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Secretion of autocrine growth‐promoting activity by renal‐carcinoma cells treated with 5‐fluorouracil
Author(s) -
Nishimura Naoki,
Kanda Shigeru,
Yogi Yasuo,
Kawamura Masaya,
Nakamura Mikio,
Hyakutake Hiroyuki,
Kanetake Hiroshi,
Saito Yutaka
Publication year - 1992
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910520119
Subject(s) - autocrine signalling , dna synthesis , cell culture , dithiothreitol , growth factor , biology , epidermal growth factor , endocrinology , cancer cell , cell growth , paracrine signalling , secretion , medicine , cancer research , biochemistry , in vitro , cancer , enzyme , genetics , receptor
A study was made of the auto‐proliferative activity of human renal‐carcinoma cells in the supernatant from a carcinoma‐cell culture in serum‐free medium to which an anticancer agent had been added (5‐FU). The human renal‐cancer cells used in this study were of 3 strains: ACHN, VMRC‐RCW and NT. When each line was cultured in medium containing no 5‐FU, the supernatant showed almost no activity for stimulating DNA synthesis. However, when the line was cultured in the presence of 5‐FU, the supernatant showed autocrine growth‐promoting activity which strongly stimulated DNA synthesis of 3 renal‐cancer cell lines in a dose‐dependent manner. Activity could be detected in a 4‐ to 6‐kDa fraction by gel filtration. This fraction increased the DNA‐synthesis‐promoting activity of epidermal growth factor, transforming growth factor‐β, basic fibroblast growth factor and insulin, and was acid‐ and heat‐stable. It was also stable against pepsin and dithiothreitol. DNA synthesis in BALB/c 3T3, adult rat hepatocytes and rabbit renal tubular cells was not affected by this fraction which was thus considered not to affect non‐cancerous cells. Renal‐cell carcinoma responds poorly to anticancer agents, and the autocrine activity of the fraction may possibly be a factor accounting for this resistance. © 1992 Wiley‐Liss, Inc.