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. 2021 Apr 23;21:456. doi: 10.1186/s12885-021-08202-y

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© The Author(s) 2021

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 — GNA14 upregulates KLF7 in UCEC. a and b The correlation between GNA14 expression and KLF7 expression was analyzed in normal samples (A, R = 0.59, p = 0.035) and UCEC samples (B, R = 0.2, p = 0.0081) from TCGA database. c IHC staining of GNA14 and KLF7 in UCEC (n = 20) and normal (n = 15) samples. Left, representative images of IHC staining. Right, quantification results of GNA14 and KLF7 in cancer and normal tissues. Spearman correlation between KLF7 and GNA14 was analyzed in cancer and normal samples based on IHC staining. d and e qRT-PCR (d) and immunoblotting (e) analysis of GAN14 and KLF7 in GAN14 knockdown and overexpressed Hec-1-A and KLE cells. GAPDH acts as the internal control. **p < 0.01