Establishment of hamster pancreatic ductal carcinoma cell line (PC-1) producing blood group-related antigens

Egami, Hiroshi; Takiyama, Yumi; Cano, Martín; Houser, William H.; Pour, Parviz M.

doi:10.1093/carcin/10.5.861

Cited by 60 publications

(29 citation statements)

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“…Two hamster pancreatic cancer cell lines were used: the weakly invasive and rarely metastatic cell line PC-1 and the highly invasive and metastatic cell line PC-1.0. The PC-1 cell line was established from pancreatic ductal/ductular adenocarcinomas induced by BoP in a Syrian golden hamster (26). The PC-1.0 cell line was established from a subcutaneous tumour produced after inoculation with PC-1 cells (27).…”

Section: Methodsmentioning

confidence: 99%

Involvement of the expression and redistribution of claudin-23 in pancreatic cancer cell dissociation

et al. 2010

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Abstract. dissociation of pancreatic cancer cells from primary sites is the critical first step in tumour invasion and metastasis. Changes in the structure and function of tight junctions are reported to be correlated with carcinogenesis and tumour development. Using cDNA microarray analysis, we recently identified claudin-23 as a differentially expressed gene related to invasion-metastasis in highly (PC-1.0) and weakly (PC-1) invasive and metastatic pancreatic cancer cells. In this study, RT-PCR, Western blotting and immunocytochemistry were used to demonstrate the involvement of the expression and redistribution of claudin-23 in pancreatic cancer cell dissociation. Claudin-23 mRNA and protein were differentially expressed in PC-1.0 and PC-1 cells. Claudin-23 expression was induced in a PC-1.0 subclone expressing mitogen-activated protein kinase kinase (MEK)-1 shorthairpin RNA (shRNA) and claudin-23 was redistributed in a PC-1.0 subclone expressing MEK2 shRNA. Furthermore, these MEK2 shRNA-expressing PC-1.0 cells aggregated and formed island-like cell colonies. By contrast, the addition of dissociation factor-conditioned medium significantly reduced claudin-23 mRNA and protein expression in PC-1 cells. The present results indicate that claudin-23 is involved in the regulation of pancreatic cancer cell dissociation through changes in gene expression and intracellular localisation. In addition, claudin-23 expression is possibly correlated with the activation of the MEK signalling pathway during pancreatic cancer cell dissociation. Claudin-23 may thus serve as a new target for molecular therapies to prevent pancreatic cancer invasion and metastasis.

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Section: Methodsmentioning

confidence: 99%

Involvement of the expression and redistribution of claudin-23 in pancreatic cancer cell dissociation

et al. 2010

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“…Two hamster pancreatic cancer cell lines, the weakly invasive and metastatic cell line PC-1 and the highly invasive and metastatic cell line PC-1.0 were used. The PC-1 cell line was established from pancreatic ductal/ductular adenocarcinomas induced by BOP in a Syrian golden hamster (1). The PC-1.0 cell line was established from a subcutaneous tumour produced after inoculation of PC-1 cells (2).…”

Section: Methodsmentioning

confidence: 99%

“…Two hamster pancreatic cancer cell lines with different potentials for invasion and metastasis after intra-pancreatic transplantation, PC-1 (low potential) and PC-1.0 (high potential), were established from a pancreatic ductal carcinoma induced by N-nitrosobis (2-oxopropyl) amine (BOP) in a Syrian golden hamster (1)(2)(3). In our previous study, gene expression differences between PC-1.0 and PC-1 cells were examined using the representational difference analysis (RDA) method.…”

Section: Introductionmentioning

confidence: 99%

MEK1 and MEK2 isoforms regulate distinct functions in pancreatic cancer cells

Zhou

Tan²,

Kamohara³

et al. 2010

Oncol Rep

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Abstract. The mitogen-activated protein kinase kinase 1/2 (MEK1/2) signalling pathway plays a central role in tumour progression. Small molecules that inhibit MEK1/2 are therefore considered attractive candidates for anti-cancer drugs. However, the exact contributions of MEK1 and MEK2 to the development of pancreatic cancer remain to be established. To differentiate the functions of MEK1 and MEK2 in a cultured pancreatic cancer cell line, we utilised shRNAmediated knockdown of their two mRNAs individually. We studied the effects of MEK1 and MEK2 knockdown on cell morphology, proliferation, mitotic arrest, and in vitro invasion capability in PC-1.0 cells. The results showed that inhibition of MEK1 expression was an effective and specific approach to inhibit cell proliferation and induce G 0 /G 1 arrest. On the other hand, MEK2 knockdown specially altered cell morphology and inhibited the invasive ability of pancreatic cancer cells. Therefore, MEK1 and MEK2 mediate different biological responses in cultured pancreatic cancer cells. These proteins could become distinct targets for the inhibition of specific cellular functions in the treatment of pancreatic cancer.

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“…Two hamster pancreatic cancer cell lines were used, the weakly invasive and rarely metastatic Analysis of invasion-metastasis in pancreatic cancer: Correlation between the expression and arrangement of tight junction protein-2 and cell dissociation in pancreatic cancer cells cell line Pc-1, and the highly invasive and metastatic cell line Pc-1.0. The Pc-1 cell line was established from pancreatic ductal/ductular adenocarcinomas induced by BoP in a Syrian golden hamster (10). The Pc-1.0 cell line was established from a subcutaneous tumour produced after the inoculation of Pc-1 cells (11).…”

Section: Methodsmentioning

confidence: 99%

Analysis of invasion-metastasis in pancreatic cancer: Correlation between the expression and arrangement of tight junction protein-2 and cell dissociation in pancreatic cancer cells

Zhou

Tan²,

Wang³

et al. 2009

Mol Med Rep

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Abstract. High frequency of invasion and metastasis is one of the key characteristics of pancreatic cancer. in our recent study, tight junction protein-2 (Tjp-2) was identified as a differentially expressed gene related to invasion-metastasis in highly (Pc-1.0) and weakly (Pc-1) invasive and metastatic pancreatic cancer cells by cdna microarray analysis. changes in the structure and function of tight junctions are correlated with carcinogenesis and tumour development. in this study, rT-Pcr, Western blotting and immunocytochemistry were used to study the correlation between the expression and localisation of Tjp-2 and cell dissociation in pancreatic cancer. Tjp-2 mrna and protein were differentially expressed in Pc-1.0 and Pc-1 cells. Furthermore, the addition of dissociation factor (DF) or U0126 (a MEK inhibitor) significantly induced changes in the mrna expression and protein intracellular localisation of Tjp-2, and in the simultaneous cell dissociation of Pc-1.0 and Pc-1 cells. However, protein expression of Tjp-2 was not affected by dF or u0126 treatment. The current results indicate that Tjp-2 is involved in the regulation of cell dissociation in pancreatic cancer cells through changes in gene expression and intracellular localisation. Tjp-2 may serve as a new target for molecular therapies that prevent the invasion and metastasis of pancreatic cancer.

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Establishment of hamster pancreatic ductal carcinoma cell line (PC-1) producing blood group-related antigens

Cited by 60 publications

References 0 publications

Involvement of the expression and redistribution of claudin-23 in pancreatic cancer cell dissociation

Involvement of the expression and redistribution of claudin-23 in pancreatic cancer cell dissociation

MEK1 and MEK2 isoforms regulate distinct functions in pancreatic cancer cells

Analysis of invasion-metastasis in pancreatic cancer: Correlation between the expression and arrangement of tight junction protein-2 and cell dissociation in pancreatic cancer cells

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