive effects on apoptosis and inflammation in LPS-stimulated HMEC-1 cells. In conclusion, Hulc knockdown partially reversed lPS-induced sepsis via the regulation of mir-128-3p/rac1 axis.

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“…The expression of miR-424 is reduced in most human BC specimens and cell lines, and increased expression of miR-424 reduces the expression of CDK1, thereby causing G2/M cell-cycle arrest and inhibiting cell proliferation [167]. MiR-128-3p inhibits the proliferation and motility of BC cells by affecting the expression of CDK4/6/cyclin D1 and CDK2/cyclin E1, leading to G0/G1 phase arrest [168]. MiR-122-5 also directly targets CDK2, CDK4, and CDK6, resulting in cell-cycle arrest [162].…”

Section: The Novel Cdk Inhibitors In Bcmentioning

confidence: 99%

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

Ding

Cao

Lin

et al. 2020

IJMS

347

216

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Cyclin-dependent kinases (CDKs) are serine/threonine kinases whose catalytic activities are regulated by interactions with cyclins and CDK inhibitors (CKIs). CDKs are key regulatory enzymes involved in cell proliferation through regulating cell-cycle checkpoints and transcriptional events in response to extracellular and intracellular signals. Not surprisingly, the dysregulation of CDKs is a hallmark of cancers, and inhibition of specific members is considered an attractive target in cancer therapy. In breast cancer (BC), dual CDK4/6 inhibitors, palbociclib, ribociclib, and abemaciclib, combined with other agents, were approved by the Food and Drug Administration (FDA) recently for the treatment of hormone receptor positive (HR+) advanced or metastatic breast cancer (A/MBC), as well as other sub-types of breast cancer. Furthermore, ongoing studies identified more selective CDK inhibitors as promising clinical targets. In this review, we focus on the roles of CDKs in driving cell-cycle progression, cell-cycle checkpoints, and transcriptional regulation, a highlight of dysregulated CDK activation in BC. We also discuss the most relevant CDK inhibitors currently in clinical BC trials, with special emphasis on CDK4/6 inhibitors used for the treatment of estrogen receptor-positive (ER+)/human epidermal growth factor 2-negative (HER2−) M/ABC patients, as well as more emerging precise therapeutic strategies, such as combination therapies and microRNA (miRNA) therapy.

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MiR-128-3p suppresses breast cancer cellular progression via targeting LIMK1

Cited by 58 publications

References 41 publications

Exosomal miRNA-128-3p from mesenchymal stem cells of aged rats regulates osteogenesis and bone fracture healing by targeting Smad5

Exosomal miRNA-128-3p from mesenchymal stem cells of aged rats regulates osteogenesis and bone fracture healing by targeting Smad5

Potential role of lncRNA HULC/miR‑128‑3p/RAC1 axis in the inflammatory response during LPS‑induced sepsis in HMEC‑1 cells

The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer

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