Abstract
ABSTRACTColorectal 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.
Highlights
Colorectal cancer (CRC) is one of the most common cancers of the gastrointestinal tract
Our data indicated that the expression of Protein Kinase C (PKC)-ζ was higher in rapidly growing CRC cells compared to the healthy cell (CCD18CO)
The expression profile of atypical PKC in the normal cell was not as robust as in cancerous cells (Figure 2). These results suggest that the atypical PKC might play an essential role in CRC cells progression
Summary
Colorectal cancer (CRC) is one of the most common cancers of the gastrointestinal tract. A significant member of ABP superfamily known as Cofilin/actin depolymerizing factor (ADF) plays an essential role in actin-filaments turnover by depolymerizing and severing filamentous actin [5,6,7]. The phosphorylation of Cofilin at Serine-3 by different kinases such as LIM kinase 1 (LIMK1) and LIM kinase 2 (LIMK2) make it unable to bind and sever filamentous actin [9,10]. Phosphatases such as Slingshot (SSH), Protein Phosphatase (PP1), Protein Phosphatase 2A (PP2A), Protein Phosphatase 2B (PP2B), and chronophin dephosphorylate Cofilin at Serine 3 to render it active [11,12,13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
