Unveiling cancer dormancy: Intrinsic mechanisms and extrinsic forces

SNAI2 enhances HPV‑negative cervical cancer cell dormancy by modulating u‑PAR expression and the activity of the ERK/p38 signaling pathway in vitro

“…By contrast, SNAI2 could trans-suppress the expression of Akt1/p-Akt1 by binding to E-box motifs in the promoter of the Akt1 gene and then inhibit the cell proliferation and tumor formation, not promote dormancy of cervical cancer cells, by upregulating p21/p27 and/or downregulating the activity of the Wnt/β-catenin signaling pathway ( 24 ). Altogether, SNAI2 is more specific to a particular type of cancer or malignant phenotype ( 34 ).…”