For α-SMA expression, significant differences were observed between control vs. OSMF (P = 0.0003), control vs. early OSMF (P = 0.036), control vs. advanced OSMF (P = 0.00008), and early vs. advanced OSMF (P = 0.0009).
Our data suggest that ZEB1 may participate in the pathogenesis of areca quid-associated OSF by activating the α-SMA promoter and inducing myofibroblast transdifferentiation from BMFs.
Heterozygous XRCC3 codon 241 [OR 2.07 (1.05-4.06)], homozygous variant of NATC481T [OR 2.81 (1.09-7.21)], and both heterozygous and homozygous variants of NAT codon 268 and 286 [OR 2.31 (1.20-4.45) and 4.98 (1.87-13.14), and 6.12 (2.75-13.62) and 2.65 (1.04-6.72)] individually influenced susceptibility to OSF in the population.
Our findings suggest arecoline promotes CD147 expression via the TGF-β1 signaling pathway in HOKs, whereas overexpression of CD147 may promote OSF progression.
Further validation was done by real time quantitative RT-PCR analysis; gene expression of Hsp-70 1B, Calreticulin, and Lumican variant were significantly increased (6.2-, 3.3-, 2.8- fold, respectively), whereas Enolase 1 was decreased by 0.5 fold in the OSMF tissues, consistent with proteomic results.
The identification of mutations in OSCC lesions but not OSMF suggests that dimer forming domain mutations in caspase 8 may be limited to malignant lesions.
Similarly, differences in the CCL2-CT expression were statistically significant between control vs. OSMF (P = 0.00086), control vs. early OSMF (P = 0.02914), and control vs. advanced OSMF (P = 0.0006).
Connective tissue growth factor (CTGF or CCN2) and early growth response-1 (Egr-1) are important mediators in the fibrotic response to TGFβ in several fibrotic disorders including OSF.
This study compared the association of OSF and polymorphisms of six collagen-related genes, collagen 1A1 and 1A2 (COL1A1 and COL1A2), collagenase-1 (COLase), transforming growth factor beta1 (TGF-beta1), lysyl oxidase (LYOXase), and cystatin C (CST3), between patients with low and high exposure to betel quids.
This study compared the association of OSF and polymorphisms of six collagen-related genes, collagen 1A1 and 1A2 (COL1A1 and COL1A2), collagenase-1 (COLase), transforming growth factor beta1 (TGF-beta1), lysyl oxidase (LYOXase), and cystatin C (CST3), between patients with low and high exposure to betel quids.
In immunohistochemical results, the expression of Loricrin and COMP showed statistically significant association with histologic grade of OSF (P = 0.03 and 0.006, respectively).
After adjusting for possible confounding factors, COX-2 -765C allele vs. -765G/G genotype (OR=0.22, 95%CI=0.12-0.39) was a protective factor against OSCC development, but was a risk factor for malignant potential of OSF (OR=3.20, 95%CI=1.32-8.94) and OL (OR=6.73, 95%CI=2.84-19.87).