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Although these results do not rule out a contribution from tumor cell extrinsic responses to the Hipp+Dxr-response in vivo, they do indicate that components of the intrinsic cell death pathway are major modifiers of the Hipp+Dxr synergy response in vivo and do so at least in part by affecting cell sensitivity to Hipp and Dxr.
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We also examined how NHERF1 expression status affects cell sensitivity to PDGFR inhibitor.
MF may inhibit A549 cells and can increase their sensitivity to RT, possibly by affecting cell cycle- and apoptosis-related signaling pathways.
Since the TF-1 erythroleukaemia cell line is relatively resistant to apoptosis induced by TNF, we first investigated whether sublethal concentrations of mithramycin would affect cells sensitivity to TNF-mediated apoptosis.
Finally, several studies suggest that vitamin D could play a role in the pathogenesis of diabetes mellitus type 2 by affecting insulin sensitivity of β cell function [ 36, 37].
Vitamin D deficiency is thought to influence insulin resistance and the pathogenesis of T2DM by affecting either insulin sensitivity, β-cell function, or both.
Altogether, these results suggest that MT2A silencing in osteosarcoma cells does not significantly affect cell viability but can enhance sensitivity to drugs such as doxorubicin by facilitating its interaction with DNA.
Since WRN affected cell growth of sgs1 top3, we next examined its effect on drug sensitivity.
Thus, lack of Hif1a may not affect cell proliferation but rescues rods by preventing cell death.
B9 affects cell growth directly.
Researchers led by members of the Department of Systems Biology at Harvard Medical School had been studying how silencing MDMX, an oncogene, affected the dynamics of p53, a natural tumor suppressor, in cancer cells when they realized those dynamics might affect the cells' sensitivity to a second, chemotherapy-like treatment.
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