通过非典型蛋白激酶c激活的Cofilin调节肌动蛋白动力学调节结直肠癌细胞的转移。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2019-12-01 Epub Date: 2018-11-18 DOI:10.1080/19336918.2018.1546513
S M Anisul Islam, Rekha Patel, Raja Reddy Bommareddy, Khandker Mohammad Khalid, Mildred Acevedo-Duncan
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引用次数: 14

摘要

结直肠癌(CRC)是美国第三大常见癌症。CRC细胞转移的确切机制尚不清楚。肌动蛋白聚合被认为是癌细胞运动周期的第一步,它驱动细胞突起的形成并确定迁移方向。Cofilin是一种重要的肌动蛋白调节分子,通过板足和丝足的形成来调节癌细胞的迁移,但对Cofilin的上游调控知之甚少。本研究研究了非典型蛋白激酶C(非典型PKC)对结直肠癌中Cofilin活性的影响。本研究表明,非典型PKC抑制通过增加磷酸化- cofilin (S3)和改变肌动蛋白组织来阻碍结直肠癌细胞的转移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells.

The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells.

The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells.

The modulation of actin dynamics via atypical Protein Kinase-C activated Cofilin regulates metastasis of colorectal cancer cells.

Colorectal cancer (CRC) is the third most common cancer in the United States. The exact mechanism of CRC cells metastasis is poorly understood. Actin polymerization is thought to be an initial step in the cancer cell motility cycle which drives the formation of cell protrusions and defines the direction of migration. Cofilin, a significant actin-regulating molecule, regulates the migration of cancer cells by the formation of lamellipodia and filopodia, however, little is known about the upstream regulation of cofilin. In this study, the effect of atypical Protein Kinase C (atypical PKC) on Cofilin activity in CRC was studied. This study demonstrates that the atypical PKC inhibition impedes the metastasis of CRC cells by increasing phospho-Cofilin (S3) and changing actin organization.

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CiteScore
7.20
自引率
4.30%
发文量
567
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