Upon binding of interferon (IFN) and epidermal growth factor (EGF) to their cell surface receptors, tyrosine phosphorylation of latent cytoplasmic Stat91 (Ras-independent signal transducer and activator of transcription, Stat1 alpha) protein is promptly induced and translocate from the cytoplasm to the nucleus to transduce the signal. The expression of mRNA for Stat91 was examined in 8 gastric carcinoma cell lines and 21 gastric carcinoma tissues as well as corresponding normal mucosa. Of the 8 gastric carcinoma cell lines, all expressed a 4.7 kb Stat91 mRNA and a 91 kD protein at various levels. In gastric carcinoma cell lines, the levels of Stat91 mRNA expression were compatible with those of Stat91 protein expression. In surgical cases, all the gastric carcinoma tissues and their adjacent non-neoplastic mucosa expressed Stat91 mRNA and protein. Interestingly, 14 (66%) out of 21 tumors expressed Stat91 mRNA at higher levels than their corresponding normal mucosas. Moreover, 6 (75%) of 8 tumor tissues expressed higher levels of Stat91 protein as compared with those of the corresponding normal gastric mucosa. No significant correlation was detected between the expression of Stat91 and clinicopathological feature of gastric carcinoma. These results suggest that the majority of gastric cancer in vivo harbour overexpression of Stat91 as a signal transducer in response to various cytokines or growth factors which may be implicated in the growth of gastric cancer.

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