MMP9公司
基质金属蛋白酶
细胞外基质
细胞生物学
卵巢癌
生物
癌症研究
化学
癌症
下调和上调
基因
遗传学
作者
Nelson A. Cook,Katie D. Finnegan,Reid A. Kallenbach,Caleb L. Lines,Shawn M. Ellerbroek
标识
DOI:10.1096/fasebj.2020.34.s1.09559
摘要
Matrix Metalloproteinase‐9 (MMP9) is an extracellular endopeptidase associated with ovarian cancer development and progression. To further understand MMP9 contributions to metastatic behavior of an established ovarian cancer cell line (OVCA433), we utilized CRISPR to generate seven cell clones null for MMP9 expression. Analysis of the pooled clones revealed MMP9‐null cells exhibited identical phenotype and growth compared to parental OVCA 433 cells. Cell adhesion and transwell migration towards type I collagen was also not impacted by MMP9 loss. MMP9‐null cells were significantly delayed, however, in non‐directional filamentous actin‐based membrane protrusions on a variety of matrix substrates in response to Epidermal growth factor stimulation. Further, over or re‐expression of MMP9 in OVCA433 or MMP9‐null cells, respectively, was sufficient to drive both lamellipodial and filopodial membrane protrusions on glass. These results indicate MMP9 directly contributes to ovarian cancer protrusive activity. Support or Funding Information Wartburg Undergraduate Research Grants
科研通智能强力驱动
Strongly Powered by AbleSci AI