The FOXO3a-FOXM1 axis can modulate cancer initiation, progression, and drug resistance by regulating the expression of genes essential for cell proliferation, survival, self-renewal, migration, angiogenesis, cell cycle/checkpoint transition, and DNA damage repair.
To date, substantial evidence has demonstrated that some key autophagic mediators, such as autophagy-related genes (ATGs), PI3K, mTOR, p53, and Beclin-1, may play crucial roles in modulating autophagic activity in cancer initiation and progression.
As E-cadherin plays a significant role in cell connection and its associated signaling pathways modulates epithelial cell fates and inflammation in gastric mucosa, inactivation of E-cadherin is critical in gastric cancer initiation and progression.
As oestrogen signalling was associated with colon cancer initiation and progression (Hogan et al, 2009), and expression of BARD1 and BARD1 isoforms can be modulated by oestrogen through ER α (Niell et al, 2004; Russo et al, 2009), we also examined the expression of ER α mRNA in colon peri-tumour and tumour tissues from males and females.
MYC activation is a hallmark of cancer initiation and maintenance.
This study demonstrates the functional significance of Mst1r during pancreatic cancer initiation and progression.
McKeown, M. R. & Bradner, J. E. MYC activation is a hallmark of cancer initiation and maintenance.
Baumgart, S. et al. Inflammation-induced NFATc1-STAT3 transcomplexn compromotesmotes pancreatic cancer initiation by KrasG12D.
Lawson, D. A. et al. Basal epithelial stem cells are efficient targets for prostate cancer initiation.
Hsieh, A. C. et al. The translational landscape of mTOR signalling steers cancer initiation and metastasis.
Diet may substantially alter prostate cancer initiation and progression.
