CAJ | 학술논문

目的：明确缺氧诱导因子－lα（ HIF－1α）在基质细胞衍生因子－1α（ SDF－1α）调控的卵巢癌细胞迁移中的作用及其机制。方法采用免疫组化分析HIF－1α在卵巢癌组织中的表达水平；将HIF－1αsiRNA转染SKOV3卵巢癌细胞，分别用SDF－1α和SDF－1α＋SB203580处理，用RT－PCR及western blotting分析HIF－1α、p38MAPK的表达水平。结果免疫组化分析表明，HIF－1α在卵巢癌组织中高表达，同时SDF－1α可明显诱导HIF－1α的mRNA及蛋白水平的表达；当用HIF－1αsiRNA转染后，细胞中HIF－1α的表达水平明显下降。当用通路抑制剂SB203580处理后，SDF－1α诱导的HIF－1α水平明显降低。结论 SDF－1α可通过p38MAPK－HIF－1α通路来调控卵巢癌细胞的迁移。因此，该研究将为卵巢癌的防治提供新的研究方向。
목적：명학결양유도인자－lα（ HIF－1α）재기질세포연생인자－1α（ SDF－1α）조공적란소암세포천이중적작용급기궤제。방법채용면역조화분석HIF－1α재란소암조직중적표체수평；장HIF－1αsiRNA전염SKOV3란소암세포，분별용SDF－1α화SDF－1α＋SB203580처리，용RT－PCR급western blotting분석HIF－1α、p38MAPK적표체수평。결과면역조화분석표명，HIF－1α재란소암조직중고표체，동시SDF－1α가명현유도HIF－1α적mRNA급단백수평적표체；당용HIF－1αsiRNA전염후，세포중HIF－1α적표체수평명현하강。당용통로억제제SB203580처리후，SDF－1α유도적HIF－1α수평명현강저。결론 SDF－1α가통과p38MAPK－HIF－1α통로래조공란소암세포적천이。인차，해연구장위란소암적방치제공신적연구방향。
Objective To observe the role and mechanism of hypoxia inducible factor-1α( HIF-1α) in ovarian cancer cell migration regulated by stromal cell-derived factor-1 alpha ( SDF-1α) .Methods The expression of HIF-1αin cervical cancer was analyzed by immunohistochemistry.HIF-1αsiRNA was transfected into ovarian cancer cell line SKOV3, and then treated with SDF-1αand SDF-1α+SB203580, respectively.The expression levels of HIF-1αand p38MAPK were confirmed by RT-PCR and western blotting.Results Immunohistochemical analysis showed that the expression of HIF-1αin ovarian cancer tissues was overexpressed, and that at the same time SDF-1αcould induce the expression of mRNA and protein levels in HIF-1α.After transfected by HIF-1αsiRNA, the HIF-1αexpression level decreased obviously.When treated by SB203580, the expression level of HIF-1αinduced by SDF-1αdecreased significantly. Conclusion SDF-1αcan regulate cells invasion by p38MAPK-HIF-1αmediated signaling in ovarian cancer.Therefore, this study will provide a new research direction for prevention and treatment of ovarian cancer.