Reports of Biochemistry and Molecular Biology

en The Investigation of Quercus Infectoria Gall Aqueous Extract Effect on the Cell Proliferation, Apoptosis and Expression of CCND1, TP53, BCL2 and BAX Genes in Cell Line of Lung, Gastric and Esophageal Cancers زیست شناسی ملکولی Molecular Biology مقالات اصلی Original Article <div class="WordSection1"> <div style="text-align: justify;">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 A549, BGC823, and KYSE-30 cell lines. Methods: A549, BGC823, and KYSE-30 cells were seeded in complete medium and incubated with different concentrations of QI gall extract for 24 hours. Cell viability was measured by an MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-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 CCND1, TP53, BCL2, 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 A549, BGC823, and KYSE-30 cell lines at IC50 concentrations of 440.1, 437.1, and 465.2 mg/ml, respectively. Additionally, compared to untreated cell population, the percentages of early apoptosis, late apoptosis, and necrosis in the A549, BGC823, and KYSE-30 cells significantly increased following treatment with QI gall extract (P< 0.05). Also, the treatment with QI gall extract influenced the expression of CCND1, TP53, BCL2, and BAX genes. Conclusions: The present findings indicated that the gall extract of QI can inhibit the growth of A549, BGC823, and KYSE-30 cells by inducing apoptosis, which may be mediated via mitochondria‑dependent pathway. </div> <div align="center" style="text-align:center"> <hr align="center" noshade="noshade" size="2" style="color:#0f243e" width="100%" ></div> </div> <div style="text-align: justify;"><div aria-label="Page Break" class="cke_pagebreak" contenteditable="false" data-cke-display-name="pagebreak" data-cke-pagebreak="1" style="page-break-after:always" title="Page Break"></div></div> Apoptosis, Cell viability, Esophageal cancer, Gastric cancer, Lung cancer, Quercus infectoria. 596 608 http://rbmb.net/browse.php?a_code=A-10-1365-1&slc_lang=en&sid=1 Pouya Tofigh 100319475328460020236 100319475328460020236 No Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran. Seyed Mehdi Mirghazanfari 100319475328460020237 100319475328460020237 No Department of Physiology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran. Zahra Hami 100319475328460020238 100319475328460020238 No Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran. Ehsan Nassireslami 100319475328460020239 100319475328460020239 No Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran. Mohsen Ebrahimi ebrahimim@ajaums.ac.ir 100319475328460020240 100319475328460020240 Yes Toxicology Research Center, AJA University of Medical Sciences, Tehran, Iran.