PDF(Pubmed)
Abstract：
UNASSIGNED: Pancreatic cancer is a highly aggressive and fatal disease with limited treatment options and poor prognosis for patients. This study aimed to investigate the impact of XYA-2 {N-(3,7-dimethyl-2,6-octadienyl)-2-aza-2-deoxychaetoviridin A}, a nitrogenated azaphilon previously reported from a deep-sea-derived fungus on the progression of pancreatic cancer cells.
UNASSIGNED: The inhibitory effects of XYA-2 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion were assessed using various assays. The CCK-8 assay, clone formation assay, flow cytometry assay, wound healing assay, and transwell assay were employed to evaluate cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion, respectively. Moreover, we employed RNA-seq and bioinformatics analyses to uncover the underlying mechanism by which XYA-2 influences pancreatic cancer cells. The revealed mechanism was subsequently validated through qRT-PCR.
UNASSIGNED: Our results demonstrated that XYA-2 dose-dependently inhibited the proliferation of pancreatic cancer cells and induced cell cycle arrest and apoptosis. Additionally, XYA-2 exerted a significant inhibitory effect on the invasion and migration of cancer cells. Moreover, XYA-2 was found to regulate the expression of genes involved in multiple cancer-related pathways based on our RNA-seq and bioinformatics analysis.
UNASSIGNED: These findings highlight the potential of XYA-2 as a promising therapeutic option for the treatment of pancreatic cancer.
UNASSIGNED: The inhibitory effects of XYA-2 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion were assessed using various assays. The CCK-8 assay, clone formation assay, flow cytometry assay, wound healing assay, and transwell assay were employed to evaluate cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion, respectively. Moreover, we employed RNA-seq and bioinformatics analyses to uncover the underlying mechanism by which XYA-2 influences pancreatic cancer cells. The revealed mechanism was subsequently validated through qRT-PCR.
UNASSIGNED: Our results demonstrated that XYA-2 dose-dependently inhibited the proliferation of pancreatic cancer cells and induced cell cycle arrest and apoptosis. Additionally, XYA-2 exerted a significant inhibitory effect on the invasion and migration of cancer cells. Moreover, XYA-2 was found to regulate the expression of genes involved in multiple cancer-related pathways based on our RNA-seq and bioinformatics analysis.
UNASSIGNED: These findings highlight the potential of XYA-2 as a promising therapeutic option for the treatment of pancreatic cancer.
摘要：
胰腺癌是一种高度侵袭性和致命性疾病，治疗选择有限，患者预后不良。本研究旨在研究XYA-2{N-(3,7-二甲基-2,6-辛二烯基)-2-氮杂-2-脱氧对甲氧苷A}的影响，以前报道的一种来自深海真菌的氮化氮杂肺对胰腺癌细胞进展的影响。
■XYA-2对细胞增殖的抑制作用，克隆潜能，细胞周期进程，凋亡，迁移,和侵袭使用各种测定进行评估。CCK-8测定，克隆形成测定，流式细胞术测定，伤口愈合试验，和transwell试验用于评估细胞增殖，克隆潜能，细胞周期进程，凋亡，迁移,和入侵,分别。此外，我们采用RNA-seq和生物信息学分析来揭示XYA-2影响胰腺癌细胞的潜在机制.随后通过qRT-PCR验证揭示的机制。
■我们的结果表明，XYA-2剂量依赖性地抑制胰腺癌细胞的增殖，并诱导细胞周期停滞和凋亡。此外,XYA-2对癌细胞的侵袭和迁移具有明显的抑制作用。此外，根据我们的RNA-seq和生物信息学分析，发现XYA-2调节参与多种癌症相关途径的基因的表达。
■这些发现凸显了XYA-2作为胰腺癌治疗的一种有希望的治疗选择的潜力。
■XYA-2对细胞增殖的抑制作用，克隆潜能，细胞周期进程，凋亡，迁移,和侵袭使用各种测定进行评估。CCK-8测定，克隆形成测定，流式细胞术测定，伤口愈合试验，和transwell试验用于评估细胞增殖，克隆潜能，细胞周期进程，凋亡，迁移,和入侵,分别。此外，我们采用RNA-seq和生物信息学分析来揭示XYA-2影响胰腺癌细胞的潜在机制.随后通过qRT-PCR验证揭示的机制。
■我们的结果表明，XYA-2剂量依赖性地抑制胰腺癌细胞的增殖，并诱导细胞周期停滞和凋亡。此外,XYA-2对癌细胞的侵袭和迁移具有明显的抑制作用。此外，根据我们的RNA-seq和生物信息学分析，发现XYA-2调节参与多种癌症相关途径的基因的表达。
■这些发现凸显了XYA-2作为胰腺癌治疗的一种有希望的治疗选择的潜力。
