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. 2023 Jul 24;13:11922. doi: 10.1038/s41598-023-39093-7

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© The Author(s) 2023

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 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/.

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The knockdown of GGCT inhibits the MEK-ERK pathway and activates the RB protein. (a) The viability of PC3, J82, A498, and A549 cells treated with control siRNA or the indicated GGCT siRNAs for 120 h was examined by the CCK-8 assay. A one-way ANOVA with Dunnett’s test was used (versus control, N = 5 per group, ****p < 0.0001). The error bars represent the S. D. (b) A Western blot analysis of GGCT, pMEK Ser217/221, pERK Thr202/Tyr204, pRB Ser780, and their non-phosphorylated forms in PC3, J82, A498, and A549 cells treated with control siRNA or the indicated GGCT siRNAs for 72 h. Vinculin is shown as a loading control. All full-length blots are presented in Supplementary Fig. S4. (c) A Western blot analysis of GGCT, pRB Ser780, and its non-phosphorylated form in control or GGCT-overexpressing NIH3T3. Vinculin is shown as a loading control. All full-length blots are presented in Supplementary Fig. S4.