Table 1.

Key references for the role of NOTCH1 in lung cancer.

References	Subtype	Key findings	Potential role of NOTCH1
[10, 11]	SCLC	NOTCH1 inhibited cell proliferation and neuroendocrine marker expression.	Tumor suppressive
[12, 13]	SCLC	NOTCH1 induced growth inhibition and cell cycle arrest.	Tumor suppressive
[30]	SCLC	NOTCH1 inhibited EMT and invasion.	Tumor suppressive
[14]	NSCLC	Knockdown of NOTCH1 inhibited cell growth; NICD1 promoted cell growth in the presence of EGF.	Oncogenic
[15, 16]	NSCLC	Hypoxia-induced HIF1α activated NOTCH1 to promote cell growth; the γ-secretase inhibitor MRK-003 induced cell apoptosis under the condition of hypoxia.	Oncogenic
[23–27]	NSCLC	Inactivation of NOTCH1 or its mediators in mouse models of NSCLC abrogated tumorigenesis.	Oncogenic
[31]	NSCLC	Inactivation of the NOTCH ligand Jagged2 inhibited EMT and metastasis.	Oncogenic
[32]	NSCLC	Galectin-1 increased Jagged2 and NOTCH1 to promote metastasis.	Oncogenic
[33]	NSCLC	ADAM10 activated NOTCH1 to promote invasion.	Oncogenic
[34]	NSCLC	NICD1 induced EMT and destroyed adherens junctions.	Oncogenic
[35]	NSCLC	NICD1 transcriptionally activated SOX9 to drive EMT and invasion.	Oncogenic
[36–39]	NSCLC	Higher NOTCH1 correlated with disease progression, metastasis, and poorer prognosis.	Oncogenic
[40]	NSCLC	Gain-of-function NOTCH1 mutations are identified in a subset of patients; activated NOTCH1 activity correlated with poorer survival of NSCLC patients without p53 mutations.	Oncogenic
[17]	NSCLC	NICD1 inhibited cell and xenograft tumor growth.	Tumor suppressive
[18]	NSCLC	NOTCH1 mediated Z-Isochaihulactone-induced growth inhibition.	Tumor suppressive
[19]	NSCLC	Endothelial DLL4 activated tumor cell NOTCH1 to inhibit growth.	Tumor suppressive
[41]	NSCLC	NOTCH1 expression negatively correlated with metastasis and predicted better survival.	Tumor suppressive
[42]	NSCLC	NICD1 was only detected in a small proportion of patient tissues and had no prognostic value.