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. 2022 Feb 21;12:2928. doi: 10.1038/s41598-022-06621-w

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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 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/.

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LEPRE1 regulates drug responsiveness in lung cancer-derived A549 cells. (a) LEPRE1 overexpression (left side) or LEPRE1 knockdown (right side) A549 cells were treated with pelitinib for 3 days. Cell viability was determined using WST-1 proliferation assays. (b) A549 cells were transfected with pcDNA3.1 and LEPRE1/pcDNA3.1 or with Negative control siRNA and LEPRE1 siRNA, as indicated. After 48 h, EGFR, AKT, and ERK expression were determined by western blot analysis. (c,d) A549 cells were transfected with pcDNA3.1 and LEPRE1/pcDNA3.1 (c) or with Negative control siRNA and LEPRE1 siRNA (d) and then treated with EGF and/or the indicated concentration of pelitinib (0, 0.1, 1, 10 μM) for 24 h. Cell extracts were prepared and immunoblotted using the indicated antibodies. GAPDH was used as an internal control. All western blots are pre-cut. Membranes were often stripped and reprobed for multiple antibodies.