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Szumiel I Jaworska A Kapiszewska M John A Gradzka I Sochanowicz B 《Radiation and environmental biophysics》2000,39(1):33-40
We examined apoptosis and expression of p53, E2F-1, bax, bclxL and bcl2 proteins in two L5178Y (LY) murine lymphoma sublines, LY-R and LY-S, which differ in radiosensitivity and double-strand
break (DSB) repair. Both sublines are heterozygous for a p53 mutation in codon 170 that precludes the transactivation function.
Accordingly, there is no G1/S arrest after irradiation.We found that there is no change in expression of E2F-1, bax, bclxL or bcl2 proteins in both LY sublines after x-irradiation. LY-R cells do not constitutively express bcl2, whereas both sublines
show high bax content. Radiation induces delayed apoptosis to a greater extent in LY-S than in LY-R cells. The apoptosis can
be seen 24 h after irradiation (2 Gy) of LY-S cells, with a maximum at 48 h. LY-R cells need 5 Gy and 72 h post-irradiation
incubation to show marked apoptosis (identified by the TUNEL method). The reported observations support the assumption that
differential radiosensitivity of LY sublines is associated with the induction of apoptosis that is not related to transactivation
by p53 and is primarily related to differential DNA repair ability.
Received: 19 August 1999 / Accepted in revised form: 30 November 1999 相似文献
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S. Colak 《Cell cycle (Georgetown, Tex.)》2016,15(12):1531-1537
There is increasing evidence that cancers are heterogeneous and contain a hierarchical organization consisting of cancer stem cells and their differentiated cell progeny. These cancer stem cells are at the core of the tumor as they represent the clonogenic cells within a tumor. Moreover, these cells are considered to contain selective therapy resistance, which suggests a pivotal role in therapy resistance and tumor relapse. Here we show that differentiated cells can re-acquire stemness through factors secreted from fibroblasts. This induced CSC state also coincides with re-acquisition of resistance to chemotherapy. Resistance induced in newly formed CSCs is mediated by the anti-apoptotic molecule BCLXL and inhibition of BCLXL with the BH3 mimetic ABT-737 sensitizes these cancer cells toward chemotherapy. These data point to an important interplay between tumor cells and their microenvironment in the regulation of stemness and therapy resistance. 相似文献
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