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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: PM2.5 promotes NSCLC carcinogenesis through translationally and transcriptionally activating DLAT-mediated glycolysis reprograming

Fig. 5

DLAT promotes the malignancy of NSCLC cells and correlates with glucose metabolism and poor prognosis in NSCLC patients. A, B Overexpression of DLAT promoted cell proliferation of NSCLC cells. C, D Knockdown of DLAT suppressed cell proliferation of A549 and PC9 cells. E, F Up-regulation of DLAT reduced apoptosis rate of PC9 and A549 cells. G, H Depletion of DLAT increased apoptosis rate of NSCLC cells. I Representative 18F-FDG PET/CT images in patients with NSCLC tumors exhibiting low or high expression of DLAT. J The expression levels (% of positive cells) of DLAT in tumor tissues were positively correlated with the SUVmax values in patients with NSCLC. K Analysis of SUVmax in the DLAT low and DLAT high groups. L DLAT expression levels in NSCLC tumor tissues increased as NSCLC progressed to more advanced stages. M Representative pictures showing that IHC signals of DLAT (brown staining) was increased along with the tumor stages of NSCLC. N Kaplan-Meier analysis showed that elevated expression of DLAT was associated with poorer overall survival (OS) in NSCLC patients. Data shown are mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

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