Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: NAT10/ac4C/JunB facilitates TNBC malignant progression and immunosuppression by driving glycolysis addiction

Fig. 7

NAT10 contributed to glycolysis elevation and T-cell inhibition by upregulating JunB expression. A Quantification of lactate production in control and remodelin treatment of mice serum. B Quantification of lactate production in the supernatant. C-F Glycolytic stress tests using the Seahorse XF bioanalyzer to measure the glycolysis level, glycolytic capacity, and reserve. GH Primary T cell was incubated with CM from NAT10-Kd or JunB-OE cells. T-cell activation was detected by flow cytometry. The data are shown as the means ± SDs; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

Back to article page