PDF(Pubmed)
Abstract：
UNASSIGNED: Pancreatic cancer is a highly aggressive and lethal disease with limited treatment options. In this study, we investigated the potential therapeutic effects of compound KL-6 on pancreatic cancer cells.
UNASSIGNED: The study involved assessing the inhibitory effects of KL-6 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion. Additionally, we examined the action mechanism of KL-6 by RNA-seq and bioinformatic analysis and validated by qRT-PCR and western blot in pancreatic cancer cells.
UNASSIGNED: Our results demonstrated that KL-6 effectively inhibited the growth of pancreatic cancer cells in a dose-dependent manner. It induced G2/M phase cell cycle arrest and apoptosis, disrupting the cell cycle progression and promoting cell death. KL-6 also exhibited inhibitory effects on cell migration and invasion, suggesting its potential to suppress the metastatic properties of pancreatic cancer cells. Furthermore, KL-6 modulated the expression of genes involved in various cancer-related pathways including apoptosis and ferroptosis.
UNASSIGNED: These findings collectively support the potential of KL-6 as a promising therapeutic option for pancreatic cancer treatment. Further research is needed to fully understand the underlying mechanisms and evaluate the clinical efficacy of KL-6 in pancreatic cancer patients.
UNASSIGNED: The study involved assessing the inhibitory effects of KL-6 on cell proliferation, clonogenic potential, cell cycle progression, apoptosis, migration, and invasion. Additionally, we examined the action mechanism of KL-6 by RNA-seq and bioinformatic analysis and validated by qRT-PCR and western blot in pancreatic cancer cells.
UNASSIGNED: Our results demonstrated that KL-6 effectively inhibited the growth of pancreatic cancer cells in a dose-dependent manner. It induced G2/M phase cell cycle arrest and apoptosis, disrupting the cell cycle progression and promoting cell death. KL-6 also exhibited inhibitory effects on cell migration and invasion, suggesting its potential to suppress the metastatic properties of pancreatic cancer cells. Furthermore, KL-6 modulated the expression of genes involved in various cancer-related pathways including apoptosis and ferroptosis.
UNASSIGNED: These findings collectively support the potential of KL-6 as a promising therapeutic option for pancreatic cancer treatment. Further research is needed to fully understand the underlying mechanisms and evaluate the clinical efficacy of KL-6 in pancreatic cancer patients.
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。在这项研究中,我们研究了化合物KL-6对胰腺癌细胞的潜在治疗作用.
■该研究涉及评估KL-6对细胞增殖的抑制作用，克隆潜能，细胞周期进程，凋亡，迁移,和入侵。此外,我们通过RNA-seq和生物信息学分析研究了KL-6在胰腺癌细胞中的作用机制，并通过qRT-PCR和westernblot进行了验证。
■我们的结果表明，KL-6以剂量依赖性方式有效抑制胰腺癌细胞的生长。诱导G2/M期细胞周期阻滞和凋亡,破坏细胞周期进程并促进细胞死亡。KL-6对细胞迁移和侵袭也表现出抑制作用，提示其抑制胰腺癌细胞转移特性的潜力。此外，KL-6调节涉及各种癌症相关途径(包括细胞凋亡和铁凋亡)的基因的表达。
■这些发现共同支持KL-6作为胰腺癌治疗的有希望的治疗选择的潜力。需要进一步的研究来充分了解胰腺癌患者KL-6的潜在机制并评估其临床疗效。
■该研究涉及评估KL-6对细胞增殖的抑制作用，克隆潜能，细胞周期进程，凋亡，迁移,和入侵。此外,我们通过RNA-seq和生物信息学分析研究了KL-6在胰腺癌细胞中的作用机制，并通过qRT-PCR和westernblot进行了验证。
■我们的结果表明，KL-6以剂量依赖性方式有效抑制胰腺癌细胞的生长。诱导G2/M期细胞周期阻滞和凋亡,破坏细胞周期进程并促进细胞死亡。KL-6对细胞迁移和侵袭也表现出抑制作用，提示其抑制胰腺癌细胞转移特性的潜力。此外，KL-6调节涉及各种癌症相关途径(包括细胞凋亡和铁凋亡)的基因的表达。
■这些发现共同支持KL-6作为胰腺癌治疗的有希望的治疗选择的潜力。需要进一步的研究来充分了解胰腺癌患者KL-6的潜在机制并评估其临床疗效。
