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Keywords {🔍}

cancer, lncropm, plag, cells, bcscs, breast, pubmed, expression, article, cell, fig, google, scholar, tumor, cas, additional, analysis, stem, file, figure, nonbcscs, data, tissues, metabolism, patients, cscs, central, rna, qrtpcr, mrna, usa, lncrnas, utr, mcf, lncrna, tumors, giripladib, clinical, target, gene, group, acid, stemness, metabolic, china, images, noncoding, phospholipid, expressed, chemoresistance,

Topics {✒️}

pglv3/h1/gfp/puro vector peroxisome proliferator-activated receptor-alpha myc/pgc-1alpha balance determines cd44+/cd24−/low cells population rna-rna interaction search mcf7 cd44+cd24−/low cells inhibiting ras-mediated transformation er−pr−her2− patients pla2g16-mediated phospholipid metabolism article download pdf h-rev107-1 stimulates growth stem/progenitor cell properties h-ras resistant fibroblasts kaplan–meier survival curve yi-xue-yuan road streptavidin-linked magnetic beads quantitative reverse-transcription pcr kaplan–meier survival analysis lncropm-pla2g16-driven bcsc properties potential metabolism-related genes ifngamma-induced cell death cisplatin-resistant mda-mb-231 cells her2-positive breast cancer 3-year disease-free survival serum-free dmem/f12 repressed stemness-related gene mir-142-5p suppresses proliferation specific lentivirus-mediated shrnas twist-positive breast cancer cd44+cd24−/low mammospheres metabolite arachid-onic acid enhanced pmir-pla2g16-3'-utr-1 activity cancer-related death due biotin-labeled rna probes disease-free survival rate dual-luciferase reporter system progression-free survival rate metabolic-related genes play adipose-specific phospholipase a2 apc-rat isotype control hippo/yap signaling pathways cd44/cd24 antibodies conjugated specially activate pi3k/akt neoadjuvant paclitaxel/radiation treatment fitc-mouse isotype control polyperoxidase-anti-rabbit igg chongqing municipal education commission called tumor-initiating cells cy3-labeled lncropm probes impaired tumor-initiating capacity

Questions {❓}

• How do lncRNAs regulate transcription?

Schema {🗺️}

WebPage:
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         headline:A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties
         description:Cancer stem cells (CSCs) are considered as the major cause to tumor initiation, recurrence, metastasis, and drug resistance, driving poor clinical outcomes in patients. Long noncoding RNAs (lncRNAs) have emerged as crucial regulators in cancer development and progression. However, limited lncRNAs involved in CSCs have been reported. The novel lncROPM (a regulator of phospholipid metabolism) in breast CSCs (BCSCs) was identified by microarray and validated by qRT-PCR in BCSCs from breast cancer cells and tissues. The clinical significance of lncROPM was evaluated in two breast cancer cohorts and TANRIC database (TCGA-BRCA, RNAseq data). Gain- and loss-of-function assays were performed to examine the role of lncROPM on BCSCs both in vitro and in vivo. The regulatory mechanism of lncROPM was investigated by bioinformatics, RNA FISH, RNA pull-down, luciferase reporter assay, and actinomycin D treatment. PLA2G16-mediated phospholipid metabolism was determined by UHPLC-QTOFMS system. Cells’ chemosensitivity was assessed by CCK8 assay. LncROPM is highly expressed in BCSCs. The enhanced lncROPM exists in clinic breast tumors and other solid tumors and positively correlates with malignant grade/stage and poor prognosis in breast cancer patients. Gain- and loss-of-function studies show that lncROPM is required for the maintenance of BCSCs properties both in vitro and in vivo. Mechanistically, lncROPM regulates PLA2G16 expression by directly binding to 3'-UTR of PLA2G16 to increase the mRNA stability. The increased PLA2G16 significantly promotes phospholipid metabolism and the production of free fatty acid, especially arachidonic acid in BCSCs, thereby activating PI3K/AKT, Wnt/β-catenin, and Hippo/YAP signaling, thus eventually involving in the maintenance of BCSCs stemness. Importantly, lncROPM and PLA2G16 notably contribute to BCSCs chemo-resistance. Administration of BCSCs using clinic therapeutic drugs such as doxorubicin, cisplatin, or tamoxifen combined with Giripladib (an inhibitor of cytoplasmic phospholipase A2) can efficiently eliminate BCSCs and tumorigenesis. Our study highlights that lncROPM and its target PLA2G16 play crucial roles in sustaining BCSC properties and may serve as a biomarker for BCSCs or other cancer stem cells. Targeting lncROPM-PLA2G16 signaling axis may be a novel therapeutic strategy for patients with breast cancer.
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            Breast cancer stem cells
            PLA2G16
            Phospholipid metabolism
            Chemo-resistance
            Oncology
            Hematology
            Cancer Research
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      headline:A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties
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         Long noncoding RNA
         Breast cancer stem cells
         PLA2G16
         Phospholipid metabolism
         Chemo-resistance
         Oncology
         Hematology
         Cancer Research
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      name:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China
      name:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China
      name:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China
      name:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China
      name:Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, USA
      name:Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China

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