The role of Snail1 transcription factor in colorectal cancer progression and metastasis

Abstract

Snail1 is a zinc-finger transcription factor, which plays a role in colorectal cancer development by silencing E-cadherin expression and inducing epithelialmesenchymal transition (EMT). During EMT tumour cells acquire a mesenchymal phenotype that is responsible for their invasive activities. Consequently, Snail1 expression in colorectal cancer is usually associated with progression and metastasis. Some studies revealed that about 77% of colon cancer samples display Snail1 immunoreactivity both in activated fibroblasts and in carcinoma cells that have undergone EMT. Therefore, expression of this factor in the stroma may indicate how many cells possess the abilities to escape from the primary tumour mass, invade the basal lamina and colonise distant target organs. Blocking snail proteins activity has the potential to avert cancer cell metastasis by interfering with such cellular processes as remodelling of the actin cytoskeleton, migration and invasion, which are clearly associated with the aggressive phenotype of the disease. Moreover, the link between factors from the snail family and cancer stem cells suggests that inhibitory agents may also prove their potency as inhibitors of cancer recurrence.

AXIN2 and SNAIL expression predict the risk of recurrence in cutaneous squamous cell carcinoma after Mohs micrographic surgery

“…Epithelial-to-mesenchymal transition (EMT) is a crucial process for cancer cell local invasion and metastasis that acts through the loss of epithelial properties and the acquisition of a mesenchymal phenotype (10). SNAIL, which is a zinc finger transcriptional repressor that functions as a crucial EMT regulator by repressing E-cadherin, is associated with poor prognosis in various types of cancer, such as breast cancer, ovarian cancer, and colorectal cancer (11)(12)(13). In cancer cells, activated canonical Wnt signaling inhibits glycogen synthase kinase 3 (GSK-3)-dependent phosphorylation of SNAIL, which subsequently leads to the inhibition of SNAIL degradation, resulting in increased SNAIL protein expression (14).…”

The effects of c-Src kinase on EMT signaling pathway in human lens epithelial cells associated with lens diseases

“…This specific process is present in embryonic development, wound healing and tissue repairment and tumor metastasis. In organ fibrosis such as renal fibrosis, pulmonary fibrosis, hepatic fibrosis and ocular fibrosis, EMT is triggered by various biomolecules and signaling pathways, such as transforming growth factor-β (TGF-β) [13], insulin-like growth factor-1 (IGF-1) [14], transcription factor snail [15], and PI3K/Akt/mTOR/NF-κB signaling [16].…”

Zinc: What Is Its Role in Lung Cancer?

“…In fact, Snail-1 has been shown to be crucial during cancer progression and metastasis. In colon cancer patients, enhanced levels of Snail1 are usually associated with poor clinical outcome [26,29]. Recent studies in Snail-1 deficient mouse embryos support the idea that transcriptional repression of E-cadherin (cellular adhesion molecules) is associated with Snail-1 activity [26].…”

“…It is generally accepted that a fundamental process for distant metastasis formation comprises epithelial-mesenchymal transition (EMT), during which tumor cells lose their epithelial properties and acquire a fibroblast-like phenotype; as a consequence, reduced intercellular adhesion, enhanced invasiveness, and increased apoptotic resistance of cells [26,27]. In the early stages of tumor, several signaling pathways are activated, such as growth factors and zinc-finger transcription factors including Snail [26,28]. In fact, Snail-1 has been shown to be crucial during cancer progression and metastasis.…”