We are analyzing https://link.springer.com/article/10.1007/s12672-023-00652-z.

Title:
RUNX1-IT1 favors breast cancer carcinogenesis through regulation of IGF2BP1/GPX4 axis | Discover Oncology
Description:
Breast cancer is the most common malignancy among women and the leading cause of cancer deaths, with complicated pathogenesis that is largely unknown. In this study, we identified a novel long non-coding RNA (lncRNA) as a critical driver of breast cancer tumorigenesis. RUNX1 intronic transcript 1 (RUNX1-IT1) was notably overexpressed in human breast cancer tissues, and knockdown of RUNX1-IT1 inhibited breast cancer cell viability and invasion, as well as tumor growth in orthotopic transplantation model. Further, RUNX1-IT1 repressed ferroptosis, a novel iron-dependent form of regulated cell death, via increasing glutathione peroxidase 4 (GPX4) expression. Specifically, RUNX1-IT1 directly bound to N6-methyladenosine m6A reader IGF2BP1 and promoted the formation of (insulin like growth factor 2 mRNA binding protein 1) IGF2BP1 liquid-liquid phase separation (LLPS) biomolecular condensates, resulting in more IGF2BP1 occupation on GPX4 mRNA, increasing GPX4 mRNA stability. Moreover, high RUNX1-IT1 was linked to poor prognosis, and a strong positive correlation between RUNX1-IT1 and GPX4 was observed in clinical breast cancer tissues. Taken together, our data reveal that RUNX1-IT1 promotes breast cancer carcinogenesis through blocking ferroptosis via elevating GPX4, targeting of the previously unappreciated regulatory axis of RUNX1-IT1/IGF2BP1/GPX4 may be a promising treatment for patient with breast cancer.
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Keywords {🔍}

runxit, cancer, breast, gpx, igfbp, fig, pubmed, article, cell, cells, google, scholar, expression, ferroptosis, cas, lncrna, mrna, protein, rna, study, assay, tissues, binding, llps, mdamb, central, analysis, function, wang, knockdown, tumor, data, death, lipid, human, levels, qrtpcr, runxitsilenced, testing, regulation, analyzed, liu, patients, mutant, results, showed, full, noncoding, model, separation,

Topics {✒️}

stat1-tincr-usp20-pd-l1 axis runx1-it1-silenced cells treated runx1-it1-silenced cells transfected liquid-liquid phase separation runx1-it1/igf2bp1 liquid droplets recent evidence shows runx1-it1-overexpressed cells transfected proto-oncogene protein eif4e runx1-it1-silenced cells article download pdf c18-reversedphase analytical column runx1-it1 affected ferroptosis downregulating mir-199a-5p runx1-it1-silenced group runx1-it1 repressed ferroptosis mda-mb-231 cell lysates gradient sds-polyacrylamide gel membrane-bound organelle dynamics maximal tumor size/burden runx1-it1-silenced t47d human pan-carcinoma tissues stable runx1-it1 knockdown runx1-it1 directly bound mda-mb-231 cell death breast cancer carcinogenesis q-exactive mass spectrometer runx1-it1 elevates gpx4 higher runx1-it1 levels emerging evidence suggests runx1-it1 induces ferroptosis shrnas targeting runx1-it1 full-length coding sequences qrt-pcr analysis testing runx1-it1-overexpressed cells study rna-protein interactions accumulated evidence shows emerging evidence shows cell-cell interaction mediated runx1-it1 expression levels regulating igf2bp1/gpx4 axis runx1-it1-mediated regulation avoid rna degradation anti-gfp magnetic beads purified gfp-igf2bp1 protein patient-derived tumor xenograft runx1-it1 promotes fatty acid oxidation runx1-it1/igf2bp1/gpx4 lung cancer cells kaplan-meier survival curve

