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Keywords {🔍}

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Topics {✒️}

tumor suppressors mir-125a-5p regulating mir-544a/fbxw7 axis tincr/stau1/cdkn2b signaling axis mir-181a-5p-mediated regulation disrupting sirt6-mediated de-acetylation generate dna–protein cross-links article download pdf accompanied epithelial-mesenchymal transition sds-page gel electrophoresis inhibiting cul4a-mediated ubiquitination impeding mir-18a repression van der stelt-frissen pi3k/akt signaling pathway ez-magna chip kit wnt/beta-catenin signaling 100 ng/ml cholera toxin anti-mir-125b rescued mir-125b significantly rescued braf-activated mapk pathway anti-mir-125b abrogated 3 ml rnase-free h2o nucleo-cytoplasmic separation experiment trastuzumab-resistant cell lines mir-125b-dependent manner mir-125b targets erythropoietin matrigel-based transwell assay mir-125b significantly suppressed epithelial-mesenchymal transition progression-free survival time 4 μm-thick tma slides progression-free survival showed anti-mir-125b reversed zinc-finger transcription factors hormone receptor-positive full access trastuzumab resistance-related metastasis kaplan-meier analysis showed tincr sponged mir-125b bt474-tr cell lines h3k27 acetylation-induced upregulation trastuzumab-res`istant cells sh-tincr-induced suppression agap2-as1 trastuzumab resistance-induced emt resistance-induced emt process tincr knockdown-induced inhibition anti-n-cadherin antibody mir-125b axis resistance-accompanied emt process negative control sh-nc

