Authors:Fatih Yulak, Zekeriya Keskin Pages: 43 - 51 Abstract: This study examines the anti-tumor, pro-apoptotic, and genotoxic effects of polo-like kinase 1 (PLK1) inhibitor RO3280 on the gastric cancer cell line SNU-16. Using the XTT assay, the antiproliferative effect of the compound was identified and showed a significant antiproliferative effect (p<0.01) with the IC50 value of 9.64 µM for 24 hours. RO3280 considerably enhanced the expression of Bax and cleaved caspase-3 (p<0.01) and dramatically lowered the BCL-2 level (p<0.01), demonstrating an apoptotic effect. It greatly raised the expression of 8-oxo-dG, a DNA damage marker, and cleaved PARP, a degraded version of the PARP enzyme involved in DNA repair (p<0.05 and p<0.01, respectively). In addition, flow cytometric studies for annexin V and caspase-3/7 revealed that RO3280 markedly improved the apoptotic cell profile (p<0.01). It reduced the mitochondrial membrane potential and DNA damage (p<0.01). These findings suggest that RO3280 has an antitumor impact by damaging DNA and inducing apoptosis in SNU-16 gastric cancer cells. PubDate: 2024-06-15 DOI: 10.3329/bjp.v19i2.71704 Issue No:Vol. 19, No. 2 (2024)
Authors:Hao Yu, Xiaoping Mei, Xueming Zhang, Neng Qian, Qingjiang Yu, Hongkun Zhou Pages: 52 - 58 Abstract: Gemcitabine is a common first-line chemotherapy agent, but gemcitabine resistance is a clinical challenge for pancreatic ductal adenocarcinoma patients. Solute carrier 39A1 (SLCA39A1) as a zinc regulator presents a crucial function in the modulation of malignancy progression. Here, the impact of SLC39A1 on the gemcitabine resistance of pancreatic ductal adenocarcinoma was investigated. Immunohistochemistry demonstrated that the SLC39A1 expression was significantly up-regulated in gemcitabine-resistant pancreatic ductal adenocarcinoma samples compared with gemcitabine-sensitive ones. Gemcitabine dose-dependently inhibited the viability of the cancer cells, and SLC39A1 knockdown aggravated this effect. Both mRNA and protein expression of SLC39A1 were elevated in the gemcitabine-resistant cancer cells. SLC39A1 knockdown also reversed AMP-activated protein kinase (AMPK) phosphorylation and S6K expression of cancer cells regulated by the gemcitabine resistance. SLC39A1 promotes gemcitabine resistance of pancreatic ductal adenocarcinoma by activating AMPK signaling, revealing SLC39A1 may be a potential target in patients with gemcitabine resistance. PubDate: 2024-06-15 DOI: 10.3329/bjp.v19i2.72787 Issue No:Vol. 19, No. 2 (2024)
Authors:Biao Zhang, Zaojun Fang, Ying Lin, Qian Wu, Jiaping Chen Pages: 59 - 64 Abstract: This study aims to investigate the effect of RU.521 on improving vascular endothelial injury in 14 acute lung injury patients. Serum myeloperoxidase, double-stranded DNA (dsDNA), IFN-β, and TNF-α levels of patients were detected by ELISA. Neutrophil extracellular traps were used to stimulate human venous endothelial cells (HUVEC). cGAS/STING pathway protein was detected by western blot. The protective effect of RU.521 on HUVEC was evaluated by CCK-8. The effects of RU.521 on cGAS/STING pathway expression were detected by PCR and western blot. The levels of myeloperoxidase and (dsDNA) in acute lung injury patients were significantly increased (p<0.05). The expression level of IFN-β in acute lung injury patients was significantly increased (p<0.05). The expression of cGAS and STING proteins in HUVEC cells was significantly increased (p<0.05), and the expression of IFN-β was significantly increased (p<0.05). RU.521 can ameliorate vascular endothelial injury. RU.521 inhibited cGAS/SRING mRNA and protein expression (p<0.05). Thus, neutrophil extracellular traps release dsDNA activates the cGAS/STING pathway-induced vascular endothelial injury in acute lung injury patients. RU.521 protects vascular endothelial injury by inhibiting the cGAS/STING pathway. PubDate: 2024-06-15 DOI: 10.3329/bjp.v19i2.72930 Issue No:Vol. 19, No. 2 (2024)
Authors:Thanh Trung Tran, Kien Trung Tran, Daeyong Kim, Nam Trung Nguyen Pages: 69 - 71 Abstract: No abstract PubDate: 2024-06-15 DOI: 10.3329/bjp.v19i2.72739 Issue No:Vol. 19, No. 2 (2024)
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