Bax is an important determinant of chemosensitivity in pediatric tumor cell lines independent of Bcl-2 expression and p53 status.

作者: McPake Cr , Houghton Ja , Poquette Ca , Harris Lc , Tillman Dm

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摘要: Susceptibility of a tumor cell to undergo chemotherapy-induced apoptosis appears be dependent upon the balance proapoptotic and survival factors that are expressed within any given cell. We have chosen evaluate how expression several these proteins influences chemosensitivity panel 10 pediatric lines from three histiotypes: neuroblastoma, rhabdomyosarcoma, glial tumors. The evaluated were p53 six members Bax/Bcl-2 family: (Bax, Bak, Bcl-xS) (Bcl-2, Bcl-xL, Mcl-1). investigated whether there was relationship between endogenous (or resistance) chemotherapeutic agents directly damage DNA (doxorubicin, actinomycin D, topotecan) mitotic spindle poison (vincristine). Even though exogenous overexpression wild-type has been associated with chemosensitive phenotype in model systems we demonstrated no such studies. In addition, levels Bcl-2, Bcl-xS, or Mcl-1 did not correlate sensitivity resistance four drugs. However, statistically significant correlation Bax protein both doxorubicin D. conclude even many as Bcl-2 shown influence drug response when exogenously overexpressed systems, unmodified may generate same results. only found across different histiotypes propose analysis more useful prognostic indicator for therapy than either Bcl-2.

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