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         headline:RETRACTED ARTICLE: Activation of LncRNA TINCR by H3K27 acetylation promotes Trastuzumab resistance and epithelial-mesenchymal transition by targeting MicroRNA-125b in breast Cancer
         description:Trastuzumab resistance followed by metastasis is a major obstacle for improving the clinical outcome of patients with advanced human epidermal growth factor receptor 2-positive (HER-2+) breast cancer. While long non-coding RNAs (lncRNAs) can modulate cell behavior, the contribution of these RNAs in trastuzumab resistance and metastasis of HER-2+ breast cancer is not well known. In this study, we sought to identify the regulatory role of lncRNA in trastuzumab resistance and accompanied Epithelial-mesenchymal Transition (EMT) process in advanced HER-2+ breast cancer. Trastuzumab-resistant SKBR-3-TR and BT474-TR cell lines were established by grafting SKBR-3 and BT474 cells into mouse models and subjected to trastuzumab treatment. LncRNA microarray followed by quantitative reverse transcription PCR (qRT-PCR) was carried out to verify the differentially expressed lncRNAs. Western blotting, bioinformatics analysis, immunofluorescence assay and immunoprecipitation assays (ChIP and RIP) were performed to identify the involvement and functional interactions between H3K27 acetylation and terminal differentiation-induced non-coding RNA (TINCR) or between TINCR and its downstream genes including miR-125b, HER-2 and Snail-1. In addition, a series of in vitro and in vivo assays were performed to assess the functions of TINCR. An increase in both, IC50 value of trastuzumab and EMT was observed in the established trastuzumab-resistant cell lines. The expression level of TINCR was significantly increased in trastuzumab-resistant cells when compared with sensitive cells. Knockdown of TINCR reversed the trastuzumab resistance and the acquired EMT in these cells. TINCR was detected in the cytoplasm of breast cancer cells and could sponge miR-125b, thereby releasing HER-2 and inducing trastuzumab resistance. In addition, Snail-1 was found to be the target gene of miR-125b and overexpression of Snail-1 could reverse the suppressed migration, invasion, and EMT caused by TINCR silencing. The upregulation of TINCR in breast cancer was attributed to the CREB-binding protein (CBP)-mediated H3K27 acetylation at the promoter region of TINCR. Clinically, HER-2+ breast cancer patients with high TINCR expression levels were associated with poor response to trastuzumab therapy and shorter survival time. TINCR could promote trastuzumab resistance and the accompanied EMT process in breast cancer. Therefore, TINCR might be a potential indicator for prognosis and a therapeutic target to enhance the clinical efficacy of trastuzumab treatment.
         datePublished:2019-01-08T00:00:00Z
         dateModified:2022-06-29T00:00:00Z
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            Trastuzumab
            TINCR
            miR-125b
            HER-2
            Snail-1
            H3K27 acetylation
            Cancer Research
            Oncology
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      headline:RETRACTED ARTICLE: Activation of LncRNA TINCR by H3K27 acetylation promotes Trastuzumab resistance and epithelial-mesenchymal transition by targeting MicroRNA-125b in breast Cancer
      description:Trastuzumab resistance followed by metastasis is a major obstacle for improving the clinical outcome of patients with advanced human epidermal growth factor receptor 2-positive (HER-2+) breast cancer. While long non-coding RNAs (lncRNAs) can modulate cell behavior, the contribution of these RNAs in trastuzumab resistance and metastasis of HER-2+ breast cancer is not well known. In this study, we sought to identify the regulatory role of lncRNA in trastuzumab resistance and accompanied Epithelial-mesenchymal Transition (EMT) process in advanced HER-2+ breast cancer. Trastuzumab-resistant SKBR-3-TR and BT474-TR cell lines were established by grafting SKBR-3 and BT474 cells into mouse models and subjected to trastuzumab treatment. LncRNA microarray followed by quantitative reverse transcription PCR (qRT-PCR) was carried out to verify the differentially expressed lncRNAs. Western blotting, bioinformatics analysis, immunofluorescence assay and immunoprecipitation assays (ChIP and RIP) were performed to identify the involvement and functional interactions between H3K27 acetylation and terminal differentiation-induced non-coding RNA (TINCR) or between TINCR and its downstream genes including miR-125b, HER-2 and Snail-1. In addition, a series of in vitro and in vivo assays were performed to assess the functions of TINCR. An increase in both, IC50 value of trastuzumab and EMT was observed in the established trastuzumab-resistant cell lines. The expression level of TINCR was significantly increased in trastuzumab-resistant cells when compared with sensitive cells. Knockdown of TINCR reversed the trastuzumab resistance and the acquired EMT in these cells. TINCR was detected in the cytoplasm of breast cancer cells and could sponge miR-125b, thereby releasing HER-2 and inducing trastuzumab resistance. In addition, Snail-1 was found to be the target gene of miR-125b and overexpression of Snail-1 could reverse the suppressed migration, invasion, and EMT caused by TINCR silencing. The upregulation of TINCR in breast cancer was attributed to the CREB-binding protein (CBP)-mediated H3K27 acetylation at the promoter region of TINCR. Clinically, HER-2+ breast cancer patients with high TINCR expression levels were associated with poor response to trastuzumab therapy and shorter survival time. TINCR could promote trastuzumab resistance and the accompanied EMT process in breast cancer. Therefore, TINCR might be a potential indicator for prognosis and a therapeutic target to enhance the clinical efficacy of trastuzumab treatment.
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      dateModified:2022-06-29T00:00:00Z
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         Breast cancer
         Trastuzumab
         TINCR
         miR-125b
         HER-2
         Snail-1
         H3K27 acetylation
         Cancer Research
         Oncology
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      name:Department of General Surgery, Hainan General Hospital, Hainan Medical University, Haikou City, China
      name:Department of General Surgery, Hainan General Hospital, Hainan Medical University, Haikou City, China
      name:Department of General Surgery, Chongqing Renji Hospital, University of Chinese Academy of Science, Chongqing, China
      name:Department of General Surgery, The Frist Affiliated Hospital, Chongqing Medical University, Chongqing, China
      name:Department of General Surgery, The Frist Affiliated Hospital, Chongqing Medical University, Chongqing, China
      name:Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

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