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-Related Anticancer Activities of Bulb Extracts Against Lung Cancer

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Specialty Biology
Date 2022 Jun 30
PMID 35769912
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Abstract

Current lung cancer treatment strategies are ineffective, and lung cancer cases continue to soar; thus, novel anticancer drugs and targets are needed, and medicinal plants are promising to offer better alternatives. This study was aimed at analysing two splice variants during the potential anticancer activities of () methanol and water extracts against different human lung cancer cell lines of varying mutation status, and these included mutant H1573 and mutant H1437 and -wild type (A549) cells. The anticancer activities of the extracts were assessed by establishing the cytotoxic effect and the apoptosis-inducing capacity of these extracts, using the MTT assay and Annexin V analysis, respectively, with the latter confirmed using fluorescence microscopy. The molecular mechanisms induced by these extracts were further evaluated using cell cycle analysis and RT-PCR. Both extracts demonstrated safety against noncancerous lung MRC-5 fibroblasts and exhibited significant anticancer potency ( < 0.001) against the H1437 (IC values: 62.50 μg/ml methanol extract and 125 μg/ml WE), H1573 (IC value: 125 μg/ml for both extracts) and A549 (IC value: 500 μg/ml ME). The water extract had no effect on the viability of A549 cells. Treated H1437 cells underwent -dependent apoptosis and S-phase cell cycle arrest while H1573 treated cells underwent -independed apoptosis and G0/G1 cell cycle arrest through upregulation of mRNA expression levels. The expression levels of , , and genes increased significantly ( < 0.001) following the treatment of H1573 cells with ME and WE. Treatment of H1437 cells with ME upregulated the , , and mRNAs. Our results indicate that the proliferative inhibitory effect of extracts on A549 and H1573 cells is correlated with the suppression of , and while that is not the case in H1437 cells. Thus, our results suggest that the dysregulation of anti-apoptotic molecules , , and in H1437 may play a role in cancer cell survival, which may consequently contribute to the development of -mutated non-small human lung cancer. Our results indicate that is a promising source of anticancer agents for the treatment of p53-mutant human non-small lung cancer cells than the p53-wild type human non-small lung cancer cells.

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