The Investigation of Quercus Infectoria Gall Aqueous Extract Effect on the Cell Proliferation, Apoptosis and Expression of CCND۱, TP۵۳, BCL۲ and BAX Genes in Cell Line of Lung, Gastric and Esophageal Cancers
Publish Year: 1402
نوع سند: مقاله ژورنالی
زبان: English
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JR_RBMB-12-4_009
تاریخ نمایه سازی: 17 تیر 1403
Abstract:
Background: The therapeutic potential of Quercus infectoria (QI) gall, including its anti-inflammatory, antioxidant, and anticancer properties, is well-known. However, its impact on lung, gastric, and esophageal cancer cells remain unclear. This study aims to explore the effects of QI gall aqueous extract on cell viability, apoptosis, and gene expression in A۵۴۹, BGC۸۲۳, and KYSE-۳۰ cell lines.
Methods: A۵۴۹, BGC۸۲۳, and KYSE-۳۰ cells were seeded in complete medium and incubated with different concentrations of QI gall extract for ۲۴ hours. Cell viability was measured by an MTT [۳-(۴, ۵-dimethylthiazol-۲-yl)-۲, ۵-diphenyl tetrazolium bromide] assay. The induction of apoptosis was assessed through flow cytometric analysis after the adding FITC-conjugated Annexin V (Annexin V-FITC) and propidium iodide (PI). The mRNA expression levels of CCND۱, TP۵۳, BCL۲, and BAX genes were determined using Real-time Quantitative Polymerase Chain Reaction analysis.
Results: The MTT assay demonstrated that treatment with QI gall extract significantly reduced the number of viable cells in the A۵۴۹, BGC۸۲۳, and KYSE-۳۰ cell lines at IC۵۰ concentrations of ۴۴۰.۱, ۴۳۷.۱, and ۴۶۵.۲ mg/ml, respectively. Additionally, compared to untreated cell population, the percentages of early apoptosis, late apoptosis, and necrosis in the A۵۴۹, BGC۸۲۳, and KYSE-۳۰ cells significantly increased following treatment with QI gall extract (P< ۰.۰۵). Also, the treatment with QI gall extract influenced the expression of CCND۱, TP۵۳, BCL۲, and BAX genes.
Conclusions: The present findings indicated that the gall extract of QI can inhibit the growth of A۵۴۹, BGC۸۲۳, and KYSE-۳۰ cells by inducing apoptosis, which may be mediated via mitochondria‑dependent pathway.
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Authors
Pouya Tofigh
Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran.
Seyed Mehdi Mirghazanfari
Department of Physiology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran.
Zahra Hami
Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran.
Ehsan Nassireslami
Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran.
Mohsen Ebrahimi
Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran.
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