Peptide pACC1-nano complex suppresses ACC1-mediated lipogenesis 5 in breast cancer cells via altering p53/NF-κB pathway of signalling

Background Cancer cells encompass comprehensively altered metabolic circuits for the growth and survival that underlie the malignant phenotype. pACC1 also referred to as peptide protein produced from chitosan, has been applied recently to develop targeted treatment that has numerous pharmacological activities towards DMBA-induced mammary cancer cells. Materials Methods Bio Concept Labs located at Delhi (India) supplied the peptide pACC1 and meanwhile Sigma Aldrich Company (America) provided us sodium tripolyphosphate and chitosan (MW-210 kDa). Antibodies were obtained from Cell Signaling Technology, USA and finally 5-tetradecyl-oxy-2-furoic acid (TOFA) offered by Santa Cruz Biotechnology from India respectively. The following methods were carried out like Cell line and culture, pACC1– Chitosan Nanoparticles, MTT assays, Flowcytometry assays, DNA fragmentation assays, detection of western blot and Gene expression analysis. A malignant tumour alters the way that cells produce energy and execute biosynthesis process. Apoptosis, or programmed cell death, could be originated and improved their ability to create new fats ( de novo lipogenesis ) at the time of interrupted. Signaling proteins linked to apoptosis are triggered by rising oxidative stress, which results in cell arrest in the G2/M phase. Notably, expression of IKK and NF-kB protein expression were remarkably altered when Acetyl-CoA Carboxylase alpha (ACC1) and fatty acid synthase (FASN), suppression taken place simultaneously by PCN influence. Duel staining and DCFH-DA Photomicrograph were further confirming the utmost oxidative stress status of cells which was influenced by PCN. ACC1 and FSN gene expression were found to be down regulated. Conclusion All the experiential evidence supported by positive control 5-(Tetradecyloxy)-2-furoic acid (TOFA) inhibitor of Fatty acid synthesis. The current study focused that PCN may potentially induce oxidative stress mediated apoptosis and down regulation of inflammatory signals in breast cancer cell.