fig5

Figure 5. Crosstalk between cell fate and cell survival pathways during cervical cancer development. GSK3β, CTNNB1 and MYC co-operatively mediate crosstalk between cell fate and cell survival regulatory mechanisms. GSK3β, a "non-hub-bottleneck node” protein in this network, acts as the crosstalk molecule between all three major cell fate regulatory pathways. MYC is the most connected protein and the "hub-bottleneck node” in this network, as it controls cell survival strategies along with cell cycle progression. CTNNB1, another "hub-bottleneck node” of this network, is the connector between GSK3β and MYC. Thus, GSK3β/CTNNB1/MYC regulatory axis concurrently controls cell fate and cell survival strategies during cervical cancer initiation, development and progression. Created with BioRender.com.