Yam H F, Wang Z H, Or P C, Wang S W, Li J, Chew E C
Department of Anatomy, Chinese University of Hong Kong, Shatin, PR China.
Anticancer Res. 1998 Jan-Feb;18(1A):209-16.
Human papillomavirus (HPV) is one of the crucial factors in cervical carcinogenesis. High risk HPV16 prototype has been demonstrated in association with the nuclear matrix in a cervical carcinoma cell line(1,2). Nuclear matrix (NM) has been established as playing an important role in various nuclear activities as well as carcinogenic processes. Dexamethasone (DEX) (glucocorticoid hormone) inhibited the growth of CC2/CUHK2 cervical carcinoma cells with concurrent induction of epithelial cell differentiation. 2D- PAGE (IEF and NEPHGE) revealed alternations in NM protein composition. Further demonstration of changes in NM was evidenced by NuMA (a novel NM protein) labelling. The HPV16 E7 oncoprotein was shown to be reduced in total cellular protein as well as in NM protein fractions in response to DEX treatment, and this suppressed expression was confirmed by RT-PCR. Thus, it is suggested that dexamethasone can down-regulate the growth of cervical cancer cells and its induced changes in NM may be a cause of this suppression.
人乳头瘤病毒(HPV)是宫颈癌发生的关键因素之一。高危型HPV16原型已在一种宫颈癌细胞系中被证明与核基质有关联(1,2)。核基质(NM)已被证实对各种核活动以及致癌过程起着重要作用。地塞米松(DEX)(糖皮质激素)抑制了CC2/CUHK2宫颈癌细胞的生长,同时诱导了上皮细胞分化。二维聚丙烯酰胺凝胶电泳(IEF和NEPHGE)显示核基质蛋白质组成发生了变化。NuMA(一种新型核基质蛋白)标记进一步证明了核基质的变化。结果表明,经地塞米松处理后,HPV16 E7癌蛋白在总细胞蛋白以及核基质蛋白组分中均减少,并且这种抑制性表达通过逆转录聚合酶链反应得到了证实。因此,提示地塞米松可下调宫颈癌细胞的生长,其诱导的核基质变化可能是这种抑制作用的原因。