PDF(Pubmed)
Abstract：
Colorectal cancer is a life-threatening and prevalent type of cancer. However, a number of current treatments have serious side effects, which increase the need for alternatives. Non-steroidal anti-inflammatory drugs have potential chemopreventive capabilities. The present study aimed to confirm this, as well as to investigate potential pathways and reasons for this trait. To accomplish this, cancerous Colo320 and healthy CCD-18 cells were treated with various concentrations of naproxen sodium (NS). A caspase-3 assay revealed a statistically significant increase in caspase-3 activity in Colo320 cells (300%; P<0.01), but not in CCD-18 cells. This chemical was also associated with a significant decrease in Colo320 cell survival (-72.888%; P<0.01), but not CCD-18 cell survival. Furthermore, NS was found to significantly decrease the migration of Colo320 cells (86.58%; P<0.01). Finally, RNA sequencing of cells treated with NS revealed the statistically significant downregulation of the mucin 5B, oligomeric mucus/gel-forming, S100 calcium binding protein A9 and mucin 5AC, oligomeric mucus/gel-forming genes, which are upregulated in colorectal cancer and are known to contribute to cancer proliferation, stemness and drug resistance. These novel biological pathway results were further confirmed using ELISAs. The present study identified a novel molecular mechanism of the anti-colorectal cancer activity of NS.
摘要：
结直肠癌是一种危及生命和流行的癌症。然而,目前的许多治疗方法都有严重的副作用，这增加了对替代品的需求。非甾体抗炎药具有潜在的化学预防能力。本研究旨在证实这一点，以及研究这种特征的潜在途径和原因。要做到这一点，用各种浓度的萘普生钠（NS）处理癌性Colo320和健康的CCD-18细胞。caspase-3分析显示Colo320细胞中caspase-3活性有统计学意义的增加(300%;P<0.01),但在CCD-18细胞中没有。该化学物质还与Colo320细胞存活率的显着降低有关（-72.888%；P<0.01），但CCD-18细胞不能存活.此外，NS显著降低Colo320细胞的迁移能力(86.58%;P<0.01)。最后,用NS处理的细胞的RNA测序显示粘蛋白5B的统计学显著下调，寡聚粘液/凝胶形成，S100钙结合蛋白A9和粘蛋白5AC，寡聚粘液/凝胶形成基因，在结直肠癌中上调，已知有助于癌症增殖，干性和耐药性。使用ELISA进一步证实了这些新的生物学途径结果。本研究确定了NS抗结直肠癌活性的新分子机制。
