In addition, we also proved that overexpressed GAS8-AS1 inhibited tumor formation <i>in vivo</i> GAS8-AS1 suppresses PTC cell growth through the miR-135b-5p/CCND2 axis.
We found rs11246050 in NLRP6 (dominant model, OR/95% CI: 2.028/1.091-3.769, p = 0.025), rs2286742 and rs3740530 in HABP2 (recessive model, OR/95% CI: 9.644/1.307-71.16, p = 0.026 and 3.989/1.413-11.26, p = 0.009), rs2736098 in TERT (recessive model, OR/95% CI: 2.322/1.028-5.242. p = 0.042) and rs62054619 in GAS8-AS1 (recessive model, OR/95% CI: 2.219/1.067-4.617, p = 0.033) were associated with the risk of PTC. rs1137282 in KRAS (dominant model, OR/95% CI: 0.5430/0.3192-0.9236, p = 0.024), rs1347591 and rs4461062 in NUP93 (dominant model, OR/95% CI: 0.6121/0.4128-0.9076, p = 0.015 and 0.6156/0.4157-0.9117, p = 0.015) were associated with low risk of distant metastatic disease in PTC patients. rs33954691 in TERT was associated with the risk of RR-PTC under dominant model (OR/95% CI: 3.161/1.596-6.262).
As a mutation hotspot, the c.713A>G/714T>C dinucleotide substitution was found among 89.1% patients with GAS8-AS1 mutations and associated with advanced PTC disease (P = 0.009).
As a mutation hotspot, the c.713A>G/714T>C dinucleotide substitution was found among 89.1% patients with GAS8-AS1 mutations and associated with advanced PTC disease (P = 0.009).