We are analyzing https://link.springer.com/article/10.1186/1471-2407-14-785.

Title:
Bmi1 regulates self-renewal and epithelial to mesenchymal transition in breast cancer cells through Nanog | BMC Cancer
Description:
Background The Bmi1 polycomb ring finger oncogene, a transcriptional repressor belonging to the Polycomb group of proteins plays an important role in the regulation of stem cell self-renewal and is elevated in several cancers. In the current study, we have explored the role of Bmi1 in regulating the stemness and drug resistance of breast cancer cells. Methods Using real time PCR and immunohistochemistry primary breast tissues were analyzed. Retro- and lentiviruses were utilized to overexpress and knockdown Bmi1, RT-PCR and Western blot was performed to evaluate mRNA and protein expression. Stemness properties were analyzed by flow cytometry and sphere-formation and tumor formation was determined by mouse xenograft experiments. Dual luciferase assay was employed to assess promoter activity and MTT assay was used to analyze drug response. Results We found Bmi1 overexpression in 64% of grade III invasive ductal breast adenocarcinomas compared to normal breast tissues. Bmi1 overexpression in immortalized and transformed breast epithelial cells increased their sphere-forming efficiency, induced epithelial to mesenchymal transition (EMT) with an increase in the expression of stemness-related genes. Knockdown of Bmi1 in tumorigenic breast cells induced epithelial morphology, reduced expression of stemness-related genes, decreased the IC50 values of doxorubicin and abrogated tumor-formation. Bmi1-high tumors showed elevated Nanog expression whereas the tumors with lower Bmi1 showed reduced Nanog levels. Overexpression of Bmi1 increased Nanog levels whereas knockdown of Bmi1 reduced its expression. Dual luciferase promoter-reporter assay revealed Bmi1 positively regulated the Nanog and NFκB promoter activity. RT-PCR analysis showed that Bmi1 overexpression activated the NFκB pathway whereas Bmi1 knockdown reduced the expression of NFκB target genes, suggesting that Bmi1 might regulate Nanog expression through the NFκB pathway. Conclusions Our study showed that Bmi1 is overexpressed in several high-grade, invasive ductal breast adenocarcinomas, thus supporting its role as a prognostic marker. While Bmi1 overexpression increased self-renewal and promoted EMT, its knockdown reversed EMT, reduced stemness, and rendered cells drug sensitive, thus highlighting a crucial role for Bmi1 in regulating the stemness and drug response of breast cancer cells. Bmi1 may control self-renewal through the regulation of Nanog expression via the NFκB pathway.
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Keywords {🔍}

bmi, cells, cancer, breast, pubmed, article, google, scholar, expression, stem, cas, cell, nanog, figure, selfrenewal, knockdown, overexpression, stemness, nfκb, control, vector, mammary, central, epithelial, tumor, activity, normal, genes, pathway, properties, emt, role, luciferase, reduced, showed, tissues, human, mdamb, study, promoter, increased, analysis, drug, shown, assay, regulates, regulating, primary, tumors, levels,

Topics {✒️}

twist1-induced epithelial-mesenchymal transition ikk-nuclear factor-kappab pathway nf-kappab/mmp-9 signaling pathway semi-quantitative rt-pcr analysis dual-luciferase assay kit inhibiting c-myc-induced apoptosis dual-luciferase assay showed induces epithelial-mesenchymal transition open access license pre-publication history nfκb promoter-luciferase plasmid article download pdf anti-α-tubulin antibody rt-pcr analysis showed hrp-coupled secondary antibodies ras/mapk signaling pathways dbt-iisc partnership programme promoter reporter assay activating nf-kappab signaling epithelial-mesenchymal transition ultra-low attachment plates undertook shrna-mediated knockdown bd facs-aria ii paranjape & geetashree mukherjee mouse xenograft experiments jacobs jj figure 2b-left panel dual luciferase assay mu-myc transgenic mice providing pbabepuro-bmi1 construct chose nble-lp cells nuclear factor-kappab induced mesenchymal morphology c-myc cooperating oncogene mammary stem cell mammary epithelial cells mammary stem cells embryonic stem cell stem cell factor nanog promoter activity graphs showing fold epithelial-mesenchymal transdifferentiation nat rev cancer acute myeloid leukemia bmi1 positively regulates anti-cancer drug doxorubicin mouse mammary epithelium secondary anti-mouse privacy choices/manage cookies nfκb promoter activity

