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Spontaneously transformed rat‐liver epithelial‐cell line producing autocrine and paracrine growth factors
Author(s) -
Narita Takeo
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.2910520321
Subject(s) - autocrine signalling , trypsinization , paracrine signalling , epidermal growth factor , cell culture , biology , growth factor , transforming growth factor , cell growth , endocrinology , medicine , microbiology and biotechnology , biochemistry , receptor , trypsin , genetics , enzyme
Abstract A spontaneously transformed rat‐liver epithelial‐cell line that could proliferate in unsupplemented, serum‐free medium and be passaged with trypsinization has been established. At the time of writing, the line has undergone more than 100 passages in serum‐free culture. This cell line produced an autocrine growth‐stimulatory factor (AGSF) and a paracrine growth‐stimulatory factor (PGSF). AGSF had a remarkable growth‐stimulatory effect on transformed rat‐liver epithelial‐cells, but had no such effect on non‐transformed rat‐liver epithelial‐cells that could not proliferate in serum‐free medium. AGSF did not show a growth‐inhibitory or stimulatory effect on normal rat kidney (NRK) cells in monolayer culture, and did not induce anchorage‐independent growth in soft‐agar culture even with epidermal growth factor (EGF) or transforming growth factor (TGF)‐p. AGSF was protease‐sensitive, but heat‐ and acid‐stable. The molecular weight was about 700 Dalton (Da) on size‐exclusion chromatography. PGSF showed a growth‐stimulatory effect on NRK cells and induced anchorage‐independent growth in soft‐agar culture without EGF or TGF‐β. On the other hand, PGSF slightly inhibited the growth of the spontaneously transformed rat‐liver epithelial cells. PGSF was heat‐, protease‐ and acid‐sensitive. The molecular weight was 30 kDa on size‐exclusion chromatography. © 1992 Wiley‐Liss, Inc.