Abstract
In the present investigation, we synthesized chalcone bearing naphthalene compound d1, and on the basis of 1H-NMR, 13C NMR, and LC-MS data we had specified the structure of the synthesized compound. The resultant compound d1 was assessed for their antiproliferative action against human cancer cell lines (HeLa, HCT116, HT29, MDA-MB-231, MCF-7, and SKBR3). The IC50 range was estimated at 5.58 to 11.13 μM shows that compound d1 had remarkable anticancer activity on HeLa cell lines. Besides, it was discovered that d1 incited the mitochondrial apoptotic pathway by controlling Bax and Bcl-2 transcripts by expanding the Caspase 3 activation. We depicted the in-vivo effects of tumor advancement and the antiangiogenic activity of d1 in the EAC animal model. Tumor growth had inhibited and without symptoms the longevity of EAC containing mice expanded by the treatment of d1. Inhibition of nuclear transcriptional factor HIF-1α in EAC cells and finally it also inhibited phosphorylation of downstream signaling proteins such as ERK1/2, p38, and JNK in HeLa cells. The present investigation uncovered that d1 indicated noteworthy tumor-repressing abilities much less concentration in in-vitro and in-vivo recommended that compound d1 as the potent anticancer medication.
Highlights
Cancer is a death-defying disease that causes a genuine medical issue around the world
Based on the MTT assay data, the resultant compound d1 was examined for in-vitro cytotoxic action in human cancer cell lines such as MDA-MB-231, MCF7, and SKBR3 (Breast adenocarcinoma), HCT116, HT29 (Colorectal Cancer), and HeLa
Our results suggested that compound d1 may disturb the ratio of BAX and Bcl2 levels in the HeLa cells
Summary
Cancer is a death-defying disease that causes a genuine medical issue around the world. Cancer is a multistage disease that is characterized by alteration in various gene expressions, prompting deregulated equalization of cell death that outcomes in the development of tumor growth [1,2,3,4]. Apoptosis is an energy-dependent manner in which the typical morphological changes occur; it includes cell membrane blebbing, cell shrinkage, and chromatin condensation, the formation of the cytoplasmic vacuole, and DNA fragmentation [8, 9]. The mitochondrial pathway is managed by initiating favourable to apoptotic proteins BAX and Bcl inhibition [12, 13]. Cell stress incites supportive of apoptotic protein BAX to move to the outside of the mitochondria, where it multiplies pores in the mitochondrial membrane and grant the arrival of cytochrome C into the cytoplasm.
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