miR-194 inhibits liver cancer stem cell expansion by regulating RAC1 pathway

Ran, Rong-zheng; Chen, Jun; Cui, Longjiu; Lin, Xiao-Lu; Fan, Mingming; Cong, Zhuangzhi; Zhang, Hai; Tan, Weifeng; Zhang, Guoqing; Zhang, Yongjie

doi:10.1016/j.yexcr.2019.03.007

Cited by 39 publications

(29 citation statements)

References 40 publications

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“…For example, linc-ROR could promote chemotherapy tolerance of breast cancer (Chen et al, 2016a), regulate gemcitabine resistance in breast cancer (Chen et al, 2016b), regulate chemoresistance in docetaxel-resistant lung adenocarcinoma cells (Pan et al, 2017), and contribute to the resistance of pancreatic cancer cells to gemcitabine (Li et al, 2016). miR-194 influences the sensitivity to docetaxel in cancer therapy (Geretto et al, 2017) and increases the chemosensitivity of nonsmall cell lung cancer cells (Zhu et al, 2016), and low expression of miR-194 was observed in chemoresistant hepatocellular carcinoma cells (Ran et al, 2019). MECP2 is overexpressed in MCF-7 cells (Lin and Nelson, 2003) and can be decreased by miR-1291 to suppress cancer cell proliferation and enhance chemosensitivity (Li et al, 2015).…”

Section: Linc-ror Promotes Cell Proliferation Migration and Invasiomentioning

confidence: 99%

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

et al. 2020

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linc‐ROR is reported to be a potential biomarker of breast cancer, but the detailed mechanism of linc‐ROR‐mediated breast cancer regulation has not been fully studied. We aimed to explore how linc‐ROR affects proliferation, metastasis, and drug sensitivity in breast cancer. Cell lines in which linc‐ROR was overexpressed or knocked down were constructed, and the cell proliferation, colony formation, cell migration, and invasion abilities of these lines were explored. A CCK‐8 assay was performed to determine the sensitivity of the breast cancer cells to rapamycin. Next‐generation sequencing was conducted to explore the detailed regulatory mechanism of linc‐ROR; differentially expressed RNAs in the linc‐ROR‐overexpressing cell line compared with the negative control were screened out, and their target genes were chosen to perform Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis, protein–protein interaction network analysis, and competing endogenous RNA (ceRNA) network analysis. The ceRNA mechanism of linc‐ROR for miR‐194‐3p, which targets MECP2, was determined through dual‐luciferase reporter assay, RT–qPCR, western blot, and rescue experiments. Finally, we found that linc‐ROR was upregulated in breast tumor tissues. linc‐ROR promoted the cell proliferation, colony formation, cell migration, and invasion of breast cancer and decreased the sensitivity of breast cancer cells to rapamycin. The overexpression of linc‐ROR triggered changes in the whole transcriptome of breast cancer cells, and a total of 85 lncRNAs, 414 microRNAs, 490 mRNAs, and 92 circRNAs were differentially expressed in the linc‐ROR‐overexpressing cell line compared with the negative control. Through a series of bioinformatic analyses, the ‘linc‐ROR/miR‐194‐3p/MECP2’ ceRNA regulatory axis was confirmed to be involved in the linc‐ROR‐mediated progression and drug sensitivity of breast cancer. In conclusion, linc‐ROR serves as an onco‐lncRNA in breast cancer and promotes the survival of breast cancer cells during rapamycin treatment by functioning as a ceRNA sponge for miR‐194‐3p, which targets MECP2.

