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. 2018 Jul 6;37(45):5926–5938. doi: 10.1038/s41388-018-0394-x

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© The Author(s) 2018

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. 3 — HMGA1 depletion in MLS trabectedin-resistant cells inhibits cell migration and invasion and favors responsiveness to the drug. a Chemotaxis and chemoinvasion assays were performed to examine the effect of HMGA1 depletion on 402-91 ET cells. Number of migrated and invading cells was presented as the means ± SD of triplicate experiments of each group (P < 0.001 and P < 0.0001, respectively). b Cell death of 402-91 WT and 402-91 ET cells, upon trabectedin treatment for the indicated time, were evaluated by Trypan blue exclusion from three independent experiments (P < 0.0001) (upper panel); total cell lysates were evaluated by WB for the expression of PARP and Hsp70 (lower panel). c 402-91 WT and 402-91 ET cells, upon depletion with HMGA1 expression, were treated for 48 h with trabectedin. Total cell lysates, derived from siScr and siHMGA1 untreated or treated cells were analyzed by WB for the expression of HMGA1, PARP, and Hsp70 (lower panel). Cell death was evaluated by Trypan blue exclusion from three independent experiments (P < 0.001) (upper panel)