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. 2022 Jan 31;41:44. doi: 10.1186/s13046-022-02252-1

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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. 1 — TRPM7 promotes the growth of ovarian cancer. A A volcano plot displayed the DEGs between sh-control SKOV3 and sh-TRPM7 SKOV3 cells. B GSEA analysis predicted that TRPM7 was involved in cell cycling and positive regulation of cell mitosis and acute inflammatory. C EdU assay exhibited that TRPM7 silencing inhibited cell proliferation. Scale bar = 50 μm. D TRPM7 silencing inhibited the growth of xenograft SKOV3 in vivo. E GO analysis exhibited that the DEGs were enriched in the indicated biological processes in the TRPM7 silencing SKOV3 cells. F Circos plot displayed the relationships between the DEGs and potential functions in TRPM7 silencing SKOV3 cells. (G) GSEA analysis predicted that TRPM7 was involved in the AMPK pathway