Table 1.
Cancer Type | GS Expression | Role of GS | Experimental Models | References |
---|---|---|---|---|
GBM | High | GS sustains nucleotide biosynthesis and cell growth of GBM in gln starved conditions | Human GBM patients, GBM PDX model |
[17,19] |
OVC | High | GS supports the proliferation of OVC cells GShigh OVC shows low invasiveness |
OVC cells | [38,39] |
Low | GSlow OVC shows high invasiveness | Xenograft mouse model | [39,40] | |
Breast cancer (luminal) | High | High expression of GS contributes to gln independence GLS inhibitor has no anti-proliferative activity |
Luminal type breast cancer cells | [13,18] |
Breast cancer (basal) | Low | Low expression of GS contributes to gln dependence GLS inhibitor has anti-proliferative activity |
Basal type breast cancer cells, Xenograft model of basal like breast cancer |
[13,18] |
Lung cancer | High | Increased GS accumulates gln in cancer cells although gln catabolism is activated | GEMs (Myc-induced lung tumors) | [41] |
- | GS confers gefitinib resistance | NSCLC cells | [42,43] | |
PDAC | High | GS contributes to cataplerotic usage of α-KG GLUL ablation suppresses tumor growth |
KPC tumor cell organoids, Orthotopic mouse model |
[44] |