Lu Lian-Jun, Zha Ding-Jun, Xue Tao, Qiu Jian-Hua
Department of Otolaryngology Head and Neck Surgery, The Fourth Military Medical University, Xi'n, Shaanxi, People's Republic of China.
Ai Zheng. 2009 Jul;28(7):691-4. doi: 10.5732/cjc.008.10801.
1Alpha,25-dihydroxy vitamin D3 [1,25(OH)2D3], the biologically active form of vitamin D3, has antiproliferative activity against various tumor cells. This study was to explore the inhibitory effect of 1,25(OH)2D3 on human laryngeal carcinoma Hep-2 cells and potential mechanisms.
Hep-2 cells were treated by 1,25(OH)2D3 (0, 1, 10 and 100 nmol/L) for 24, 48, 72 and 96 h, respectively. Cell proliferation was measured by MTT assay. Cell apoptosis was measured by flow cytometry (FCM). The expression and phosphorylation of ERK, p38MAPK, and JNK proteins were detected by Western blot.
1,25(OH)2D3 significantly inhibited Hep-2 cell proliferation and induced cell apoptosis. 1,25(OH)2D3 increased p38MPAK phosphorylation but not ERK and JNK phosphorylation. The 1,25(OH)2D3-induced apoptosis of Hep-2 cells was partly blocked by p38 inhibitor SB2035080.
1,25(OH)2 D3 could induce apoptosis of Hep-2 cells and p38MAPK plays an important role in this process.
1α,25 - 二羟基维生素D3[1,25(OH)2D3]是维生素D3的生物活性形式，对多种肿瘤细胞具有抗增殖活性。本研究旨在探讨1,25(OH)2D3对人喉癌Hep - 2细胞的抑制作用及其潜在机制。
分别用1,25(OH)2D3（0、1、10和100 nmol/L）处理Hep - 2细胞24、48、72和96小时。采用MTT法检测细胞增殖。通过流式细胞术（FCM）检测细胞凋亡。用蛋白质印迹法检测ERK、p38MAPK和JNK蛋白的表达及磷酸化情况。
1,25(OH)2D3显著抑制Hep - 2细胞增殖并诱导细胞凋亡。1,25(OH)2D3增加p38MPAK磷酸化，但不增加ERK和JNK磷酸化。p38抑制剂SB2035080部分阻断1,25(OH)2D3诱导的Hep - 2细胞凋亡。
1,25(OH)2D3可诱导Hep - 2细胞凋亡，且p38MAPK在此过程中起重要作用。
