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. 2022 Aug 10;41:241. doi: 10.1186/s13046-022-02443-w

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Targeted inhibition of CDK7 reverses chemoresistance in pancreatic cancer. A Western blotting of TB32047 and MIA PaCa-2 gemcitabine- and paclitaxel-resistant cells (TBGPR, MIAR) and parental cells (TBWT, MIAWT). B The CDK7 inhibitor THZ1 synergistically enhances the antiproliferative effects of GEM and PTX in TBGPR and MIAGPR cells. The proliferation was determined after 72 h of treatment with THZ1 and GEM/PTX alone or in combination. Below is a plot of the fraction impacted versus the combination index. CI < 1.0, synergism. C Diagrammatic representation of the research outcome. Gemcitabine and paclitaxel combined with CDK7 inhibition induces DNA damage, G2-M arrest, and subsequent apoptosis