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. 2023 Apr 14;13:73. doi: 10.1186/s13578-023-01020-8

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© The Author(s) 2023

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. 8 — Malignancy reppression and ferroptosis facilitation of BCL6 in GC cells are down-regulated by RhoC. A, B BCL6 depletion reversed the inhibition of cell proliferation, migration and invasion induced by RhoC depletion in AGS and SGC-7901 cells (Scale bar, 100 μm) (*p < 0.05, **p < 0.01, ***p < 0.001). C, D BCL6 depletion reversed cell death induced by erastin or RSL3 in RhoC-depleted AGS and SGC-7901 cells (***p < 0.001)