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This pathway, known to influence cell proliferation, adhesion, and differentiation, is frequently deregulated in carcinogenesis

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In line with these findings, the inhibition of Gln metabolism with V9302 and Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide (BPTES) in murine syngeneic colorectal carcinoma model increases PD-L1 expression in tumor cells, activates T-cell-mediated Fas cell death signaling, and synergizes with anti-PD-L1 immunotherapy [90]