Fig. 8: KMT5A expression was significantly correlated with activated MARK4/YAP signaling in triple-negative breast cancer.
From: KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling
a Representative images of KMT5A, SNIP1K301me1, and MARK4 in 100 clinical TNBC metastatic lymph node tissues. Scale bars, 50 μm. b Correlation of expression levels between KMT5A, SNIP1K301me1, and MARK4 in (a). c Prognosis comparison of breast cancer patients with KMT5A/SNIP1K301me1 or KMT5A/MARK4 ectopic differential expression using Kaplan–Meier survival analysis. d Representative immunoblots showing KMT5A, SNIP1K301me1, and MARK4 expression in normal breast specimen (N) and paired tumor tissues (T) (n = 3). e Correlation between TNBC stages and IHC scores of KMT5A and SNIP1K301me1. f Representative IHC staining of KMT5A, SNIP1K301me1, and MARK4 in primary TNBC and matched metastatic lymph nodes (n = 100 paired samples). Scale bars: 50 μm. g A working model of KMT5A-promoted Hippo/YAP signaling pathway modification and triple-negative breast cancer metastasis through the SNIP1 methylation status. KMT5A methylated SNIP1 at K301, which released KAT2A for activated histone acetyltransferase (HAT) and recruited by c-MYC, leading to enhanced KAT2A anchoring onto the MARK4 promoter and MARK4 transcription, ultimately activating the Hippo/YAP signaling pathway. Data information: In (b), Statistical analysis was performed by chi-square test. In (c), by log-rank test. In (e), by two-tailed t-test. *P < 0.05, ***P < 0.001. Data are represented as mean ± SEM. Panel (d) shows one experiment representative of three independent experiments with similar results.
