We are analyzing https://link.springer.com/article/10.1186/s12943-018-0826-9.

Title:
Enhanced expression of histone chaperone APLF associate with breast cancer | Molecular Cancer
Description:
DNA damage-specific histone chaperone Aprataxin PNK-like factor (APLF) regulates mesenchymal-to-epithelial transition (MET) during cellular reprogramming. We investigated the role of APLF in epithelial-to-mesenchymal transition (EMT) linked to breast cancer invasiveness and metastasis. Here, we show that a significant manifestation of APLF is present in tumor sections of patients with invasive ductal carcinoma when compared to their normal adjacent tissues. APLF was significantly induced in triple negative breast cancer (TNBC) cells, MDAMB-231, in comparison to invasive MCF7 or normal MCF10A breast cells and supported by studies on invasive breast carcinoma in The Cancer Genome Atlas (TCGA). Functionally, APLF downregulation inhibited proliferative capacity, altered cell cycle behavior, induced apoptosis and impaired DNA repair ability of MDAMB-231 cells. Reduction in APLF level impeded invasive, migratory, tumorigenic and metastatic potential of TNBC cells with loss in expression of genes associated with EMT while upregulation of MET-specific gene E-cadherin (CDH1). So, here we provided novel evidence for enrichment of APLF in breast tumors, which could regulate metastasis-associated EMT in invasive breast cancer. We anticipate that APLF could be exploited as a biomarker for breast tumors and additionally could be targeted in sensitizing cancer cells towards DNA damaging agents.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

cells, aplf, expression, mdamb, cancer, control, breast, aplfkd, additional, file, cell, figure, fig, level, foxa, invasive, genes, dna, repair, analysis, downregulation, ezh, histone, article, emt, significant, metastatic, promoter, significantly, performed, recruitment, pubmed, demonstrated, observed, tcga, potential, tumor, cdh, macroha, chromatin, enhanced, factor, analyzed, carcinoma, normal, induced, negative, loss, enrichment, tumors,

Topics {✒️}

g1/s-phase specific marker forkhead transcription factors met-specific gene e-cadherin histones h3/h4 tetramer female nod/scid mice article download pdf student t-test function web-based bioinformatics tool rbi = relative band intensity cancer research program aplf-shrna-resistant cells khaja moheiddin syed emt-specific gene promoters histone chaperone aplf g2/m-phase population aplf-downregulation impeded invasive histone modification patterns invasive breast cancer γh2ax-positive foci cells epithelial-mesenchymal transition aplf-kd mdamb-231 cells emt-specific genes correlated met-favoring cdh1 level g1-phase population compared ananda mukherjee invasive breast carcinoma molecular signature database cancer including melanoma invasive ductal carcinoma privacy choices/manage cookies breast cancer letter cancer genome atlas breast cancer cells showed significant increase open chromatin resulting comprehensive molecular portraits lateral tail vein aprataxin pnk regional cancer centre demonstrated significant correlation creative commons license histone modifying enzymes histone variant macroh2a base excision repair breast cancer subtypes breast cancer metastasis sensitizing cancer cells debasree dutta histone chaperone aplf-downregulation significantly reduced

Questions {❓}

But, eventually, what drives the upregulation of FOXA1 in APLF-kd cells?
But, how APLF could regulate FOXA1?
But, is this effect of APLF restricted to tumor-specific cells or is a global phenomenon?
But, mechanistically how APLF could regulate these genes?
Then how binding of FOXA1 could be facilitated under this condition?
We were intrigued to understand whether this is a general phenomenon prevalent in any cancer or restricted to breast cancer only?

