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Aditi , Majumder and Khaja Moheiddin , Syed and Ananda, Mukherjee and Manendra , Babu Lankadasari and Juberiya Mohammed, Azeez and Sreeja, S and KB, Harikumar and Pillai , MR and Debasree, Dutta (2018) Enhanced expression of histone chaperone APLF associate with breast cancer. Molecular cancer, 17 (1). ISSN 1476-4598

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Abstract

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.

Item Type: Article
Uncontrolled Keywords: Histone chaperone, APLF, Invasive breast cancer, EMT
Subjects: Cancer Research
Depositing User: Central Library RGCB
Date Deposited: 28 Jun 2018 09:06
Last Modified: 28 Jun 2018 09:06
URI: http://rgcb.sciencecentral.in/id/eprint/628

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