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.

中文翻译：

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通过非典型蛋白激酶C激活的Cofilin对肌动蛋白动力学的调节可调节结直肠癌细胞的转移。

结直肠癌（CRC）是美国第三大最常见的癌症。CRC细胞转移的确切机制了解甚少。肌动蛋白的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的方向。Cofilin是一种重要的肌动蛋白调节分子，通过形成片状脂蛋白和丝状伪足来调节癌细胞的迁移，但是，对cofilin的上游调节知之甚少。在这项研究中，研究了非典型蛋白激酶C（非典型PKC）对CRC中Cofilin活性的影响。这项研究表明，非典型的PKC抑制作用通过增加磷酸Cofilin（S3）和改变肌动蛋白的组织来阻止CRC细胞的转移。