[Studies on the phenotype deviation of the single-cell subclones of human stomach carcinoma MGC-803 cell line].
The diversity of phenotypes of tumor cells is the main reason for the differences of drug-sensitivity, immunology, metastatic properties and cellular growth rate, and thus raises difficulties in tumor diagnosis and therapy. In order to investigate the mechanisms involved in the expression, correlation, development and regulation of the diversed malignant phenotypes, cell models from single-cell subclones of human stomach carcinoma cell line MGC-803 were studied. According to the growing time needed for the process of separation of each single-cell subclone, they were categoried into 3 groups as fast growing, moderatly and slowly growing subclones and named. From each group, representative subclones were selected--M17 fast. M6 moderate and M3 slow, for further comparative studies. Foci frequency in soft agar was very high with M17, very low with M3, and M6, the middle. The difference in the major transformed phenotype among the 3 subclones were statistically significant. There were differences in the function of gap junctional intercellular communication as detected by scrape-loading and dye transfer method. M17 negative, while M6 and M3 were positive with dye transfer. Immunocytochemical staining of cytoskeleton elements showed heavy disruption of microtubule and microfilament networks and appearance of F-actin aggregates in M17 cells. On the other hand, M3 showed less disruptive changes and more normal appearance of microtubules and microfilament organization. Immunofluorescent staining showed marked differences in gene expression of c-myc, c-Ha-ras and c-met between M17 and M3. M17 expressed intense fluorescence of the 3 onco-proteins while M3 was negative with c-myc and c-Ha-ras, only weak c-met fluorescence in the cytoplasm.
Han
Y L
YL
School of Oncology, Beijing Insititute for Cancer Research, Beijing Medical University.
Zhang
Z Q
ZQ
Cai
X F
XF
Zhang
W J
WJ
Lin
Z X
ZX
D002288:Adenocarcinoma, Mucinous / Q000235:genetics / Q000473:pathology*; D002450:Cell Communication; D002455:Cell Division; D003599:Cytoskeleton; D017629:Gap Junctions; D015870:Gene Expression; D016259:Genes, myc; D011905:Genes, ras; D006801:Humans; D010641:Phenotype; D013274:Stomach Neoplasms / Q000235:genetics / Q000473:pathology*; D014407:Tumor Cells, Cultured