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Insulin-like growth factor-I can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro.
J Clin Invest. 1988 Jul; 82(1):354-9.JCI

Abstract

The effect of insulin-like growth factor I (IGF-I) on growth of small cell lung cancer (SCLC) cell lines was studied. Western blot analysis of whole cell lysates of cell lines NCI-H345 and NCI-N417 demonstrated the presence of a 16-kD band consistent with an IGF-I precursor molecule. Scatchard plot analysis of cell line NCI-H345 using 125I-labeled IGF-I demonstrated two high affinity specific binding sites (Kd 1.3 and 4.0 nM with maximal rate (Bmax) 200 and 500 fmol/mg protein, respectively). The exogenous addition of IGF-I, IGF-II, or insulin resulted in marked proliferation of human SCLC cells as evaluated using an in vitro growth assay. These peptides stimulated the growth of SCLC cell lines NCI-H82, NCI-H209, NCI-H345, and NCI-N417. The concentration of IGF-I producing maximal SCLC cell growth was 10-100-fold less than that of insulin or IGF-II, whereas the maximal growth stimulated by the optimal concentration of these peptides were similar. An MAb that specifically binds to the IGF-I receptor (but not to the insulin receptor) mediates a dose-dependent inhibition of cell growth in basal media as well as IGF-I, IGF-II, or insulin-supplemented media. The IGF-I receptor thus appears to be the common pathway for the mitogenic activity by IGF-I, IGF-II, and insulin for human SCLC cell lines. The demonstration of an IGF-I precursor molecule, specific IGF-I receptor binding, IGF-I-mediated growth stimulation, and inhibition of basal cell growth by an MAb to the IGF-I receptor suggests that an IGF-I-like molecule can function in vitro as an autocrine growth factor for human SCLC cell lines.

Authors+Show Affiliations

Navy Medical Oncology Branch, National Cancer Institute, Bethesda, Maryland 20814.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2839551

Citation

Nakanishi, Y, et al. "Insulin-like Growth factor-I Can Mediate Autocrine Proliferation of Human Small Cell Lung Cancer Cell Lines in Vitro." The Journal of Clinical Investigation, vol. 82, no. 1, 1988, pp. 354-9.
Nakanishi Y, Mulshine JL, Kasprzyk PG, et al. Insulin-like growth factor-I can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro. J Clin Invest. 1988;82(1):354-9.
Nakanishi, Y., Mulshine, J. L., Kasprzyk, P. G., Natale, R. B., Maneckjee, R., Avis, I., Treston, A. M., Gazdar, A. F., Minna, J. D., & Cuttitta, F. (1988). Insulin-like growth factor-I can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro. The Journal of Clinical Investigation, 82(1), 354-9.
Nakanishi Y, et al. Insulin-like Growth factor-I Can Mediate Autocrine Proliferation of Human Small Cell Lung Cancer Cell Lines in Vitro. J Clin Invest. 1988;82(1):354-9. PubMed PMID: 2839551.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Insulin-like growth factor-I can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro. AU - Nakanishi,Y, AU - Mulshine,J L, AU - Kasprzyk,P G, AU - Natale,R B, AU - Maneckjee,R, AU - Avis,I, AU - Treston,A M, AU - Gazdar,A F, AU - Minna,J D, AU - Cuttitta,F, PY - 1988/7/1/pubmed PY - 1988/7/1/medline PY - 1988/7/1/entrez SP - 354 EP - 9 JF - The Journal of clinical investigation JO - J. Clin. Invest. VL - 82 IS - 1 N2 - The effect of insulin-like growth factor I (IGF-I) on growth of small cell lung cancer (SCLC) cell lines was studied. Western blot analysis of whole cell lysates of cell lines NCI-H345 and NCI-N417 demonstrated the presence of a 16-kD band consistent with an IGF-I precursor molecule. Scatchard plot analysis of cell line NCI-H345 using 125I-labeled IGF-I demonstrated two high affinity specific binding sites (Kd 1.3 and 4.0 nM with maximal rate (Bmax) 200 and 500 fmol/mg protein, respectively). The exogenous addition of IGF-I, IGF-II, or insulin resulted in marked proliferation of human SCLC cells as evaluated using an in vitro growth assay. These peptides stimulated the growth of SCLC cell lines NCI-H82, NCI-H209, NCI-H345, and NCI-N417. The concentration of IGF-I producing maximal SCLC cell growth was 10-100-fold less than that of insulin or IGF-II, whereas the maximal growth stimulated by the optimal concentration of these peptides were similar. An MAb that specifically binds to the IGF-I receptor (but not to the insulin receptor) mediates a dose-dependent inhibition of cell growth in basal media as well as IGF-I, IGF-II, or insulin-supplemented media. The IGF-I receptor thus appears to be the common pathway for the mitogenic activity by IGF-I, IGF-II, and insulin for human SCLC cell lines. The demonstration of an IGF-I precursor molecule, specific IGF-I receptor binding, IGF-I-mediated growth stimulation, and inhibition of basal cell growth by an MAb to the IGF-I receptor suggests that an IGF-I-like molecule can function in vitro as an autocrine growth factor for human SCLC cell lines. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/2839551/Insulin_like_growth_factor_I_can_mediate_autocrine_proliferation_of_human_small_cell_lung_cancer_cell_lines_in_vitro_ L2 - https://doi.org/10.1172/JCI113594 DB - PRIME DP - Unbound Medicine ER -