Neither was the association between the MALAT-1 SNPs and progression factors of HCC, including TNM staging, metastasis, and cancer embolus; Overall, this study suggested that tagSNPs rs11227209, rs619586, and rs3200401 at MALAT-1 were not significantly associated with HCC susceptibility.
A stratified analysis showed that younger patients (<55 years) with the MALAT1 rs619586 G allele had a decreased risk of HCC under a codominant model (AOR = 0.289, 95% CI: 0.108-0.773, p = 0.013) and dominant model (AOR = 0.286, 95% CI: 0.107-0.765, p = 0.013).
In the present study, SNPs rs7763881 in HULC and rs619586 in MALAT1 were genotyped in 70 HBV-positive HCC, 70 HBV patients, and 70 healthy controls in Egyptian population and the level of serum lncRNA-AF085935 and lncRNA-uc003wbd of all the subjects was assayed by quantitative real-time polymerase chain reaction.
In addition, the two-way interaction of <i>HOTTIP</i> rs17501292-<i>MALAT1</i> rs619586 polymorphisms showed a decreased effect on HCC risk (<i>P</i><sub>interaction</sub> = 0.028, OR = 0.30) and epistasis with each other.
Furthermore, the variant genotypes of rs619586 was associated with decreased HCC risk with a borderline significance (AG/GG vs. AA: adjusted OR = 0.81, 95% CIs = 0.65-1.01, P = 0.057).
Taken together, this study provides additional evidence that genetic variation of the ANRIL rs9632884 and MALAT1 rs3200401 can mediate lipid levels in MI patients.
Our study indicated that miR-214 inhibited MALAT1 expression by directly binding to the G allele of MALAT1 rs619586 polymorphism, thus inhibiting CTNNB1 expression and promoting cell proliferation in the pathogenesis of DTC.
Neither was the association between the MALAT-1 SNPs and progression factors of HCC, including TNM staging, metastasis, and cancer embolus; Overall, this study suggested that tagSNPs rs11227209, rs619586, and rs3200401 at MALAT-1 were not significantly associated with HCC susceptibility.
In conclusion, our results suggest that there is no contribution of MALAT1 rs3200401 and rs619586 polymorphisms or polymorphisms in the core promoter that could be associated with the risk of melanoma skin cancer in this specific study setting.
<b>Conclusion:</b> Our study demonstrated that the GC genotype and the recessive model of rs4102217 potentially increased CAD risk in some specific group.
In conclusion, our study suggests that the rs619586 G variant may have potential protective effects conferring a decreased risk of recurrent miscarriage in the southern Chinese population.
Since the association between rs619586 A > G polymorphism and ESCC risk was not significant after FDR adjustment, there was a minor possibility that rs619586 A > G might be a protective factor for ESCC.
In conclusion, our results suggest that there is no contribution of MALAT1 rs3200401 and rs619586 polymorphisms or polymorphisms in the core promoter that could be associated with the risk of melanoma skin cancer in this specific study setting.
<b>Conclusions:</b> Our findings su</span>ggested that MALAT1 SNP rs619586 could serve as a potential indicator for PTC susceptibility and pathogenesis.
<i>In vitro</i> and <i>in vivo</i> experiments showed that the rs664589 C to G mutation facilitated carcinogenesis and metastasis of colorectal cancer.
<i>In vitro</i> and <i>in vivo</i> experiments showed that the rs664589 C to G mutation facilitated carcinogenesis and metastasis of colorectal cancer.
<i>In vitro</i> and <i>in vivo</i> experiments showed that the rs664589 C to G mutation facilitated carcinogenesis and metastasis of colorectal cancer.
<i>In vitro</i> and <i>in vivo</i> experiments showed that the rs664589 C to G mutation facilitated carcinogenesis and metastasis of colorectal cancer.
In addition, females with genotype CT of rs3200401 had a lower risk of BC in the codominant model (OR: 0.75, 95%CI: 0.559-1.007) and over-dominant model (OR: 0.741, 95%CI: 0.552-0.993).