Ovarian carcinoma cell line, inhibition

Fig. 3. Cross-resistance profiles for the 41M/41McisR, CH 1/CH1 c sR and A2 780/A2780cisR pairs of human ovarian-carcinoma cell lines for cisplatin itself carboplatin, tetraplatin (1,2-diaminocyclohexane)tetrachloroplatinum(IV)), JM216, JM118 (the major metabolite of JM216) andAMD473. Resistance Factor = IC50 resistant/parent cell line. Drug exposure was for 96 h, sulforhodamine B growth-inhibition assay, bars = SEM, n = 3-4.

Comparisons of reactions of cis- versus fran -DDP with sulfur donors and other cellular components may afford some insight into their relative biological effects, however. /rans-DDP is much more reactive than the cis isomer with GSH (6, 27). Depletion of GSH with use of the inhibitor BSO had no effect on the cisplatin sensitivity of two human ovarian carcinoma cell lines, but made them 2.7 times more sensitive to trans-DY) (4). In a related finding, it was necessary to add 14 times more trans- than ds-DDP to cells in culture to achieve the same percent inhibition of in vivo SV40 DNA replication (23). These results suggest that part of the differential activity of these isomers in biological systems may arise from the differential reactivity of fran -DDP toward cellular components other than DNA. Thus trani-DDP could be more effectively inactivated prior to encountering DNA, or be better blocked as monofunctional platinum-DNA cross-links. 

Many HATs are involved in cancer pathogenesis and several are proposed as cancer biomarkers due to correlations of expression levels with outcomes, including a positive correlation between p300 expression levels and prostate cancer recurrence, and a negative correlation between hMOF and primary breast carcinomas. A series of isothiazolone PCAF-p300 inhibitors has shown inhibition of growth of a panel of colon and ovarian tumour cell lines. ... 

Additionally, several reports indicate that -resveratrol inhibits the proliferation of a wide variety of human cancer cells including breast, prostate, colon, gastric, lung, pancreatic, liver, thyroid, and ovarian cancers, leukemia, lymphoma, osteosarcoma, squamous cell carcinoma, multiple myeloma, and medulloblastoma [135]. Among the other stilbenoids, piceatannol, a- and s-viniferin, hopeaphenol, pallidol, ampelopsin A, vaticanol B and C, and pterostilbene also showed cytotoxicity and/or antiproliferative effect on different tumor cell lines [136-145]. 

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