TFs and their role in cancer

Name Description Role in cancer
NF-κB A dimeric TF that combines NF-κB and Rel protein. It regulates the expression of several genes related to inflammation, innate and adaptive immunity and stress response. It plays an important role in tumorigenesis, inflammation, preventing apoptosis, supporting angiogenesis and metastasis.
p53 Also known as TP53 functions as TF when forms a tetramer. It plays important role in DNA damage, cell-cycle regulation and apoptosis. It acts as a tumour suppressor. Most tumours have mutations in the p53 gene. Mutated proteins cannot bind DNA effectively and cells lose their control on cell cycle regulation and apoptosis.
c-Myb As an oncogenic TF, it controls the several genes related to cell proliferation, differentiation and apoptosis. It plays a key role in haematopoietic cell proliferation and lineage differentiation. Over expression of c-Myb is noticed in breast, colon and haematopoietic cancer. In solid tumours, c-Myb is required for proliferation and in leukaemia, c-Myb controls several downstream genes necessary to maintain the proliferation of leukaemic cells.
MLL-AF9 A chimeric TF formed by chromosomal translocation of the N-terminal DNA binding part of the MLL protein (lysine-specific methyltransferase 2A located in chromosome 11) with the c-terminal part of AF9 protein (gene is located in chromosome 9). This TF can bind promoters of a wide range of proteins as well as the enhancer elements. The RUNX1 gene (runt-related TF1) is one of the most well documented downstream targets of MLL-AF9. RUNX1 is a TF that controls granulocytic differentiation. MLL-AF9 driven overexpression of RUNX1 mediates leukemogenic transformation.
c-MYC Oncogenic TF which is responsible to control cell proliferation and apoptosis. Overexpression of c-MYC is observed in more than 40% of tumours. Overexpression caused by gene amplification deregulates the cell proliferation and apoptosis pathways.
STAT3 A master TF that controls the expression of several genes related to the innate and adaptive immunity. It plays an integral part to transduce the signal from receptors to the transduction factors to relocate in the nucleus. It acts as a key player in supporting tumour microenvironment which includes maintaining hypoxic condition, blood vessels and extracellular matrix (ECM) formation, immune cells, and inflammatory cells proliferation.
AML1-ETO A fusion protein generated by chromosomal translocation in AML. The fusion protein comprises of conserved runt homology (which is the DNA binding domain) from the hematopoietic TF RUNX1 (also known as AML1) and ETO repressor protein. It is considered as a transcriptional repressor of all RUNX1 target genes. AML1 acts as a transcriptional activator but this fusion protein acts as a transcriptional repressor in granulocytic differentiation and drives granulocytes in the mode of continuous uncontrolled proliferation.
HIF-1 A key TF that regulates the physiological response to the low oxygen concentration or in hypoxia. It plays a crucial role in maintaining the hypoxic tumour microenvironment by regulating several genes related to this phenomenon. Elevated expression of this TF is associated with poor prognosis and high metastasis.
AP1 It forms a heterodimer with the oncoproteins c-FOS or c-JUN and regulates genes related to the cell proliferation, differentiation, apoptosis and angiogenesis. It acts as an oncogenic factor or tumour suppressor depending on the nature of the cell types, stage of the tumour and its genotypes.