From: H3K36 trimethylation-mediated biological functions in cancer
Cancer subtype | Signaling pathway | Category | Mechanism | Function | Role |
---|---|---|---|---|---|
Colorectal cancer | Wnt/β-catenin signaling pathway | KDM4C: overexpression | Upregulating MALAT1 expression | Metastasis | Promoter |
SETD2: mutation | Aberrant Dvl2 alternative splicing | Tumorigenesis | Suppressor | ||
Liver cancer | AP-1 pathway | SETD2: mutation | Dysregulated cholesterol homeostasis | Tumorigenesis | Suppressor |
P53 inhibition | |||||
Pancreatic cancer | / | SETD2: mutation | Promoting acinar-to-ductal transition | Transformation | Suppressor |
Progression | |||||
Lung cancer | CXCL1-associated signaling pathway | SETD2: mutation | Aberrant FGFR-2 gene alternative splicing | Tumorigenesis | Promoter |
CXCL1-mediated activation of cell cycle | Proliferation | Suppressor | |||
P53 inactivation | metastasis | ||||
Dysregulation of gene expression | Prognosis | ||||
Breast cancer | / | SETD2: mutation | Unstrained expression of oncogenes | Metastasis | Suppressor |
H3 mutation | Prognosis | ||||
Renal cancer | Wnt/β-catenin signaling pathway | SETD2: mutation; loss | Genome reprogramming | Tumorigenesis | Suppressor |
Defective DNA methylation | Prognosis | ||||
Defective DSBs repair | |||||
P53 inhibition | |||||
Pediatric cancer | / | H3F3A/H3F3B: mutation | Histone methylation reprogramming | Transformation | Suppressor |
SETD2: mutation; loss | Upregulation of oncogenes | Tumorigenesis | Promoter? | ||
Impair MMR | |||||
Prostate cancer | AMPK signaling pathway | SETD2: mutation | Altering histone methylation landscape | Progression | Suppressor |
Hematological malignant tumor | / | SETD2: mutation | Dysregulation and malignant transformation of hematopoietic stem cells | Tumorigenesis | Suppressor |