Characteristics of three human gastric cancer cell lines, NU-GC-2, NU-GC-3 and NU-GC-4

Abstract

Three human gastric cancer cell lines, NU-GC-2, NU-GC-3 and NU-GC-4 were established in vitro from the cancer tissues obtained from 3 patients during surgery. The pathological findings of the gastric tumors of these cases revealed poorly differentiated adenocarcinoma (and partial signet-ring cell carcinoma in the case of NU-GC-4). NU-GC-2 and NU-GC-4 were originally obtained from metastatic paragastric lymph nodes and NU-GC-3 was obtained from a metastatic tumor in the brachial muscle. The cells of NU-GC-2 and NU-GC-3 are polygonal in shape and grow as a monolayer sheet. NU-GC-4 cells, however, are mainly spherical in shape with a few free floating cells. Electron microscopy revealed epithelial characteristics in all 3 cell lines. The average doubling time of NU-GC-2 was 36.1 hours, that of NU-GC-3 was 38.2 hours and that of NU-GC-4 was 29.9 hours. The modal chromosome number of NU-GC-2 was 62, that of NU-GC-3 was 58 and those of NU-GC-4 grown in in vitro and in vivo were 52-54 and 53, respectively. In vitro and in vivo lines of NU-GC-4 were established from the same tumor. These two cell lines are quite similar in morphology, but slightly different in karyotype. The in vitro sensitivity to anticancer agents was highest in NU-GC-4 and lowest in NU-GC-2. Of the anticancer agents, mitomycin C and adriamycin were most effective on the cells of all 3 cell lines.

A novel DNA topoisomerase inhibitor: dehydroebriconic acid, one of the lanostane‐type triterpene acids from Poria cocos

“…We also analyzed the kinetics of compound 5, and obtained similar results (data not shown). In the kinetic analysis, poly(dA)/oligo(dT) [12][13][14][15][16][17][18] and dTTP were used as the DNA template-primer and nucleotide substrate, respectively. Double-reciprocal plots of the results show that inhibition of pol α activity by compound 6 was noncompetitive with the DNA template and the nucleotide substrate.…”

“…Activities of DNA polymerases were measured by the methods described previously. 24,25) The substrates of DNA polymerases used were poly(dA)/oligo(dT) [12][13][14][15][16][17][18] and dTTP as template-primer DNA and nucleotide substrate, respectively. One unit of each DNA polymerase activity was defined as the amount of enzyme that catalyzes the incorporation of 1 nmol of deoxyribonucleotide triphosphate (i.e., dTTP) into the synthetic template-primers (i.e., poly(dA)/oligo(dT) [12][13][14][15][16][17][18] , A/T=2/1) in 60 min at 37°C under the normal reaction conditions for each of the enzymes.…”

“…Therefore, information concerning the structural characteristics of these inhibitors may provide valuable insight for the design of new anti-cancer agents. [12][13][14][15][16][17][18] were purchased from Amersham Biosciences (Buckinghamshire, UK). Supercoiled pUC19 plasmid DNA was obtained from TaKaRa (Tokyo).…”

“…All other reagents were of analytical grade and were purchased from Wako Chemical Industries. NUGC-3, a human gastric cancer cell line (JCRB0822), 15) was supplied by the Health Science Research Resources Bank.…”

Clinicopathologic significance of sialyl Le xexpression in advanced gastric carcinoma

“…Some authors have subsequently described that CD44H Table 6 Relationship between SLX staining status and postoperative liver metastasis and peritoneal dissemination in patients with curative resection plays an important role in peritoneal dissemination of a gastric carcinoma (Nishimura et al, 1996;Nakashio et al, 1997). Using a gastric carcinoma cell line which was established from undifferentiated carcinoma (Akiyama et al, 1988) and had a high potential for peritoneal dissemination, Nakashio et al (1997) indicated that both CD44H and β 1 integrin were involved in peritoneal dissemination. Interestingly, their flow-cytometric analysis indicated that SLX expression was weak in the gastric carcinoma cells with a high potential for peritoneal dissemination, and that peritoneal dissemination was not inhibited by anti-SLX antibody.…”