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. 2022 Jan 17;29:3. doi: 10.1186/s12929-022-00787-1

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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. 9 — Clinical relevance. Samples obtained from lung cancer patients were used to study the mRNAs of Sp1 and CD44 including the standard form (CD44s) and short form (CD44st) by q-PCR. After three independent experiments were completed, the results were quantitated, and statistical analysis was performed with a Pearson Correlation analysis, r < 0: negative correlation (A). Samples of normal and tumor tissues obtained from 8 cohorts were used to study the levels of Sp1 and CD44 by Western blotting with anti-Sp1 and anti-CD44 antibodies (B). The levels of Sp1 and CD44 in 51 lung cancer clinical cohorts were studied by IHC. All the cohorts were divided into two groups, high and low, based on the signal (C, a), and the survival rates (C, b) of women and men with lung cancer based on Sp1 and CD44 levels were analyzed. The survival rates of younger (< 55 years) lung cancer patients with Sp1-low or Sp1-high (C, c), Sp1-low/CD44-high or Sp1-high/CD44-low (C, d) levels were analyzed with Kaplan–Meier survival curves. Working model: E2 increases RNF4 expression to enhance Sp1 degradation, thereby decreasing miR-3194-5p expression and resulting in an increase in CD44 expression in younger female lung cancer patients (D)