Overexpression of phospholipase C-γ1 in rat 3Y1 fibroblast cells leads to malignant transformation

Jong Soo Chang; Dong Young Noh; In Ae Park; Myung Jong Kim; Hebok Song; Sung Ho Ryu; Pann Ghill Suh

Overexpression of phospholipase C-γ1 in rat 3Y1 fibroblast cells leads to malignant transformation

Jong Soo Chang, Dong Young Noh, In Ae Park, Myung Jong Kim, Hebok Song, Sung Ho Ryu, Pann Ghill Suh^*

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Article › peer-review

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Abstract

Phospholipase C-γ1 (PLC-γ1) mediates signals from various extracellular origins to evoke cellular events such as mitogenesis. Previously, we reported that PLC-γ1 was highly expressed in colorectal cancer and familial adenomatous polyposis, suggesting that PLC-γ1 might be oncogenic. In this study, we have established rat 3Y1 fibroblasts that overexpress whole PLC-γ1 and src homology 2 (SH2)-SH2-SH3 domain of PLC- γ1. These cells showed a transformed phenotype and were tumorigenic when transplanted into nude mice. These results indicate that overexpression of PLC-γ1 could transform rat fibroblasts, and the transformation is mediated by SH2-SH2-SH3 domain of PLC-γ1.

Original language	English (US)
Pages (from-to)	5465-5468
Number of pages	4
Journal	Cancer Research
Volume	57
Issue number	24
State	Published - Dec 15 1997

ASJC Scopus subject areas

Oncology
Cancer Research

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title = "Overexpression of phospholipase C-γ1 in rat 3Y1 fibroblast cells leads to malignant transformation",

abstract = "Phospholipase C-γ1 (PLC-γ1) mediates signals from various extracellular origins to evoke cellular events such as mitogenesis. Previously, we reported that PLC-γ1 was highly expressed in colorectal cancer and familial adenomatous polyposis, suggesting that PLC-γ1 might be oncogenic. In this study, we have established rat 3Y1 fibroblasts that overexpress whole PLC-γ1 and src homology 2 (SH2)-SH2-SH3 domain of PLC- γ1. These cells showed a transformed phenotype and were tumorigenic when transplanted into nude mice. These results indicate that overexpression of PLC-γ1 could transform rat fibroblasts, and the transformation is mediated by SH2-SH2-SH3 domain of PLC-γ1.",

author = "Chang, {Jong Soo} and Noh, {Dong Young} and Park, {In Ae} and Kim, {Myung Jong} and Hebok Song and Ryu, {Sung Ho} and Suh, {Pann Ghill}",

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T1 - Overexpression of phospholipase C-γ1 in rat 3Y1 fibroblast cells leads to malignant transformation

AU - Chang, Jong Soo

AU - Noh, Dong Young

AU - Park, In Ae

AU - Kim, Myung Jong

AU - Song, Hebok

AU - Ryu, Sung Ho

AU - Suh, Pann Ghill

PY - 1997/12/15

Y1 - 1997/12/15

N2 - Phospholipase C-γ1 (PLC-γ1) mediates signals from various extracellular origins to evoke cellular events such as mitogenesis. Previously, we reported that PLC-γ1 was highly expressed in colorectal cancer and familial adenomatous polyposis, suggesting that PLC-γ1 might be oncogenic. In this study, we have established rat 3Y1 fibroblasts that overexpress whole PLC-γ1 and src homology 2 (SH2)-SH2-SH3 domain of PLC- γ1. These cells showed a transformed phenotype and were tumorigenic when transplanted into nude mice. These results indicate that overexpression of PLC-γ1 could transform rat fibroblasts, and the transformation is mediated by SH2-SH2-SH3 domain of PLC-γ1.

AB - Phospholipase C-γ1 (PLC-γ1) mediates signals from various extracellular origins to evoke cellular events such as mitogenesis. Previously, we reported that PLC-γ1 was highly expressed in colorectal cancer and familial adenomatous polyposis, suggesting that PLC-γ1 might be oncogenic. In this study, we have established rat 3Y1 fibroblasts that overexpress whole PLC-γ1 and src homology 2 (SH2)-SH2-SH3 domain of PLC- γ1. These cells showed a transformed phenotype and were tumorigenic when transplanted into nude mice. These results indicate that overexpression of PLC-γ1 could transform rat fibroblasts, and the transformation is mediated by SH2-SH2-SH3 domain of PLC-γ1.

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Overexpression of phospholipase C-γ1 in rat 3Y1 fibroblast cells leads to malignant transformation

Abstract

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