Journal Article

Overexpression of midkine in lung tumors induced by <i>N</i>-nitrosobis(2-hydroxypropyl)amine in rats and its increase with progression

Hiroyuki Sakitani, Masahiro Tsutsumi, Kenji Kadomatsu, Shinya Ikematsu, Makoto Takahama, Katsumichi Iki, Toshifumi Tsujiuchi, Takashi Muramatsu, Sdatoshi Sakuma, Toshisuke Sakaki and Yoichi Konishi

in Carcinogenesis

Volume 20, issue 3, pages 465-469
Published in print March 1999 | ISSN: 0143-3334
Published online March 1999 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/20.3.465
Overexpression of midkine in lung tumors induced by N-nitrosobis(2-hydroxypropyl)amine in rats and its increase with progression

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The expression of midkine (MK) in lung tumors induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) in rats was examined. The animals were administered 2000 p.p.m. of BHP in their drinking water for 12 weeks, then maintained without further treatment until being killed 20–28 weeks after the beginning of the experiment. MK mRNA expression of adenocarcinomas and squamous cell carcinomas assessed by means of the reverse transcriptase–polymerase chain reaction and northern blot analysis was significantly higher than in rat embryonic tissues (positive controls) and contrasted strongly with the lack in normal lungs. MK protein was detected immunohistochemically in 58.3% of alveolar hyperplasias, 92.3% of adenomas and 100% of adenocarcinomas and squamous cell carcinomas. The extent of staining significantly increased along with malignant progression in adenomatous (pre-)neoplastic lesions and tended to become more pronounced with malignant progression in squamous lesions. The results suggest that MK may play some essential roles in the development and progression of lung tumors induced by BHP in rats.

Keywords: BHP, N-nitrosobis(2-hydroxypropyl)amine; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; MK, midkine; RT–PCR, reverse transcriptase–polymerase chain reaction; SDS, sodium dodecyl sulfate; SSC, standard saline citrate.

Journal Article.  4007 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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