Fig. 7: Correlations among ENSA, SREBP2, pSTAT3-Tyr705 and survival in clinical samples. | Nature Communications

Fig. 7: Correlations among ENSA, SREBP2, pSTAT3-Tyr705 and survival in clinical samples.

From: Copy number amplification of ENSA promotes the progression of triple-negative breast cancer via cholesterol biosynthesis

Fig. 7

a, b Representative IHC images (a) and IHC scores (b) of ENSA staining in 8 paired TNBC tissues and adjacent normal tissues. n = 8 paired samples. Two-tailed paired Student’s t test. c Immunohistochemical staining of ENSA in 138 TNBC specimens. Representative images are shown. Scale bars, 100 µm. d Kaplan–Meier analysis of the relapse-free survival and overall survival of 138 TNBC patients. A log-rank test was used to determine the statistical significance between the low-ENSA expression group (n = 96) and the high ENSA expression group (n = 42). e IHC staining of SREBP2 and pSTAT3-Tyr705 in 138 TNBC specimens. Representative images are shown. Scale bars, 100 µm. n = 138 samples. f Correlation analysis of ENSA with SREBP2 and pSTAT3-Tyr705 expression levels in 138 TNBC tissues. Correlation coefficients were calculated using the Spearman test. Two-tailed P-values were given. g Proposed working model. In TNBC, ENSA is amplified, highly expressed and inhibits the function of PP2A, resulting in STAT3 Tyr705 phosphorylation and activation. STAT3 activation induces SREBP2 transcription to upregulate cellular cholesterol biosynthesis and facilitate tumor progression. Inhibition of STAT3 signaling with Stattic might serve as an effective treatment strategy for 1q21.3-amplified and ENSA-highly expressed TNBC. Source data are provided as a Source Data file. IHC immunohistochemistry, Amp amplification, SRE sterol regulatory element.

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