Antiproliferative and Pro-Apoptotic Effects of Glaucium Flavum Extract on A549 Lung Cancer Cells

Introduction: Glaucium Flavum has recently been studied by researchers and pharmacists and has been attributed to its antioxidant, antiproliferative properties. The alkaloid compounds of this plant are also widely used in the pharmaceutical industry as decongestants and antitussives. Materials and Methods: In this experiment, first, the cell class (A549) was cultured in DMEM culture medium containing 10% FBS and then treated with different concentrations of Glaucium Flavum. MTT assay was performed to determine IC50 and compare the viability percentage of treated cells with different concentrations of Glaucium Flavum on days 1, 3, and 5. The qRT-PCR test was used to investigate the effects of Glaucium Flavum with IC50 concentration on the induction of apoptosis, and expression of genes including P53, Bax, Bad, and Bcl2. Obtained results were analyzed by SPSS software using ANOVA test. Results: MTT results showed that Glaucium Flavum causes cell death and reduces the viability of cancer cells, which was observed in the form of cell shrinkage, nucleus shrinkage, and chromatin density and determination of 10 μg/ml concentration as IC50 of A549 cells. An increase in the expression of Bax, P53 and bad apoptotic genes, and a decrease in the expression of the Bcl2 gene also indicate the induction of apoptotic death and the lethal effect of Glaucium Flavum. Conclusion: Finally, it can be said that Glaucium Flavum, due to its rich content of alkaloid and antioxidant compounds, can be a good option to replace it with chemical drugs in the treatment of lung cancer

A Novel Homozygous MYO7A Mutation: Case Report

MYO7A is an unconventional myosin that is essential for ordinary hearing and vision; mutations in the MYO7A gene result in Usher syndrome type 1B and other disorders. In this manuscript, we reported a mutation (c.4705delA) in exon 35, causing the alteration of a Ser amino acid to Ala at codon 1569 (p.H2027del) located within the first FERMdomain of the human protein myosin VIIA. This mutation involved in the pathogenesis of hearing loss, congenital night blindness, muscular weakness, skin problem, and difficulty in keeping balance in the 13-year-old female. After checkup the patient’s DNA was extracted from peripheral blood and amplification was performed by PCR. Sequencing method was performed for identification of the mutation. The c.4705delA mutation in exon 35 was found in the patient in heterozygosis form; this means that her mother and father were carriers. This mutation is located on the tail of the myosinVIIA protein and is associated with several disorders