Schema {🗺️}

WebPage:
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         headline:Enhanced expression of histone chaperone APLF associate with breast cancer
         description:DNA damage-specific histone chaperone Aprataxin PNK-like factor (APLF) regulates mesenchymal-to-epithelial transition (MET) during cellular reprogramming. We investigated the role of APLF in epithelial-to-mesenchymal transition (EMT) linked to breast cancer invasiveness and metastasis. Here, we show that a significant manifestation of APLF is present in tumor sections of patients with invasive ductal carcinoma when compared to their normal adjacent tissues. APLF was significantly induced in triple negative breast cancer (TNBC) cells, MDAMB-231, in comparison to invasive MCF7 or normal MCF10A breast cells and supported by studies on invasive breast carcinoma in The Cancer Genome Atlas (TCGA). Functionally, APLF downregulation inhibited proliferative capacity, altered cell cycle behavior, induced apoptosis and impaired DNA repair ability of MDAMB-231 cells. Reduction in APLF level impeded invasive, migratory, tumorigenic and metastatic potential of TNBC cells with loss in expression of genes associated with EMT while upregulation of MET-specific gene E-cadherin (CDH1). So, here we provided novel evidence for enrichment of APLF in breast tumors, which could regulate metastasis-associated EMT in invasive breast cancer. We anticipate that APLF could be exploited as a biomarker for breast tumors and additionally could be targeted in sensitizing cancer cells towards DNA damaging agents.
         datePublished:2018-03-26T00:00:00Z
         dateModified:2018-03-26T00:00:00Z
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            APLF
            Invasive breast cancer
            EMT
            Cancer Research
            Oncology
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ScholarlyArticle:
      headline:Enhanced expression of histone chaperone APLF associate with breast cancer
      description:DNA damage-specific histone chaperone Aprataxin PNK-like factor (APLF) regulates mesenchymal-to-epithelial transition (MET) during cellular reprogramming. We investigated the role of APLF in epithelial-to-mesenchymal transition (EMT) linked to breast cancer invasiveness and metastasis. Here, we show that a significant manifestation of APLF is present in tumor sections of patients with invasive ductal carcinoma when compared to their normal adjacent tissues. APLF was significantly induced in triple negative breast cancer (TNBC) cells, MDAMB-231, in comparison to invasive MCF7 or normal MCF10A breast cells and supported by studies on invasive breast carcinoma in The Cancer Genome Atlas (TCGA). Functionally, APLF downregulation inhibited proliferative capacity, altered cell cycle behavior, induced apoptosis and impaired DNA repair ability of MDAMB-231 cells. Reduction in APLF level impeded invasive, migratory, tumorigenic and metastatic potential of TNBC cells with loss in expression of genes associated with EMT while upregulation of MET-specific gene E-cadherin (CDH1). So, here we provided novel evidence for enrichment of APLF in breast tumors, which could regulate metastasis-associated EMT in invasive breast cancer. We anticipate that APLF could be exploited as a biomarker for breast tumors and additionally could be targeted in sensitizing cancer cells towards DNA damaging agents.
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      dateModified:2018-03-26T00:00:00Z
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         Histone chaperone
         APLF
         Invasive breast cancer
         EMT
         Cancer Research
         Oncology
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            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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            name:Manipal Academy of Higher Education
            address:
               name:Manipal Academy of Higher Education, Manipal, India
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            address:
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            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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      name:Juberiya Mohammed Azeez
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            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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      name:Sreeharshan Sreeja
      affiliation:
            name:Cancer Research Program, Thycaud PO
            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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            name:Cancer Research Program, Thycaud PO
            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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      name:Madhavan Radhakrishna Pillai
      affiliation:
            name:Cancer Research Program, Thycaud PO
            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
               type:PostalAddress
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      name:Debasree Dutta
      url:http://orcid.org/0000-0003-2745-9180
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            name:Cancer Research Program, Thycaud PO
            address:
               name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
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      email:[email protected]
PostalAddress:
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Manipal Academy of Higher Education, Manipal, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Manipal Academy of Higher Education, Manipal, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India
      name:Rajiv Gandhi Centre for Biotechnology, Cancer Research Program, Thycaud PO, Thiruvananthapuram, India

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