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. 2023 Mar 14;13:1123192. doi: 10.3389/fonc.2023.1123192

Figure 2.

Figure 2

Glutamine metabolism in tumor metastases. (A) In lung, the expression of ASCT2 can maintain the intracellular glutamine level by seizing in the microenvironment. Upregulation of GLS1 in CRC cells can enhance glutamine metabolism to promote the formation of lung metastases. The expression of GDH1 contributes to anoikis resistance and pro-metastatic signals in LKB1-deficient lung metastasis. xCT can promote cystine uptake to increase the generation of GSH to constrain ROS levels, and enhance the invasiveness of breast cancer cells. (B) In liver, the expression of GLS1 can generate GSH to attenuate ROS accumulation. However, knockdown of GOT2 can promote hematogenous and intrahepatic metastasis of HCC cells. (C) In peritoneum, upregulated GLS1 expression is closely related to high invasiveness of OvCa cells. Moreover, glutamine metabolism can perturb T cell mitochondrial respiration to induce immune evasion of OvCa cells. (D) In brain, glutamine can be used as an alternative fuel to avoid energy deficiency in metastatic cells. In addition, the expression of ASCT2 is upregulated in human glioma cells, and overexpression of xCT can resist oxidative stress to promote metabolic adaptation of brain metastasis in breast cancer cells.