Interstitial Reactions in the Progress of Gastric Carcinoma

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To clarify the mechanism of the development of gastric carcinona, NKN-28 and KATO-III gastric carcinoma cells of different histological types were grown in synchronous cultures, and the differences in collagen metabolism and GAG (glycosaminoglycans) production were investigated in relation to the cell cycle. The effects of conditioned medium on the collagen metabolism of fibroblasts at various phases of the gastric carcinoma cell cycle were also studied.1) MKN-28, KATO-III and fibroblasts all produced collagen and collagenase and showed high values in the losarithaic growthphase.2) Good synchronization was obtained with both the MKN-28 and KATO-III cells, 87.0% and 74.6%, respectively.3) Collagen metabolism of gastric carcinoma cells was significantly promoted in the S phase (P<0.01) of the cell cycle regardless of the histological type.4) The collagen synthesizing capacity of both poorly and well differentiated types of gastric carcinoma cells was compared at various cell cycles, and … More no significant differences were found.5) Since collagenase activity in the S phase of KATO-III cells of scirrhus gastric carcinoma origin was significantly higher than that in the S phase of 9KN-28 cells of well-differentiated tubular adenocarcinoma origin, it appeared that collagenase is closely related to the type of carcinoma development and that since it causes collagen decomposition it is deeply involved in extensive cancer cell infiltrative growth, one of factors in the mechanism of formation of scirrhus gastric carcinoma.6) Because the conditioned medium of the KATO-III in the S phase promoted collagen synthesis by fibroblasts, it appeared that humoral factors released from carcinoma cells play an important role in the fibroplasia of scirrhus gastric carcinoma.7) GAG production was promoted in the S phase of cell cycle regardless of histological type. Its main component was hyaluronic acid (HA), and HA production in the S phase of KATO-III was higher than that in the S phase of NKN-28. Since accompanying carcinoma cell infiltration and proliferation HA increases and inhibits collagen fibrosis, it is surmised that this facilitates the progress of the carcinoma. Less