Xiaofei Huang1, Jun Qian2, Lingchang Li3, Xiaozhen Zhang1, Guoli Wei3, Jian Lv1, Fengxia Qin1, Jialin Yu3, Ya Xiao3, Zhen Gong4, Jiege Huo3. 1. Department of Emergency, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China. 2. Department of Diagnostics of Chinese Medicine, School of Chinese Medicine, School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China. 3. Department of Oncology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China. 4. Department of Gynaecology and Obstetrics, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Abstract
BACKGROUND: Curcumol was presented to unleash antitumor effects in a variety of cancers, including gastric cancer. However, the relevance between curcumol and cisplatin resistance in gastric cancer still remains unclear. Therefore, the current research was performed to survey the role of curcumol in cisplatin sensitivity in gastric cancer. METHODS: First, BGC-823 and BGC-823/DDP cells were incubated with cisplatin for 48 hr and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) analysis was applied to determine the inhibition rate of cell proliferation and the half-maximal inhibitory concentration (IC50 ) of cisplatin. In addition, BGC-823 and BGC-823/DDP cells were treated with curcumol for 48 hr followed with detection of cell viability and apoptosis using MTT and flow cytometry assay, respectively. Moreover, MTT analysis was applied to test the effects of curcumol on cisplatin sensitivity in gastric cancer cells. Lastly, Western blot assay and qRT-PCR analysis were utilized to check the functions of curcumol on PI3K/AKT pathway-related markers. RESULTS: We found that BGC-823/DDP cells exhibited stronger resistance to cisplatin compared with BGC-823 cells. Furthermore, curcumol evidently reduced cell proliferation and facilitated cell apoptosis in BGC-823/DDP and BGC-823 cells. Moreover, results from MTT assay demonstrated that curcumol notably promoted the suppression effect of cisplatin and decreased the IC50 of cisplatin in BGC-823/DDP and BGC-823 cells. It was also presented that curcumol suppressed the PI3K/AKT pathway dose-dependently in BGC-823/DDP and BGC-823 cells. CONCLUSION: The findings in the current research demonstrated that curcumol could promote the sensitivity of gastric cancer cells to cisplatin-based chemotherapies via inhibiting the phosphatidylinositol 3-kinase (PI3K)/Protein Kinase B (AKT) pathway.
BACKGROUND:Curcumol was presented to unleash antitumor effects in a variety of cancers, including gastric cancer. However, the relevance between curcumol and cisplatin resistance in gastric cancer still remains unclear. Therefore, the current research was performed to survey the role of curcumol in cisplatin sensitivity in gastric cancer. METHODS: First, BGC-823 and BGC-823/DDP cells were incubated with cisplatin for 48 hr and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) analysis was applied to determine the inhibition rate of cell proliferation and the half-maximal inhibitory concentration (IC50 ) of cisplatin. In addition, BGC-823 and BGC-823/DDP cells were treated with curcumol for 48 hr followed with detection of cell viability and apoptosis using MTT and flow cytometry assay, respectively. Moreover, MTT analysis was applied to test the effects of curcumol on cisplatin sensitivity in gastric cancer cells. Lastly, Western blot assay and qRT-PCR analysis were utilized to check the functions of curcumol on PI3K/AKT pathway-related markers. RESULTS: We found that BGC-823/DDP cells exhibited stronger resistance to cisplatin compared with BGC-823 cells. Furthermore, curcumol evidently reduced cell proliferation and facilitated cell apoptosis in BGC-823/DDP and BGC-823 cells. Moreover, results from MTT assay demonstrated that curcumol notably promoted the suppression effect of cisplatin and decreased the IC50 of cisplatin in BGC-823/DDP and BGC-823 cells. It was also presented that curcumol suppressed the PI3K/AKT pathway dose-dependently in BGC-823/DDP and BGC-823 cells. CONCLUSION: The findings in the current research demonstrated that curcumol could promote the sensitivity of gastric cancer cells to cisplatin-based chemotherapies via inhibiting the phosphatidylinositol 3-kinase (PI3K)/Protein Kinase B (AKT) pathway.