
Stimulatory Effect of Interleukin‐1α on Proliferation through a Ca 2+ /Calmodulindependent Pathway of a Human Thyroid Carcinoma Cell Line, NIM 1
Author(s) -
Inokuchi Nobuo,
Zeki Kazuya,
Morimoto Isao,
Nakano Yoichiro,
Fujihira Takashi,
Yamashita Uki,
Yanagihara Nobuyuki,
Izumi Futoshi,
Eto Sumiya
Publication year - 1995
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1995.tb02451.x
Subject(s) - endocrinology , medicine , calmodulin , cell culture , nicardipine , cell growth , protein kinase c , signal transduction , cytokine , biology , microbiology and biotechnology , chemistry , calcium , biochemistry , genetics , blood pressure
NIM 1 cells, a human thyroid cell line established from a patient with thyroid papillary adenocarcinoma, produce cytokines such as interleukin‐1α (IL‐1α) and granulocyte‐colony stimulating factor. In the present study, we investigated the signal transduction pathway in the proliferation of NIM 1 cells evoked by IL‐1α. Incubation of NIM 1 cells with IL‐1α for 48 h increased the incorporation of 3 H‐thymidine ( 3 H‐TdR). The stimulatory effect of IL‐1α was evident at 0.01 ng/ml and the maximal effect was seen at 10 ng/ml. IL‐1α evoked an influx of 45 Ca into NIM 1 cells within 3 min in a concentration‐dependent manner (0.01–1 ng/ml). These stimulatory effects of IL‐1α on both 3 H‐TdR incorporation and 45 Ca influx were similarly inhibited by nicardipine, an inhibitor of voltage‐dependent Ca 2+ channels, in a concentration‐dependent manner (10–1000 nM). The stimulatory effect of IL‐1α on 3 H‐TdR incorporation was inhibited by N‐(6‐aminohexyl)‐5‐chloro‐1‐naphthalenesulfonamide (W‐7), an antagonist of calmodulin, but not by 1‐(5‐isoquinoline sulfonyl)‐2‐methylpiperazine (H‐7), an inhibitor of protein kinase C. While the culture medium initially contained 0.75 m M Ca 2+ , inhibition of 3 H‐TdR incorporation by nicardipine and W‐7 under these baseline conditions was also recognized. These results suggest that IL‐1α stimulates cell proliferation through a Ca 2+ /calmodulin‐dependent pathway in NIM 1 cells.