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. 2023 Jun 8;13:103. doi: 10.1186/s13578-023-01061-z

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© The Author(s) 2023

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 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. 7 — Silencing CAV2, PHLDA1, and VDAC3 separately significantly increases sensitivity to cisplatin. A–C qRT-PCR and Western blot showing CAV2, PHLDA1, and VDAC3 knockdown 48 and 72 h after transfection with CAV2-targeting, PHLDA1-targeting and VDAC3-targeting siRNAs. D: cytotoxicity curves of the LUAD cell lines A549, PC9 and ESCC cell line TE1 transfected with nontargeting (ctrl) or CAV2-targeting, PHLDA1-targeting and VDAC3-targeting siRNAs and treated for 48 h with different concentrations of cisplatin (0, 2.5, 5, 10, 20, 40 μM). E EdU for A549, PC9 and TE1 transfected with nontargeting (ctrl) or CAV2-targeting, PHLDA1-targeting and VDAC3-targeting siRNAs and treated for 48 h with cisplatin (10 μM)