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Section: Linc-ror Promotes Cell Proliferation Migration and Invasiomentioning

confidence: 99%

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

et al. 2020

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“…In the past several decades, emerging evidence indicates that CSC is considered to have the ability to retain stem cell-like properties through self-renewal and differentiation and be responsible for tumor initiation, propagation, recurrence and resistance to therapy [14,39]. Moreover, CSC has now been suggested to bear a distinct metabolic phenotype and targeting CSC metabolism may provide a selective advantage to eventually take over and drive relapse of cancers [39,40]. Increasing evidence has indicated the existence of CSCs in OS [29,41] and yet, the mechanism of these CSCs in the progression of OS remains vague.…”

Section: Discussionmentioning

confidence: 99%

Untargeted LC–MS/MS analysis reveals metabolomics feature of osteosarcoma stem cell response to methotrexate

et al. 2020

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Background: Cancer stem cell (CSC) is identified in osteosarcoma (OS) and considered resistant to chemotherapeutic agents. However, the mechanism of osteosarcoma stem cell (OSC) resistant to chemotherapy remains debatable and vague, and the metabolomics feature of OSC is not clarified. Materials and methods: OSC was isolated by using sphere forming assay and identified. Untargeted LC-MS/MS analysis was performed to reveal the metabolomics feature of OSC and underlying mechanisms of OSC resistant to methotrexate (MTX). Results: OSC was efficiently isolated and identified from human OS 143B and MG63 cell lines with enhanced chemoresistance to MTX. The untargeted LC-MS analysis revealed that OSC showed differential metabolites and perturbed signaling pathways, mainly involved in metabolisms of fatty acid, amino acid, carbohydrate metabolism and nucleic acid. After treated with MTX, metabolomics feature of OSC was mainly involved metabolisms of amino acid, fatty acid, energy and nucleic acid. Moreover, compared with their parental OS cells response to MTX, the differential metabolites and perturbed signaling pathways were mainly involved in metabolism of amino acid, fatty acid and nucleic acid. What's more, Rap1 signaling pathway and Ras signaling pathway were involved in OS cells and their SCs response to MTX. Conclusion: Sphere-forming assay was able to efficiently isolate OSC from human OS cell lines and the untargeted LC-MS/MS analysis was suggested a sufficient methodology to investigate metabolomics features of OS cells and OSCs. Moreover, the metabolomics features of OSCs response to MTX might reveal a further understanding of chemotherapeutic resistance in OS.

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“…Thus, lower expression of miR-194 is a poor prognosis biomarker for HCC patients. 33 In another study, long noncoding RNA (lncRNA) MCM3AP antisense RNA 1 (MCM3AP-AS1) as a novel oncogene was suggested that is overexpressed in HCC tissues and positively correlated with large tumor size, high tumor grade, advanced tumor stage, and poor prognosis of HCC patients. MCM3AP-AS1 shows its oncogenic role via acting as endogenous RNA (ceRNA) for targeting and downregulating miR-194 and subsequently promoting FOXA1 expression.…”

Section: Hepatocellular Carcinomamentioning

confidence: 99%

Functional mechanisms of miR‐192 family in cancer

Mishan

Tabari

Parnian

et al. 2020

Genes Chromosomes & Cancer

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By growing research on the mechanisms and functions of microRNAs (miRNAs, miRs), the role of these noncoding RNAs gained more attention in healthcare. Due to the remarkable regulatory role of miRNAs, any dysregulation in their expression causes cellular functional impairment. In recent years, it has become increasingly apparent that these small molecules contribute to development, cell differentiation, proliferation, apoptosis, and tumor growth. In many studies, the miR-192 family has been suggested as a potential prognostic and diagnostic biomarker and even as a possible therapeutic target for several cancers. However, the mechanistic effects of the miR-192 family on cancer cells are still controversial. Here, we have reviewed each family member of the miR-192 including miR-192, miR-194, and miR-215, and discussed their mechanistic roles in various cancers.

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miR-194 inhibits liver cancer stem cell expansion by regulating RAC1 pathway

Cited by 39 publications

References 40 publications

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

Linc‐ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR‐194‐3p targeting MECP2

Untargeted LC–MS/MS analysis reveals metabolomics feature of osteosarcoma stem cell response to methotrexate

Functional mechanisms of miR‐192 family in cancer

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