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. 2021 Mar 5;6:108. doi: 10.1038/s41392-021-00495-6

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© The Author(s) 2021

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. 8 — Regulation of SRSF1 in autophagy in cancer cells. a In normal conditions, SRSF1 disrupts the interaction between Beclin1 and PIK3C3 through promoting the production of Bcl-xL and directly binding to PIK3C3, thereby suppressing autophagy and stimulating gefitinib-resistant cancer cell proliferation. b Under starvation conditions, SRSF1 is degraded via starvation-induced autophagy, thus to stimulate the formation of Beclin1-PIK3C3 complex and activate autophagy. The resulting gefitinib-resistant cancer cells will be eliminated through autophagy