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WebPage:
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         headline:Bmi1 regulates self-renewal and epithelial to mesenchymal transition in breast cancer cells through Nanog
         description:The Bmi1 polycomb ring finger oncogene, a transcriptional repressor belonging to the Polycomb group of proteins plays an important role in the regulation of stem cell self-renewal and is elevated in several cancers. In the current study, we have explored the role of Bmi1 in regulating the stemness and drug resistance of breast cancer cells. Using real time PCR and immunohistochemistry primary breast tissues were analyzed. Retro- and lentiviruses were utilized to overexpress and knockdown Bmi1, RT-PCR and Western blot was performed to evaluate mRNA and protein expression. Stemness properties were analyzed by flow cytometry and sphere-formation and tumor formation was determined by mouse xenograft experiments. Dual luciferase assay was employed to assess promoter activity and MTT assay was used to analyze drug response. We found Bmi1 overexpression in 64% of grade III invasive ductal breast adenocarcinomas compared to normal breast tissues. Bmi1 overexpression in immortalized and transformed breast epithelial cells increased their sphere-forming efficiency, induced epithelial to mesenchymal transition (EMT) with an increase in the expression of stemness-related genes. Knockdown of Bmi1 in tumorigenic breast cells induced epithelial morphology, reduced expression of stemness-related genes, decreased the IC50 values of doxorubicin and abrogated tumor-formation. Bmi1-high tumors showed elevated Nanog expression whereas the tumors with lower Bmi1 showed reduced Nanog levels. Overexpression of Bmi1 increased Nanog levels whereas knockdown of Bmi1 reduced its expression. Dual luciferase promoter-reporter assay revealed Bmi1 positively regulated the Nanog and NFκB promoter activity. RT-PCR analysis showed that Bmi1 overexpression activated the NFκB pathway whereas Bmi1 knockdown reduced the expression of NFκB target genes, suggesting that Bmi1 might regulate Nanog expression through the NFκB pathway. Our study showed that Bmi1 is overexpressed in several high-grade, invasive ductal breast adenocarcinomas, thus supporting its role as a prognostic marker. While Bmi1 overexpression increased self-renewal and promoted EMT, its knockdown reversed EMT, reduced stemness, and rendered cells drug sensitive, thus highlighting a crucial role for Bmi1 in regulating the stemness and drug response of breast cancer cells. Bmi1 may control self-renewal through the regulation of Nanog expression via the NFκB pathway.
         datePublished:2014-10-28T00:00:00Z
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            Drug-resistance
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            Surgical Oncology
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            Biomedicine
            general
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      headline:Bmi1 regulates self-renewal and epithelial to mesenchymal transition in breast cancer cells through Nanog
      description:The Bmi1 polycomb ring finger oncogene, a transcriptional repressor belonging to the Polycomb group of proteins plays an important role in the regulation of stem cell self-renewal and is elevated in several cancers. In the current study, we have explored the role of Bmi1 in regulating the stemness and drug resistance of breast cancer cells. Using real time PCR and immunohistochemistry primary breast tissues were analyzed. Retro- and lentiviruses were utilized to overexpress and knockdown Bmi1, RT-PCR and Western blot was performed to evaluate mRNA and protein expression. Stemness properties were analyzed by flow cytometry and sphere-formation and tumor formation was determined by mouse xenograft experiments. Dual luciferase assay was employed to assess promoter activity and MTT assay was used to analyze drug response. We found Bmi1 overexpression in 64% of grade III invasive ductal breast adenocarcinomas compared to normal breast tissues. Bmi1 overexpression in immortalized and transformed breast epithelial cells increased their sphere-forming efficiency, induced epithelial to mesenchymal transition (EMT) with an increase in the expression of stemness-related genes. Knockdown of Bmi1 in tumorigenic breast cells induced epithelial morphology, reduced expression of stemness-related genes, decreased the IC50 values of doxorubicin and abrogated tumor-formation. Bmi1-high tumors showed elevated Nanog expression whereas the tumors with lower Bmi1 showed reduced Nanog levels. Overexpression of Bmi1 increased Nanog levels whereas knockdown of Bmi1 reduced its expression. Dual luciferase promoter-reporter assay revealed Bmi1 positively regulated the Nanog and NFκB promoter activity. RT-PCR analysis showed that Bmi1 overexpression activated the NFκB pathway whereas Bmi1 knockdown reduced the expression of NFκB target genes, suggesting that Bmi1 might regulate Nanog expression through the NFκB pathway. Our study showed that Bmi1 is overexpressed in several high-grade, invasive ductal breast adenocarcinomas, thus supporting its role as a prognostic marker. While Bmi1 overexpression increased self-renewal and promoted EMT, its knockdown reversed EMT, reduced stemness, and rendered cells drug sensitive, thus highlighting a crucial role for Bmi1 in regulating the stemness and drug response of breast cancer cells. Bmi1 may control self-renewal through the regulation of Nanog expression via the NFκB pathway.
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         Bmi1
         Breast cancer stem cells
         Drug-resistance
         Epithelial to mesenchymal transition
         Nanog
         NFκB
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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                     type:PostalAddress
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                  name:Indian Institute of Science
                  address:
                     name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
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                  name:Indian Institute of Science
                  address:
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                     type:PostalAddress
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         type:PostalAddress
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         type:PostalAddress
      name:Kidwai Memorial Institute of Oncology
      address:
         name:Department of Pathology, Kidwai Memorial Institute of Oncology, Bangalore, India
         type:PostalAddress
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            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
            name:Kidwai Memorial Institute of Oncology
            address:
               name:Department of Pathology, Kidwai Memorial Institute of Oncology, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Sai A Balaji
      affiliation:
            name:Indian Institute of Science
            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Tamoghna Mandal
      affiliation:
            name:Indian Institute of Science
            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Esthelin Vittal Krushik
      affiliation:
            name:Indian Institute of Science
            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Pradeep Nagaraj
      affiliation:
            name:Indian Institute of Science
            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Geetashree Mukherjee
      affiliation:
            name:Kidwai Memorial Institute of Oncology
            address:
               name:Department of Pathology, Kidwai Memorial Institute of Oncology, Bangalore, India
               type:PostalAddress
            type:Organization
      name:Annapoorni Rangarajan
      affiliation:
            name:Indian Institute of Science
            address:
               name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
      name:Department of Pathology, Kidwai Memorial Institute of Oncology, Bangalore, India
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India
      name:Department of Pathology, Kidwai Memorial Institute of Oncology, Bangalore, India
      name:Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India

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