Background:Brain acid soluble protein 1 (BASP1) is identified as a novel potential tumor suppressor in several cancers. However, its role in thyroid cancer has not been investigated yet. In the present study, the antitumor activities of BASP1 against the growth and migration of thyroid cancer cells were evaluated.Methods:BASP1 expression in thyroid cancer tissues and normal tissues were examined by immunohistochemical staining and the association between its expression and prognosis was analyzed. pcDNA-BASP1 carrying full length of BASP1 cDNA was constructed to restore the expression of BASP1 in thyroid cancer cell lines (BHT-101 and KMH-2). The cell proliferation in vitro and in vivo was evaluated by WST-1 assay and xenograft tumor models, respectively. Cell cycle distribution after transfection was analyzed using flow cytometry. Cell apoptosis after transfection was examined by annexin V/propidium iodide assay. The migration was examined using transwell assay.Results:BASP1 expression was abundant in normal tissues while it is significantly decreased in cancer tissues (P = 0.000). pcDNA-BASP1 restored the expression of BASP1 and significantly inhibited the growth of BHT-101 and KMH-2 cells as well as xenograft tumors in nude mice (P = 0.000). pcDNA-BASP1 induced G1 arrest and apoptosis in BHT-101 and KMH-2 cells. In addition, pcDNA-BASP1 significantly inhibited the cell migration.Conclusions:Downregulation of BASP1 expression may play a role in the tumorigenesis of thyroid cancer. Restoration of BASP1 expression exerted extensive antitumor activities against growth and migration of thyroid cancer cells, which suggested that BASP1 gene might act as a potential therapeutic agent for the treatment of thyroid cancer.

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.

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