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. 2024 Nov 25;14:29133. doi: 10.1038/s41598-024-72408-w

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 5 — SLC4A4 knockdown induces cell cycle arrest in PCa cells by increasing hypophosphorylation of retinoblastoma protein (RB1) (A) SLC4A4 knockdown decreased total RB expression and induced hypophosphorylation at serine 608 (S608) of RB. (B) Co-immunoprecipitation (Co-IP) results showed that SLC4A4 KD stable cells had diminished total RB interaction with the SLC4A4 protein (C) Cell cycle distribution analysis showed the percentage of PCa cells in G0/G1, S and G2/M. SLC4A4 knockdown induced G0/G1 cell cycle arrest in PCa cells. The results are presented as means ± standard error of three independent experiments.