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. 2022 Dec 16;128(5):896–906. doi: 10.1038/s41416-022-02095-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a The expression of BCKDK and BCKDH were determined by western blotting of protein lysates from the indicated cell lines. The results shown are representative of the three experiments and were also quantified (Fig. S1). b, c The sensitivity of OVCAR-4 (b) or MCF-7 (c) cells to paclitaxel was measured in cell growth assays after knockdown of BCKDK with 3 separate siRNA. The relative cell number was determined by staining with SRB and the results (mean ± S.D., n = 3) were normalised to the absorbance measured in the absence of paclitaxel (labelled “C” on the axis). d, e The potency of paclitaxel in cell growth assays using the indicated ovarian (d) or breast cancer cells (e) after knockdown of BCKDK with siRNA was quantified. The results (mean IC₅₀ ± S.D., n = 3) are significantly different from those measured in cells transfected with a non-targeting siRNA (NT-1; ***P < 0.001; **P < 0.01; *P < 0.05; paired t test) where indicated. f BCAA were measured in either OVCAR-4 or MCF-7 cells exposed to 100 µM CMVA or DCBC for 48 h and intracellular BCAA measured. The results (mean ± SD, n = 3) were normalised to total protein per well and are significantly different to that measured in cells treated with the drug vehicle as indicated (*P < 0.05; **P < 0.01 paired t test). g Combinations of paclitaxel and the indicated concentrations of either CMVA or DCBC (which on their own inhibited cell growth by <5%) were assessed in cell growth assays and the combination index determined. The results (mean ± S.D., n = 3) were significantly different from unity were indicated (***P < 0.001; **P < 0.01; *P < 0.05; paired t test). h Combinations of paclitaxel and either CMVA or DCBC (both 100 µM) in the presence or absence of exogenous BCAA (1 mM) were assessed in cell growth assay. The combination index (mean ± S.D., n = 3) were significantly altered by the inclusion of exogenous BCAA where indicated (***P < 0.001; **P < 0.01; *P < 0.05; paired t test).