Fig. 8: Clinical implication and plausible action mechanism of vimentin in promoting metastasis and immune suppression. | Cell Death & Differentiation

Fig. 8: Clinical implication and plausible action mechanism of vimentin in promoting metastasis and immune suppression.

From: PLK1/vimentin signaling facilitates immune escape by recruiting Smad2/3 to PD-L1 promoter in metastatic lung adenocarcinoma

Fig. 8

a Clinical association between the expression of PLK1/VIM/CD274 and the cumulative OS times of LUAD patients. The survival times of all (n = 631), stage 1 (n = 346), and stage 2 (n = 118) LUAD patients were analysed according to their PLK1/VIM/CD274 expression levels using KM PLOTTER. High (Hi) vs. low (Lo) expression was split by mean value. n.s., not significant. b Phosphorylation of vimentin by PLK1 at S339, T327, and S83 facilitates metastatic tumorigenesis and immune escape through the activation of TGF-β/Smad signaling and the expression of PD-L1 in LUAD. p-Vimentin S339 upregulates PD-L1 by activating Smad2/3 and interacting with p-Smad2 for nuclear translocation, where it recruits them to the PD-L1 promoter regions for transcriptional activation, immune escape, and tumor survival. Vimentin acts as a coordinator for metastatic tumorigenesis in LUAD via its phosphorylation, activation of TGF-β signaling for metastasis, and interaction with p-Smad2/3, which it recruits to the PD-L1 promoter for tumor survival.

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