cd44 rs13347c>t variants in 3'utr and prostate neoplasms: a case-control study and bioinformatics approach

Cd44, a cell-surface receptor and a key player in cellular signaling, can act as both tumor suppressor and promoter. this study aimed to investigate the association of cd44 rs13347c>t variants with prostate neoplasms, including both benign prostatic hyperplasia (bph) and prostate cancers using a case-control and bioinformatics approach. genomic dna was extracted from 545 blood samples (225 bph, 225 prostate cancers, and 95 control) and the cd44 rs13347c>t genotypes were identified using pcr-rflp. we explored mirna interactions using the mirnasnp-v3 database and genemania for co-expression networks. results showed cancer patients had significantly higher psa levels compared to both controls (p= 0.03) and bph (p= 0.01). additionally, digital rectal examination-positive and smoker bph patients showed significantly the increased cancer risk (p= 0.004, p= 0.046). prostate cancer group indicated significantly higher frequency of cd44 rs13347c>t mutant allele compared to control and bph groups, particularly in tt and ct+tt genotypes (p < 0.05). mirna snp-v3 database predicted the mutant allele of cd44 rs13347c>t could lose 1 and gain 6 mirnas for a new site created. co-expression analysis revealed a direct interaction between cd44 and aryl hydrocarbon receptor (ahr), a gene known to be dysregulated in smokers. furthermore, these genes alone display co-expression interactions with integrin subunit alpha 4 (itga4), protein plays a paradoxical role, both suppressing and promoting tumors. based on the findings, the mutant allele of cd44 rs13347c>t may disrupt mirna binding, which may potentially impact cd44, ahr, and itga4 expression in smokers, possibly contributing to prostate cancer progression.