Identifying the factors and signal pathways necessary for anchorage-independent growth of Ha-ras oncogene-transformed NIH/3T3 cells

Tsuey Yu Chang, Wen Jiuan Tsai, Chao Kai Chou, Nan-Haw Chow, Tzeng-Horng Leu, Hsiao-Sheng Liu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Ha-rasVal 12 overexpression was positively correlated with colony formation by NIH/3T3 derivative "2-12" cells harboring an inducible Ha-rasVal 12 transgene. The ras-farnesylation inhibitor, Lovastatin, completely suppressed colony formation at higher dosages. However, Ha-ras oncogene overexpression alone could not stimulate colony formation under serum-deprived conditions, suggesting that ras is required but not sufficient for supporting colony formation. Substituting cow colostrum (AC-2®) for serum did not result in colony formation from 2-12 cells in soft agar, suggesting the colostrum lacked or contained insufficient amounts of factors that stimulate colony formation. Supplementation of AC-2®-containing medium with growth factors, such as insulin-like growth factor-1 (IGF-1), partially restored the capability of anchorage-independent cell growth induced by Ha-ras overexpression. Consistently, antibodies specific for IGF-1 receptors only partially blocked colony formation from 2-12 cells. The data indicate that multiple factors, including IGF-1, are required for Ha-ras-dependent colony formation. Signal transduction studies revealed that, under Ha-ras overexpression conditions, IGF-1 utilizes phosphatidyl inositol 3-kinase and NF-κB to transduce colony formation-related signaling.

Original languageEnglish
Pages (from-to)1265-1274
Number of pages10
JournalLife Sciences
Volume73
Issue number10
DOIs
Publication statusPublished - 2003 Jul 25

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NIH 3T3 Cells
ras Genes
Somatomedins
Signal Transduction
Colostrum
Growth
Prenylation
Somatomedin Receptors
Lovastatin
Signal transduction
Cell growth
Phosphatidylinositols
Serum
Transgenes
Agar
Intercellular Signaling Peptides and Proteins
Phosphotransferases
Derivatives
Antibodies

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

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title = "Identifying the factors and signal pathways necessary for anchorage-independent growth of Ha-ras oncogene-transformed NIH/3T3 cells",
abstract = "Ha-rasVal 12 overexpression was positively correlated with colony formation by NIH/3T3 derivative {"}2-12{"} cells harboring an inducible Ha-rasVal 12 transgene. The ras-farnesylation inhibitor, Lovastatin, completely suppressed colony formation at higher dosages. However, Ha-ras oncogene overexpression alone could not stimulate colony formation under serum-deprived conditions, suggesting that ras is required but not sufficient for supporting colony formation. Substituting cow colostrum (AC-2{\circledR}) for serum did not result in colony formation from 2-12 cells in soft agar, suggesting the colostrum lacked or contained insufficient amounts of factors that stimulate colony formation. Supplementation of AC-2{\circledR}-containing medium with growth factors, such as insulin-like growth factor-1 (IGF-1), partially restored the capability of anchorage-independent cell growth induced by Ha-ras overexpression. Consistently, antibodies specific for IGF-1 receptors only partially blocked colony formation from 2-12 cells. The data indicate that multiple factors, including IGF-1, are required for Ha-ras-dependent colony formation. Signal transduction studies revealed that, under Ha-ras overexpression conditions, IGF-1 utilizes phosphatidyl inositol 3-kinase and NF-κB to transduce colony formation-related signaling.",
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Identifying the factors and signal pathways necessary for anchorage-independent growth of Ha-ras oncogene-transformed NIH/3T3 cells. / Chang, Tsuey Yu; Tsai, Wen Jiuan; Chou, Chao Kai; Chow, Nan-Haw; Leu, Tzeng-Horng; Liu, Hsiao-Sheng.

In: Life Sciences, Vol. 73, No. 10, 25.07.2003, p. 1265-1274.

Research output: Contribution to journalArticle

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AU - Chang, Tsuey Yu

AU - Tsai, Wen Jiuan

AU - Chou, Chao Kai

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AU - Leu, Tzeng-Horng

AU - Liu, Hsiao-Sheng

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AB - Ha-rasVal 12 overexpression was positively correlated with colony formation by NIH/3T3 derivative "2-12" cells harboring an inducible Ha-rasVal 12 transgene. The ras-farnesylation inhibitor, Lovastatin, completely suppressed colony formation at higher dosages. However, Ha-ras oncogene overexpression alone could not stimulate colony formation under serum-deprived conditions, suggesting that ras is required but not sufficient for supporting colony formation. Substituting cow colostrum (AC-2®) for serum did not result in colony formation from 2-12 cells in soft agar, suggesting the colostrum lacked or contained insufficient amounts of factors that stimulate colony formation. Supplementation of AC-2®-containing medium with growth factors, such as insulin-like growth factor-1 (IGF-1), partially restored the capability of anchorage-independent cell growth induced by Ha-ras overexpression. Consistently, antibodies specific for IGF-1 receptors only partially blocked colony formation from 2-12 cells. The data indicate that multiple factors, including IGF-1, are required for Ha-ras-dependent colony formation. Signal transduction studies revealed that, under Ha-ras overexpression conditions, IGF-1 utilizes phosphatidyl inositol 3-kinase and NF-κB to transduce colony formation-related signaling.

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