Data on the negative regulation of invadopodia activity by MLCK.
Data on the negative regulation of invadopodia activity by MLCK.
复制标题
MLCK 对侵袭伪足活性负调控的数据。
DOI：
10.1016/j.dib.2019.103939
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发表时间：
2019
期刊：
影响因子：
1.2
通讯作者：
Parekh,Aron
中科院分区：
文献类型：
--
作者：
Jerrell,RachelJ;Parekh,Aron
肌动球蛋白的收缩性可以促进癌细胞中侵袭伪足对细胞外基质（ECM）的降解。然而，我们以前发现，抑制肌球蛋白轻链激酶（MLCK）的siRNA并没有改变力产生的头颈部鳞状细胞癌（HNSCC）细胞系SCC-61。我们在此提供的数据表明，这种MLCK敲低（KD）的靶向方法导致ECM降解量、主动降解侵袭伪足数量和形成的总侵袭伪足数量显著增加。这些数据与题为“Matrix rigidity differentially regulates invadopodia activity through ROCK 1 and ROCK 2”Jerrell and Parekh，2016的研究文章相关。
Actomyosin contractility can promote extracellular matrix (ECM) degradation by invadopodia in cancer cells. However, we previously found that inhibiting myosin light chain kinase (MLCK) with siRNA did not change force generation by the head and neck squamous cell carcinoma (HNSCC) cell line SCC-61. We provide data here that this targeted method of MLCK knockdown (KD) resulted in a significant increase in the amount of ECM degradation, number of actively degrading invadopodia, and the number of total invadopodia formed. These data are related to the research article entitled “Matrix rigidity differentially regulates invadopodia activity through ROCK1 and ROCK2” Jerrell and Parekh, 2016.