MIR612 (MicroRNA 612)

While the pooled data analysis did not reveal any association, a subgroup analysis demonstrated country-specific differences in allele frequencies of all the four miRNAs in various genetic models, implying ethnicity-based risk. Our results suggested that miRNA-SNPS can still be considered as a potential risk factor to be explored in more populations.

This review aims to summarize the expression of CENP-H, the relationship between CENP-H expression and prognostic features, growth and metastasis of cancer in patients, as well as the mechanism of CENP-H in cancer. It also proposes a new candidate molecule for treating patients with cancer.

Knockdown of CCL28 inhibited cell proliferation and invasion and counteracted miR-612 inhibitor-caused tumour-promoting effects. Our findings unveil that WTAP-mediated m6A modification of circSMOC1 facilitates the tumorigenesis of NSCLC by regulating the miR-612/CCL28 axis.

Stronger effect estimates of benzene/BTX exposure were found in carriers of miR-196a-2-related rs11614913 heterozygotes and of wild homozygotes of miR-1269b-related rs12451747, miR-612-related rs12803915, and miR-4804-related rs266437. Our findings provide further support of the involvement of BTX co-exposure, mirSNPs, and their gene-environment interactions in determining the severity of DNA strand break in a complex manner.

The expression of BANCR gradually increased with the progression of endometriosis during malignant transformation, and promoted the proliferation and migration of endometrial cells via the miR-612/CPNE3 pathway. BANCR may represent a novel target for monitoring the malignant transformation of endometriosis.

The A allele of rs41291179 and the G allele of rs12803915 were associated with decreased risk of CIN (OR = 0.05, 95% CI: 0.01-0.39; OR = 0.61, 95% CI: 0.49-0.76) and CC (OR = 0.08, 95% CI: 0.01-0.66; OR = 0.71, 95% CI: 0.59-0.86), respectively. Our results suggest that polymorphisms in miRNA genes of the AMPK signaling pathway are associated with the development of CC.

miR-612 also suppressed HCC cell proliferation and metastasis by enhancing RSL3- and lovastatin-induced ferroptosis in vivo. Overall, miR-612 promotes ferroptosis in HCC cells and affects HCC proliferation and metastasis by downregulating CoQ10 and increasing cellular PUFA levels and lipid peroxides via the HADHA-mediated MVA pathway.

Our study highlights the significant association between the miR-149 rs2292832 genetic variant and childhood ALL susceptibility in the Chinese population. These findings expand our understanding of the complex genetic landscape underlying ALL and have implications for the development of personalized therapeutic strategies.

Our results indicated a four-miRNA signature that has a robust predictive effect on the prognosis of PTC. Accordingly, we would recommend more radical therapy and closer follow-ups for high-risk groups.

Additionally, there was a statistically significant relationship between the polymorphisms of pri-miR-34b/c rs4938723 (in the homozygote and recessive models) and miR-612 rs12803915 (in the allele and dominant models) and childhood acute lymphoblastic leukemia risk. These findings suggest that the rs4938723 and rs12803915 polymorphisms may have a role in the development of childhood acute lymphoblastic leukemia.

Our data indicated that the A allele of the rs12402181 polymorphism may be considered as a genetic biomarker of preB-ALL susceptibility. Likewise, it was identified that the A allele of the rs12402181 polymorphism is an independent risk factor for ALL.