The 4-nitroquinoline 1-oxide (4-NQO) model for carcinogenesis has been used to investigate cancer stem cells (CSC), but no study has addressed the role of the p75 neurotrophin receptor (p75<sup>NTR</sup>) in 4-NQO-induced oral dysplasia and oral squamous cell carcinoma (OSCC).
<i>N</i>-Glycan deletion on β4-integrin impaired β4-dependent cancer cell migration, invasion, and growth <i>in vitro</i> and diminished tumorigenesis and proliferation <i>in vivo</i> The reduced abilities of β4-integrin were accompanied with decreased phosphoinositol-3 kinase (PI3K)/Akt signals and were restored by the overexpression of the constitutively active p110 PI3K subunit.
Several transcriptional targets and cellular functions of CUX1 affect tumorigenesis; however, we have yet to develop a mechanistic framework to reconcile the opposite roles of CUX1 in cancer protection and progression.
Although the implication of the two pathways investigated in our study in carcinogenesis is well established, our null results suggest that common genetic variants in CDP-choline and Rho GTPases-related genes are not risk factors for lung cancer.
Overexpression of constitutively active p110 phosphoinositol-3-kinase subunit was sufficient to restore invasion and tumorigenesis in transformed cells lacking laminin-332/collagen VII interaction in a manner independent of cellular adhesion.
Taken together, these results suggest that aberrant expression of the CDP/Cux p75 isoform in mammary epithelial cells may be associated with the process of tumorigenesis in breast cancer.