The first section is about studies on the in vitro and in vivo anti-tumor activity of PH Ⅱ -7 and it's possible mechanisms, the second section is about identification and validation of drug resistance-related gene candidates with cDNA microarray, which will provide potential new targets for the diagnosis and therapy of clinical drug resistant tumor.
Objective To observe the expression of adhesion molecular integrin β 1 in drug resistant tumor cells and its influence on programmed cell death so as to find a possible way to invert drug resistance.
Conclusion The successful construction of expressive vectors containing MDR1 promoter provides an experimental basis for targeted gene therapy to the multidrug resistant tumor cells.
Results PHⅡ-7inhibited the proliferation of various human tumor cells derived from different tumor cell lines. The IC 50 values varied from0.34~18.61μmol/L. Especially,PHⅡ-7had strong inhibitory effect on multidrug resistant tumor cells,whereas adriamycin(ADR)was resistant.
dah, C. foe, C. dah 1-3 and Cfoe-1 on all tested neoplastic cell lines revealed that they were effective on both drug-resistant tumor and drug-sensitive tumor.
Conclusions: p14 ARF can suppress the growth of the p53 positive tumor cell lines in a p53-relevant manner, while in the p53 negative, drug-resistant tumor cells, p14 ARF has strong inhibitory effect, indicating the inhibitory effect of p14 ARF on growth of drug-resistant tumor cells is independent on p53, at least in KB-v200 and MCF7/ADR drug-resistant cells.
Conclutions TS and p16 double promoters are capable of inducting TK target killing of 5 FU drug fast cancer cells, thus protecting normal cells and improving safety of gene therapy.
We have shown that neither great increase in the level of YB-1 mRNA nor substantial increase in the number of cells with nuclear localization of YB-1 are obligatory traits of drug resistant tumor cell populations.
Our data suggest that although YB-1 regulates several MDR genes, it could not be regarded as a global marker of already formed drug resistant tumor cell populations.
This method can also be used to screen drugs which may block efflux of a chemotherpeutic drug and thus increase chemosensitivity of a drug resistant tumor.
Anexperimental anti-cancer drug, SH 30demonstrated highly selective and potentcytotoxic activity against a number ofmulti-drug resistant tumor cell lines in vitro.
The unresponsiveness of multidrug resistant tumor cells to antineoplastic chemotherapy is often associated with reduced cellular drug accumulation accomplished by overexpressed transport molecules.
Studies in multidrug resistant tumor models confirm P-gp as the in vivo target of PSC-833 and demonstrate the ability of PSC-833 to reverse MDR leukemias and solid tumors in mice.
The inhibition of these anti-apoptotic gene products by rituximab sensitizes drug-resistant tumor cells to apoptosis induced by a variety of cytotoxic chemotherapeutic drugs.
All pleiotropic (PDR) drug-resistant tumor sublines had decreased membrane potentials (membrane depolarized) compared with their corresponding drug-sensitive parental tumors.