Wang Xiaobo, Ye Xuxing, Zhang Yili, Ji Feng
Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Traditional Medicine Center, Jinhua Hospital, Zhejiang University, Jinhua, Zhejiang 321000, P.R. China.
Oncol Lett. 2020 Nov;20(5):132. doi: 10.3892/ol.2020.11993. Epub 2020 Aug 20.
Colorectal cancer is an aggressive disease with a poor prognosis and low survival rate at the advanced stage, therefore new innovative targets are urgently required. Flurbiprofen has been reported to exhibit therapeutic effects in other types of cancer, such as esophageal cancer, breast cancer and colorectal cancer. Therefore, the present study aimed to investigate the function of flurbiprofen in colorectal cancer. SW620 colorectal cancer cells were treated with different concentrations of flurbiprofen to determine the optimum concentration. Subsequently, COX2 expression affected by flurbiprofen was tested using western blotting, reverse transcription-quantitative PCR and immunofluorescence. Enzyme-linked immunosorbent assay was used to determine the levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β. Cell Counting Kit-8, colony formation and flow cytometry assays were used to assess the proliferation and apoptosis of SW620 cells in various groups. Western blotting was performed to investigate the expression of proliferation-, apoptosis- and migration-related proteins after different treatments. Wound healing and Transwell assays were performed to measure the invasion and migration of colorectal cancer cells, respectively. The results demonstrated that flurbiprofen inhibited colorectal cancer cell proliferation. Furthermore, it was identified that flurbiprofen inhibited the expression of COX2. Notably, flurbiprofen suppressed the expression of inflammatory factors by inhibiting COX2. Moreover, flurbiprofen inhibited the proliferation, invasion and migration of colorectal cancer cells by inhibiting COX2. In conclusion, the present study revealed that flurbiprofen inhibited COX2 expression in colorectal cancer, and affected the proliferation, invasion, migration and apoptosis of colorectal cancer cells. These results expand the understanding of the function of COX2 in colorectal cancer and the effect of flurbiprofen on COX2 expression.
结直肠癌是一种侵袭性疾病,预后较差,晚期生存率低,因此迫切需要新的创新靶点。据报道,氟比洛芬在其他类型的癌症中具有治疗作用,如食管癌、乳腺癌和结直肠癌。因此,本研究旨在探讨氟比洛芬在结直肠癌中的作用。用不同浓度的氟比洛芬处理SW620结直肠癌细胞以确定最佳浓度。随后,使用蛋白质免疫印迹法、逆转录-定量聚合酶链反应和免疫荧光检测受氟比洛芬影响的COX2表达。采用酶联免疫吸附测定法测定肿瘤坏死因子-α、白细胞介素(IL)-6和IL-1β的水平。使用细胞计数试剂盒-8、集落形成和流式细胞术检测评估各组SW620细胞的增殖和凋亡。进行蛋白质免疫印迹法以研究不同处理后增殖、凋亡和迁移相关蛋白的表达。分别进行伤口愈合和Transwell检测以测量结直肠癌细胞的侵袭和迁移。结果表明,氟比洛芬抑制结直肠癌细胞增殖。此外,发现氟比洛芬抑制COX2的表达。值得注意的是,氟比洛芬通过抑制COX2来抑制炎症因子的表达。此外,氟比洛芬通过抑制COX2抑制结直肠癌细胞的增殖、侵袭和迁移。总之,本研究表明氟比洛芬抑制结直肠癌中COX2的表达,并影响结直肠癌细胞的增殖、侵袭、迁移和凋亡。这些结果扩展了对COX2在结直肠癌中的作用以及氟比洛芬对COX2表达影响的认识。