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Objective:To analyze the p16INK4a genomic alteration and expression status in 3 human pancreatic carcinoma cell lines with different potential of metastasis. Methods: Using PCR-SSCP, Dot-blot and immunohistochemistry. the p16INK4a genomic mutation and expression were analyzed on DNA, mRNA and protein levels in 3 human pancreatic carcinoma cell lines Patu8902, Patu8988 and SW1990, which had different potential of metastasis. Results :(1) On DNA level: there was no deletion of p16INK4a Exon I in 3 cell lines; p16INK4a Exon II was only deleted in Patu8902 while no deletion in Patu8988 and SW1990. No insertion, microdeletion and point mutation were found in the 3 cell lines. (2) On RNA level: the expression of p16INK4a protein was negative in Patu8902. low expressed in SW1990, but highly expressed in Patu8988. (3) On protein level: P16 protein was strongly stained in Patu8988, much lower in SW1990, but not stained in Patu8902. Conclusion :The genomic type and expression of p16INKa4 are quite different in 3 pancreatic carcinoma cell lines which have different potential of metastasis. It is suggested that genomic ho-mozygous deletion and low expression of mRNA might relate to the potential of metastasis of pancreatic cell lines. In other words, dysfunction of p16INK4a might be an important mechanism in the metastasis of pancreatic carcinoma.
Objective: To analyze the p16INK4a genomic alteration and expression status in 3 human pancreatic carcinoma cell lines with different potential of metastasis. Methods: Using PCR-SSCP, Dot-blot and immunohistochemistry. The p16INK4a genomic mutation and expression were analyzed on DNA, mRNA and Results: (1) On DNA level: there was no deletion of p16INK4a Exon I in 3 cell lines; p16INK4a Exon II was only deleted in Patu8902 while no deletion in Patu8988 and SW1990. No insertion, microdeletion and point mutation were found in the 3 cell lines. (2) On RNA level: the expression of p16INK4a protein was negative in Patu8902. low expressed in SW1990, but highly expressed in Patu8988. (3) On protein level: P16 protein was strongly stained in Patu8988, much lower in SW1990, but not stained in Patu8902. Conclusion: The genomic type and expression of p16INKa4 are qui te different in 3 pancreatic carcinoma cell lines which have different potential of metastasis. It is suggested that genomic ho-mozygous deletion and low expression of mRNA might relate to the potential of metastasis of pancreatic cell lines. In other words, dysfunction of p16INK4a might be an important mechanism in the metastasis of pancreatic carcinoma.