Barbolina Maria V, Adley Brian P, Kelly David L, Shepard Jaclyn, Fought Angela J, Scholtens Denise, Penzes Peter, Shea Lonnie D, Stack M Sharon
Department of Chemical and Biological Engineering, Northwestern University, Chicago, IL, USA.
Int J Cancer. 2009 Aug 15;125(4):816-25. doi: 10.1002/ijc.24347.
Epithelial ovarian carcinoma (EOC) is a leading cause of death from gynecologic malignancies, due mainly to the prevalence of undetected metastatic disease. The process of cell invasion during intraperitoneal anchoring of metastatic lesions requires concerted regulation of many processes, including modulation of adhesion to the extracellular matrix and localized invasion. Exploratory cDNA microarray analysis of early response genes (altered after 4 hr of 3D collagen culture) coupled with confirmatory real-time reverse-transcriptase polymerase chain reaction, multiple 3D cell culture matrices, Western blot, immunostaining, adhesion, migration and invasion assays were used to identify modulators of adhesion pertinent to EOC progression and metastasis. cDNA microarray analysis indicated a dramatic downregulation of connective tissue growth factor (CTGF) in EOC cells placed in invasion- mimicking conditions (3D Type I collagen). Examination of human EOC specimens revealed that CTGF expression was absent in 46% of the tested samples (n = 41), but was present in 100% of normal ovarian epithelium samples (n = 7). Reduced CTGF expression occurs in many types of cells and may be a general phenomenon displayed by cells encountering a 3D environment. CTGF levels were inversely correlated with invasion such that downregulation of CTGF increased, while its upregulation reduced collagen invasion. Cells adhered preferentially to a surface comprised of both collagen I and CTGF relative to either component alone using alpha6beta1 and alpha3beta1 integrins. Together these data suggest that downregulation of CTGF in EOC cells may be important for cell invasion through modulation of cell-matrix adhesion.
上皮性卵巢癌(EOC)是妇科恶性肿瘤导致死亡的主要原因,主要是由于未被检测到的转移性疾病普遍存在。转移性病变在腹腔内锚定过程中的细胞侵袭过程需要对许多过程进行协同调节,包括调节与细胞外基质的粘附和局部侵袭。通过对早期反应基因(在三维胶原培养4小时后发生改变)进行探索性cDNA微阵列分析,并结合实时逆转录聚合酶链反应进行验证、多种三维细胞培养基质、蛋白质免疫印迹、免疫染色、粘附、迁移和侵袭试验,以鉴定与EOC进展和转移相关的粘附调节因子。cDNA微阵列分析表明,在模拟侵袭条件(三维I型胶原)下培养的EOC细胞中,结缔组织生长因子(CTGF)显著下调。对人类EOC标本的检测显示,46%的测试样本(n = 41)中不存在CTGF表达,但100%的正常卵巢上皮样本(n = 7)中存在CTGF表达。CTGF表达降低发生在多种类型的细胞中,可能是细胞在三维环境中呈现的普遍现象。CTGF水平与侵袭呈负相关,即CTGF下调增加,而其上调则减少胶原侵袭。相对于单独的任何一种成分,细胞使用α6β1和α3β1整合素优先粘附于由I型胶原和CTGF组成的表面。这些数据共同表明,EOC细胞中CTGF的下调可能通过调节细胞-基质粘附对细胞侵袭很重要。