Schema {🗺️}

WebPage:
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         headline:RUNX1-IT1 favors breast cancer carcinogenesis through regulation of IGF2BP1/GPX4 axis
         description:Breast cancer is the most common malignancy among women and the leading cause of cancer deaths, with complicated pathogenesis that is largely unknown. In this study, we identified a novel long non-coding RNA (lncRNA) as a critical driver of breast cancer tumorigenesis. RUNX1 intronic transcript 1 (RUNX1-IT1) was notably overexpressed in human breast cancer tissues, and knockdown of RUNX1-IT1 inhibited breast cancer cell viability and invasion, as well as tumor growth in orthotopic transplantation model. Further, RUNX1-IT1 repressed ferroptosis, a novel iron-dependent form of regulated cell death, via increasing glutathione peroxidase 4 (GPX4) expression. Specifically, RUNX1-IT1 directly bound to N6-methyladenosine m6A reader IGF2BP1 and promoted the formation of (insulin like growth factor 2 mRNA binding protein 1) IGF2BP1 liquid-liquid phase separation (LLPS) biomolecular condensates, resulting in more IGF2BP1 occupation on GPX4 mRNA, increasing GPX4 mRNA stability. Moreover, high RUNX1-IT1 was linked to poor prognosis, and a strong positive correlation between RUNX1-IT1 and GPX4 was observed in clinical breast cancer tissues. Taken together, our data reveal that RUNX1-IT1 promotes breast cancer carcinogenesis through blocking ferroptosis via elevating GPX4, targeting of the previously unappreciated regulatory axis of RUNX1-IT1/IGF2BP1/GPX4 may be a promising treatment for patient with breast cancer.
         datePublished:2023-04-10T00:00:00Z
         dateModified:2023-04-10T00:00:00Z
         pageStart:1
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            Breast cancer
            Ferroptosis
            m6A reader
            mRNA stability
            Oncology
            Cancer Research
            Surgical Oncology
            Molecular Medicine
            Radiotherapy
            Internal Medicine
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ScholarlyArticle:
      headline:RUNX1-IT1 favors breast cancer carcinogenesis through regulation of IGF2BP1/GPX4 axis
      description:Breast cancer is the most common malignancy among women and the leading cause of cancer deaths, with complicated pathogenesis that is largely unknown. In this study, we identified a novel long non-coding RNA (lncRNA) as a critical driver of breast cancer tumorigenesis. RUNX1 intronic transcript 1 (RUNX1-IT1) was notably overexpressed in human breast cancer tissues, and knockdown of RUNX1-IT1 inhibited breast cancer cell viability and invasion, as well as tumor growth in orthotopic transplantation model. Further, RUNX1-IT1 repressed ferroptosis, a novel iron-dependent form of regulated cell death, via increasing glutathione peroxidase 4 (GPX4) expression. Specifically, RUNX1-IT1 directly bound to N6-methyladenosine m6A reader IGF2BP1 and promoted the formation of (insulin like growth factor 2 mRNA binding protein 1) IGF2BP1 liquid-liquid phase separation (LLPS) biomolecular condensates, resulting in more IGF2BP1 occupation on GPX4 mRNA, increasing GPX4 mRNA stability. Moreover, high RUNX1-IT1 was linked to poor prognosis, and a strong positive correlation between RUNX1-IT1 and GPX4 was observed in clinical breast cancer tissues. Taken together, our data reveal that RUNX1-IT1 promotes breast cancer carcinogenesis through blocking ferroptosis via elevating GPX4, targeting of the previously unappreciated regulatory axis of RUNX1-IT1/IGF2BP1/GPX4 may be a promising treatment for patient with breast cancer.
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      dateModified:2023-04-10T00:00:00Z
      pageStart:1
      pageEnd:13
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         Long non-coding RNA
         Breast cancer
         Ferroptosis
         m6A reader
         mRNA stability
         Oncology
         Cancer Research
         Surgical Oncology
         Molecular Medicine
         Radiotherapy
         Internal Medicine
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      name:School of Medicine, Xi’an Jiaotong University, Xi’an, China
      name:Clinical Medical Center, Xi’an Peihua University, Xi’an, China
      name:Clinical Medical Center, Xi’an Peihua University, Xi’an, China

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