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. 2019 Apr 9;9:5839. doi: 10.1038/s41598-019-42303-w

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© The Author(s) 2019

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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Reduced B7-H3 levels abolish dacarbazine (DTIC) resistance in DTIC resistant cells. FEMX-V cells with sensitivity (FEMX-V sensitive) or induced resistance to DTIC (FEMX-V DR), where knocked down for B7-H3. (A) Representative immunoblot of B7-H3 and α-tubulin expression in the four FEMX-V cell variants. (B) When these cells were subjected to DTIC treatment, little effect of DTIC was seen in the ability of drug resistant DR and DR shSCR cells to form colonies. FEMX-V DR shB7-H3 cells, however, displayed a reduced capacity to form colonies. Results show the average of two independent experiments ± SEM. (C) This effect was also seen in vivo, where FEMX-V shB7-H3 cells and FEMX-V sensitive cells displayed reduced relative tumor growth ± SEM compared to FEMX-V DR and FEMX-V DR shSCR cells (n = 7–8 in each group).