Preferential Alternative Splicing in Cancer Generates a K-sam Messenger RNA with Higher Transforming Activity

Hiroshi Itoh, Yutaka Hattori, Hiromi Sakamoto, Hideshi Ishii, Tatsuya Kishi, Hiroki Sasaki, Teruhiko Yoshida, Masashi Koono, Takashi Sugimura, Masaaki Terada

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

K-sam, also designated fibroblast growth factor receptor 2/BEK, was originally cloned from a stomach cancer cell line KATO-III. The gene is amplified and overexpressed preferentially in poorly differentiated types of stomach cancers. The major K-sam transcript in KATO-III cells encodes a receptor protein with a truncated carboxyl terminus and with a high-affinity binding site for keratinocyte growth factor. This truncated type is produced by an alternative splicing mechanism, and in normal tissues, the truncated type is far less prevalent than the untruncated form. The variant K-sam complementary DNA lacks tyrosine 769, which is a putative phospholipase Cγ1 association site, and showed a higher transforming activity to NIH3T3 cells than the untruncated form, which is identical with the keratinocyte growth factor receptor.

Original languageEnglish
Pages (from-to)3237-3241
Number of pages5
JournalCancer Research
Volume54
Issue number12
Publication statusPublished - 1994 Jun 15
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Preferential Alternative Splicing in Cancer Generates a K-sam Messenger RNA with Higher Transforming Activity'. Together they form a unique fingerprint.

  • Cite this

    Itoh, H., Hattori, Y., Sakamoto, H., Ishii, H., Kishi, T., Sasaki, H., Yoshida, T., Koono, M., Sugimura, T., & Terada, M. (1994). Preferential Alternative Splicing in Cancer Generates a K-sam Messenger RNA with Higher Transforming Activity. Cancer Research, 54(12), 3237-3241.