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. 2022 Jun 21;22:679. doi: 10.1186/s12885-022-09789-6

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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. 5 — A schema of the function and role of LSR in endometrial cancer. LSR is highly expressed in endometrial cancer cells and regulates cell proliferation, invasion, and migration through the MEK/ERK signaling pathway and subsequent MT1-MMP and MMP2. By these mechanisms, LSR contributes to a poor prognosis of patients with endometrial cancer. The newly developed anti-LSR monoclonal antibody which exerted a significant antitumor effect in the xenograft mouse model has the potential to be a novel therapeutic agent for endometrial cancer