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Let‐7f was reported to be downregulated in patients with colorectal cancer (CRC). However, little is known about the role of let‐7f in CRC carcinogenesis. The aim of this study was to investigate the correlation between genetic polymorphisms in the flanking region of pri‐let‐7f and CRC risk, as well as the potential role of let‐7f in CRC cell migration and invasion. The pri‐let‐7f‐1 rs10739971 and pri‐let‐7f‐2 rs17276588 were genotyped using TaqMan (Applied Biosystems, Foster City, CA) assay. The luciferase activity was detected using Dual‐Luciferase Reporter Assay. CRC cell migration and invasion were evaluated using transwell chamber assay. The rs17276588 AG and AG/AA genotypes had a significantly increased CRC risk (AG vs. GG: adjusted odds ratio [OR] = 1.48, 95% confidence interval [CI] = 1.19–1.83, p < 0.001; AG/AA vs. GG: adjusted OR = 1.43, 95% CI = 1.17–1.75, p < 0.001). Stratification analyses showed that the increased risk was observed in CRC patients with well‐moderately differential status, patients with clinical Stages I–II, and patients without lymph node metastasis. The rs17276588A allele displayed a decreased transcriptional activity and low levels of let‐7f. Moreover, let‐7f inhibited migration and invasion in Caco‐2 and Lovo cells. These findings indicate that the rs17276588 AG/AA genotypes increased CRC risk by reducing the expression of tumor suppressor let‐7f. [ABSTRACT FROM AUTHOR]

• The progression of papillary thyroid carcinoma might be linked to the long non-coding RNA TINCR. • The rs8101923 within the enhancer region of TINCR was a risk factor for the development of PTC in the Chinese population. • Our results could be helpful for papillary thyroid carcinoma risk assessment and diagnosis in future. Single nucleotide polymorphisms (SNPs) in the enhancer region have been demonstrated to confer to altered enhancer activities, aberrant gene expression, and cancer susceptibility. In this study, we aimed to examine the association between an SNP, rs8101923, within terminal differentiation-induced non-coding RNA (TINCR) and the risk of papillary thyroid carcinoma (PTC). Blood samples from 559 patients with PTC and 445 healthy individuals were collected. The rs8101923 was genotyped by using polymerase chain reaction-restriction fragment length polymorphism assay. The impact of the rs8101923 on TINCR expression and enhancer activity was evaluated by quantitative real-time PCR and dual-luciferase reporter assay. The binding of AP-2α to TINCR enhancer was determined by chromatin immunoprecipitation. The rs8101923 G allele was significantly associated with a higher risk of PTC (adjusted OR = 1.37; 95% CI: 1.15–1.64). Mechanistically, the rs8101923 was related to increased transcriptional levels and enhancer activities (P < 0.05). Transcription factor AP-2α binds to the enhancer region of TINCR containing the rs8101923 locus, and promotes cell proliferation in PTC. These findings suggest the rs8101923 as a risk factor in the pathogenesis of PTC, which provides evidence for explaining the mechanism of the rs8101923 risk allele predisposing to PTC. [ABSTRACT FROM AUTHOR]