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Hedgehog signaling pathway regulates ovarian cancer invasion and migration via adhesion molecule CD24

机译:刺猬信号通路通过粘附分子CD24调节卵巢癌的侵袭和迁移

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摘要

Hedgehog (Hh) signalling plays an important role in cancer; however, its mechanism in ovarian cancer migration and invasion remains unclear. In the present study, we aimed to clarify the effect of the Hh signalling pathway on ovarian cancer migration and invasion through the regulation of CD24 expression, both in vitro and in vivo. Patients with ovarian cancer (n = 97) were recruited for this study. Evaluation of the explored the role parameters of patients indicated that CD24 expression was negatively associated with age, histological type and lymph node metastasis (p>0.05), but was positively associated with the clinical stage and pathological grading (p<0.05).The in vitro results indicated that the activator (sonic hedgehog, Shh) and inhibitor (GANT61) of Hh signalling significantly enhanced and reduced CD24 expression, respectively, at both the gene and protein levels (p<0.05).The addition of Shh significantly enhanced cellular migration and invasion of SKOV3 cells in vitro (p<0.05) Down regulation of CD24 using siRNA inhibited the tumour-promoting effects of Shh, and the in vivo results confirmed that GANT61 significantly inhibited CD24 expression and reduced tumour growth (p<0.01). In conclusion, the expression of CD24 can be regulated by Hh signalling, and downregulation of CD24 could play an important role in inhibiting ovarian cancer progression.
机译:刺猬(Hh)信号在癌症中起重要作用;然而,其在卵巢癌迁移和侵袭中的机制仍不清楚。在本研究中,我们旨在通过体外和体内CD24表达的调节来阐明Hh信号通路对卵巢癌迁移和侵袭的影响。招募患有卵巢癌的患者(n = 97)进行这项研究。对患者角色参数进行的评估表明,CD24表达与年龄,组织学类型和淋巴结转移呈负相关(p> 0.05),但与临床分期和病理分级呈正相关(p <0.05)。体外实验结果表明,Hh信号的激活剂(Sonic Hedgehog,Shh)和抑制剂(GANT61)分别在基因和蛋白质水平上均显着增强和降低了CD24的表达(p <0.05).Shh的添加显着增强了细胞迁移SKOV3细胞的体外侵袭和侵袭(p <0.05)使用siRNA下调CD24抑制Shh的促肿瘤作用,体内结果证实GANT61显着抑制CD24表达并降低肿瘤生长(p <0.01)。总之,CD24的表达可以通过Hh信号来调节,而CD24的下调可能在抑制卵巢癌的进展中起重要作用。

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