Since tenascin C is a factor expressed highly in the tumorassociated matrix, it would be a desirable first step for targeting the tumor-specific microenvironment. In fact, a high level of tenascin C expression has been reported in most solid tumors, including lung cancer, colon cancer and glioblastoma. Therefore, the targeted binding of tenascin C in tumor stroma would inhibit tumor metastasis by modulating cancer cell growth and migration. We isolated a peptide that bound to tenascin C by phage display peptide library selection, and the selected peptide specifically recognized tenascin C protein in xenograft mouse tissue. We also observed exclusive staining of tenascin C by the selected peptide in tumor patient tissues. Moreover, the peptide reduced tenascin C-induced cell rounding and migration. We propose that the tenascin C targeting peptide may be useful as a specific anti-cancer diagnostic and therapeutic tool for most human solid tumors.
Background/Aims
This study was tried to determine the role of β-catenin in invasion in pancreatic cancer.
Methods
We analyzed cancer invasiveness according to β-catenin expression in pancreatic cancer cell line. We also investigated the change in cancer invasiveness when β-catenin expression was changed. To enhance β-catenin activity, we treated low β-catenin cancer cell line, PANC1, with Wnt-3a conditioned media and transected β-catenin. We also treated high β-catenin expressing cell line, BxPC3, with XAV939, β-catenin inhibitor and siRNA for β-catenin to inhibit β-catenin expression.
Results
The high β-catenin expressing cancer cell line, BxPC3 showed higher invasiveness, and low β-catenin expressing cell lines, PANC1and MIA-PaCa-2, were less invasive. By adding the Wnt-3a conditioned media or performing transfection with β-catenin in PANC1, cell invasiveness was increased (
p
< 0.05 and
p
< 0.01, respectively). On inhibition of β-catenin by XAV939 and siRNA in BxPC3 cell line, invasiveness was significantly decreased (
p
< 0.01). It was not correlated with the expression of cluster of differentiation 44 (CD44) or CD44 variant 6 (CD44v6), the invasion related protein. On analysis of association with metastasis in human tissue, Wnt-3a expression was statistically correlated with the development of metastasis (
p
= 0.029).
Conclusions
Based on our data, β-catenin may be involved in cancer invasion in pancreatic cancer, and it is not associated with CD44, the invasion related protein.
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