MicroRNA 628 suppresses migration and invasion of breast cancer stem cells through targeting SOS1

Lin, Chao‐Nan; Gao, Bin; Yan, Xuemao; Lei, Zixiong; Chen, Kebing; Li, Yuquan; Zeng, Qing; Chen, Zeqin; Li, Haomiao

doi:10.2147/ott.s164575

Cited by 33 publications

(27 citation statements)

References 27 publications

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“…Previous studies have demonstrated that mirnas serve an important role in the development of tumors; the aberrant overexpression or downregulation of multiple mirnas are often detected in a variety of tumors, suggesting that mirnas have different roles in different processes, such as tumor occurrence, development and metastasis (11,12). Previous studies have reported the abnormal expression of mirna (mir)-628 in numerous malignant tumor tissues (13,14); however, there are few studies observing the effects of mir-628 in colorectal cancer.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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Microrna (mir)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of mir-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of mir-628-5p in colorectal cancer. reverse transcription-quantitative Pcr (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of mir-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm mir-628-5p target genes. The expression levels of cyclin d1 (ccnd1) and related genes were determined using rT-qPcr or/and western blotting analysis. mir-628-5p mimics and ccnd1 plasmids were used to overexpress mir-628-5p and ccnd1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. mir-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. ccnd1, a downstream effector of mir-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by mir-628-5p mimics. in conclusion, the present study suggested that colorectal cancer progression may be regulated through the mir-628-5p/ccnd1 axis, and mir-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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“…Regarding the downregulated miRNAs, a low expression of miR-24-3p have been observed in the paclitaxel-resistant prostate cancer cell (PCa) [ 47 ], and associated to etoposide (VP16) and cisplatin (DDP) resistance in small cell lung cancer [ [48] , [49] , [50] ]. In the case of miRNA-628 and mir-766-3p, they have been implied with tumor suppressor functions in leukemia [ 51 , 52 ] and hepatocellular carcinoma [ 53 , 54 ], respectively.…”

Section: Discussionmentioning

confidence: 99%

miRNA signature associated with R–CHOP refractoriness in patients diagnosed with diffuse large B cell lymphoma

Fajardo-Ramírez

Villela

Campa-Carranza

et al. 2020

Non-coding RNA Research

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Refractoriness remains as one of the challenges in patients with lymphoma under chemotherapy, and among biological regulators in cells driving this type of response are microRNAs (miRNAs). Different genes are constantly turned on or off according to the miRNAs expression profiles affecting the drug response in patients and their stability in serum and plasma makes them potential prognostic biomarkers in several diseases. Here we described a profile of miRNAs in plasma of diffuse large B cell lymphoma (DLBCL) patients. miRNA expression arrays were carried using pre-treatment plasma samples of sixteen patients, followed by a comparison between the responder and the non-responders. After six cycles of R–CHOP treatment, twelve out of sixteen patients were clinically diagnosed with complete response while in four patients no clinical response was observed. Between these groups, a signature of fifteen differential expressed miRNAs was found. The circulating miRNAs in plasma of patients with no response were related to the drug resistance in other types of cancer, by targeting genes involved in cell proliferation and apoptosis, among other cell processes.

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“…By using hTERT promoter-driven VISA delivery of miR-34a plasmid, they further showed TV-miR-34a markedly suppressed tumor-initiating properties of BCSC in vitro and in vivo and also reported that TV-miR-34a plasmid synergizes with docetaxel for eradicating BCSC by targeting C22ORF28 [96]. miR-628, another important miRNA deregulated in human cancer pathogenesis, has been shown to suppresses BCSC stemness features by targeting Ras/Rac guanine nucleotide exchange factor 1 (SOS1) [138]. Interestingly, hypoxia or hypoxic tumor microenvironments or tumor vicinity has been well-known as a tumorigenic stimulus via targeting a number of biological mechanisms including miRNAs.…”

Section: Breast Cancermentioning

confidence: 94%

Role of miRNA-Regulated Cancer Stem Cells in the Pathogenesis of Human Malignancies

Khan

Ahmed

Elareer

et al. 2019

Cells

238

168

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Recent biomedical discoveries have revolutionized the concept and understanding of carcinogenesis, a complex and multistep phenomenon which involves accretion of genetic, epigenetic, biochemical, and histological changes, with special reference to MicroRNAs (miRNAs) and cancer stem cells (CSCs). miRNAs are small noncoding molecules known to regulate expression of more than 60% of the human genes, and their aberrant expression has been associated with the pathogenesis of human cancers and the regulation of stemness features of CSCs. CSCs are the small population of cells present in human malignancies well-known for cancer resistance, relapse, tumorigenesis, and poor clinical outcome which compels the development of novel and effective therapeutic protocols for better clinical outcome. Interestingly, the role of miRNAs in maintaining and regulating the functioning of CSCs through targeting various oncogenic signaling pathways, such as Notch, wingless (WNT)/β-Catenin, janus kinases/ signal transducer and activator of transcription (JAK/STAT), phosphatidylinositol 3-kinase/ protein kinase B (PI3/AKT), and nuclear factor kappa-light-chain-enhancer of activated B (NF-kB), is critical and poses a huge challenge to cancer treatment. Based on recent findings, here, we have documented the regulatory action or the underlying mechanisms of how miRNAs affect the signaling pathways attributed to stemness features of CSCs, such as self-renewal, differentiation, epithelial to mesenchymal transition (EMT), metastasis, resistance and recurrence etc., associated with the pathogenesis of various types of human malignancies including colorectal cancer, lung cancer, breast cancer, head and neck cancer, prostate cancer, liver cancer, etc. We also shed light on the fact that the targeted attenuation of deregulated functioning of miRNA related to stemness in human carcinogenesis could be a viable approach for cancer treatment.

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MicroRNA 628 suppresses migration and invasion of breast cancer stem cells through targeting SOS1

Cited by 33 publications

References 27 publications

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

miRNA signature associated with R–CHOP refractoriness in patients diagnosed with diffuse large B cell lymphoma

Role of miRNA-Regulated Cancer Stem Cells in the Pathogenesis of Human Malignancies

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