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Int J Oncol. 2018 Sep;53(3):1118-1128. doi: 10.3892/ijo.2018.4475. Epub 2018 Jul 9.

Loss of profilin 2 contributes to enhanced epithelial-mesenchymal transition and metastasis of colorectal cancer.

Author information

1
Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
2
Department of General Surgery, Jiading District Central Hospital Affiliated Shanghai University of Medicine & Health Sciences, Shanghai 201800, P.R. China.

Abstract

Profilin 2 (PFN2) functions as an actin cytoskeleton regulator and serves an important role in cell motility. However, a role for PFN2 in the progression of colorectal cancer (CRC), particularly in metastasis, has yet to be clarified. The aim of the present study was to investigate whether PFN2 served specific roles in the progression of human CRC. The results demonstrated that PFN2 was differentially expressed in CRC tissues and cell lines by reverse transcription-quantitative polymerase chain reaction and western blotting. PFN2 expression was also negatively associated with the degree of tumor metastasis. Low PFN2 expression in CRC cells was related with enhanced epithelial-mesenchymal transition (EMT) and, in turn, may increase migratory capabilities. Overexpression of PFN2 in CRC cell lines with a low level of endogenous PFN2 inhibited the EMT process, as well as the associated migration; in addition, myosin light chain (MLC) phosphorylation was upregulated. Inhibition of MLC phosphorylation attenuated the inhibition of EMT and cell migratory abilities induced by PFN2 overexpression in CRC cell lines, the results suggested that PFN2 may suppress cancer EMT and the subsequent metastasis by regulating cytoskeletal reorganization. These results demonstrated that PFN2 may serve a suppressive role in the metastasis of CRC and therefore may provide a new potential target for cancer therapeutics.

PMID:
30015842
PMCID:
PMC6065425
DOI:
10.3892/ijo.2018.4475
[Indexed for MEDLINE]
Free PMC Article

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