ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Linc-ROR induces epithelial-mesenchymal transition and contributes to drug resistance and invasion of breast cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025Review
- Key genes and molecular mechanisms related to Paclitaxel Resistance.Cancer cell international · 2024Review
- Autophagy-related lncRNAs in tumor progression and drug resistance: A double-edged sword.Genes & diseases · 2024Review
- H1Innovative approaches to combat anti-cancer drug resistance: Targeting lncRNA and autophagy.Clinical and translational medicine · 2023Review
- Long Noncoding RNAs in Taxane Resistance of Breast Cancer.International journal of molecular sciences · 2023Review
- Differential Expression ofIranian journal of public health · 2023Article
- Functional Relevance of the Long Intergenic Non-Coding RNA Regulator of Reprogramming (Linc-ROR) in Cancer Proliferation, Metastasis, and Drug Resistance.Non-coding RNA · 2023Review
- The Mechanisms of lncRNA-Mediated Multidrug Resistance and the Clinical Application Prospects of lncRNAs in Breast Cancer.Cancers · 2022Review
- Downregulation of LINC02615 Is Correlated with The Breast Cancer Progress: A Novel Biomarker for Differential Identification of Breast Cancer Tissues.Cell journal · 2021Article
- Review
- LncRNAs and microRNAs as Essential Regulators of Stemness in Breast Cancer Stem Cells.Biomolecules · 2021Review
- LINC00467, Driven by Copy Number Amplification and DNA Demethylation, Is Associated with Oxidative Lipid Metabolism and Immune Infiltration in Breast Cancer.Oxidative medicine and cellular longevity · 2021Article
- The Role of Non-Coding RNAs in Breast Cancer Drug Resistance.Frontiers in oncology · 2021Review
- Mechanisms of Taxane ResistanceCancers · 2020Review
- Connecting the Missing Dots: ncRNAs as Critical Regulators of Therapeutic Susceptibility in Breast Cancer.Cancers · 2020Review
- Dual Effects of Non-Coding RNAs (ncRNAs) in Cancer Stem Cell Biology.International journal of molecular sciences · 2020Review
- Linc-ROR promotes the progression of breast cancer and decreases the sensitivity to rapamycin through miR-194-3p targeting MECP2.Molecular oncology · 2020Article
- Non-Coding RNAs as Regulators and Markers for Targeting of Breast Cancer and Cancer Stem Cells.Cancers · 2020Review
- Relevance Function of Linc-ROR in the Pathogenesis of Cancer.Frontiers in cell and developmental biology · 2020Review
- Emerging Roles of Long Noncoding RNA Regulator of Reprogramming in Cancer Treatment.Cancer management and research · 2020Review
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5 authors.
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Abstract
We aimed to investigate the role of large intergenic noncoding RNA regulator of reprogramming (linc-ROR) in the chemotherapy resistance of human breast cancer (BC) cells and its mechanism. A total of 142 patients diagnosed with BC in the First Affiliated Hospital, Zhejiang University between January 2012 and January 2014 were enrolled in our study. The BC tissues and the adjacent normal tissues (5 cm away from tumor tissue) of the enrolled patients were selected, and human BC cell lines (MCF10A, SK-BR-3, MCF-7, Bcap-37, MDA-MB-231, and T47D) were also selected. Quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, 3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS) assay, and Transwell were applied in our study. Expression level of linc-ROR messenger RNA (mRNA) in BC tissues was clearly higher than that in adjacent normal tissues, and significant difference was found between expression level of linc-ROR mRNA and lymph node metastasis (all P < 0.05). Linc-ROR was highly expressed in others BC cell lines compared with that in immortalized mammary epithelial cells (MECs) MCF10A (both P < 0.05), while MDA-MB231 cell presented the higher expression (P < 0.001). Under different concentrations of 5-FU and paclitaxel in MDA-MB231 cell, E-cadherin mRNA and protein expressions increased gradually with the increase of concentrations, and Vimentin and N-cadherin mRNA and protein expressions decreased gradually with the decrease of concentrations (all P < 0.05). Compared with shCtrl group, MDA-MB231 cell in shROR group presented higher sensibility of 5-FU and paclitaxel with increased E-cadherin expression, decreased Vimentin and N-cadherin expression and invasion ability (all P < 0.05). Compared with vector cell, overexpressed linc-ROR cell presented decreased sensibility of 5-FU and paclitaxel with decreased E-cadherin expression, increased Vimentin, N-cadherin expression, and invasion ability (all P < 0.05). Our study demonstrated that linc-ROR is an important marker for multidrug resistance of BC, and its up-regulation is important for chemotherapy tolerance and invasion of BC.
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