Kumala Sławomir, Niemiec Paweł, Wideł Maria, Hancock Ronald, Rzeszowska-Wolny Joanna
Department of Experimental and Clinical Radiobiology, Center of Oncology, Wybrzeze AK 15, 44-100 Gliwice, Poland.
Cell Mol Biol Lett. 2003;8(3):655-65.
We compared the extent to which apoptosis is induced and clonogenicity reduced in three tumour cell lines - the human melanoma Me45 and promyelocytic leukaemia HL-60, and the rat rhabdomyosarcoma R1 - after exposure to the anticancer drugs etoposide and cis-platinum or to gamma radiation; each induces different types of DNA damage. Cells which readily underwent apoptosis did not necessarily show a correlated loss of clonogenicity; for example, Me45 cells showed the highest sensitivity to all three agents in clonogenic assays but much lower levels of apoptotic cells than R1 or HL-60 cells. These results show that the efficiency of the eradication of clonogenic cells by genotoxic agents does not solely depend on the induction of apoptotic processes, and suggest that the induction of apoptosis and suppression of clonogenicity are independent processes.
我们比较了三种肿瘤细胞系——人黑色素瘤Me45、早幼粒细胞白血病HL-60以及大鼠横纹肌肉瘤R1,在暴露于抗癌药物依托泊苷和顺铂或γ射线后,诱导凋亡的程度以及克隆形成能力降低的程度;每种处理诱导不同类型的DNA损伤。容易发生凋亡的细胞不一定表现出克隆形成能力的相应丧失;例如,在克隆形成试验中,Me45细胞对所有三种试剂的敏感性最高,但凋亡细胞水平比R1或HL-60细胞低得多。这些结果表明,遗传毒性试剂根除克隆形成细胞的效率并不完全取决于凋亡过程的诱导,并表明凋亡的诱导和克隆形成能力的抑制是独立的过程。