Decoding the prognostic significance of integrator complex subunit 9 (INTS9) in glioma: links to TP53 mutations, E2F signaling, and inflammatory microenvironments

Table 2 Integrator’s role in tumorigenesis

Subunit	Cancer type	Role in the Tumorigenesis	Refs
INTS3	LEUK	Loss of INTS3 → tumorigenesis	[47]
INTS3	HCC	Increased INTS3 → tumorigenesis.	[48]
INTS6	LUAD	Loss of INTS6 → tumorigenesis	[36, 37]
	ESCA		[38]
	PRAD		[39, 40]
	ALL		[41]
	HCC		[42]
INTS7	LUAD	Increased INTS7→ poor prognosis. Tumor proliferation↑, migration↑, invasion↑ Tumor apoptosis↓	[43]
INTS7	PAAD	INTS7 mutation → cancer driver	[49]
INTS8	STAD	Increased INTS8 → poor prognosis.	[46]
	PTCL	INTS8 mutation → cancer driver	[44]
	HCC	Increased INTS8 → poor prognosis. Epithelial-to-mesenchymal transition↑ Metastatic potential↑	[50]
	CHOL	Increased INTS8 → poor prognosis. Tumor apoptosis↓	[45]

* ALL = Acute lymphoblastic leukemia; AML = Acute lymphoblastic leukemia; CHOL = Cholangiocarcinoma; ESCA = Esophageal carcinoma; HCC = hepatocellular carcinoma; LEUK = Leukemia; LUAD = Lung adenocarcinoma; PAAD = Pancreatic adenocarcinoma; PRAD = Prostate adenocarcinoma; PTCL = Peripheral T cell lymphoma; STAD = stomach adenocarcinoma

ISSN: 1475-2867