[S-phase arrest associated apoptosis leads to diversities of drug resistance and mutation rate in human breast cancer cells].
To find out different abilities of drug resistance and mutation rate and its fundamental mechanism among the human breast cancer cells, two variants, L-2 and Br-1, derived from a common parent cell line of MDA-MB-435, were assayed for sensitivity to PALA and determined for their mutation rate to drug resistance by clone formation and fluctuation analysis respectively. Further, by means of cell growth rate test, flow cytometry, measurement of DNA fragmentation and western blot, the relationship between drug resistance and mutation rate and cell cycle control and apoptosis was explored. The results showed that the mechanism of S-phase arrest associated apoptosis created such a different ability of drug resistance and stability of genome in two cell lines with identical p53 mutation.
Ying
H
H
Labratory Animal Center, WCUMS, Chengdu 610041.
Subrata
S
S
D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D006801:Humans; D010746:Phosphonoacetic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D017354:Point Mutation / Q000235:genetics; D016196:S Phase; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics
D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53; D001224:Aspartic Acid; C013195:sparfosic acid; D010746:Phosphonoacetic Acid