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. Author manuscript; available in PMC: 2014 May 21.
Published in final edited form as: Crit Rev Oncog. 2013;18(4):327–340. doi: 10.1615/critrevoncog.2013007254

FIGURE 2. The KRAS Variant and Tumorigenesis.

FIGURE 2

The SNP rs61764370 is located within the 3'-UTR of KRAS in the binding site of the miRNA let-7. The variant allele (G) disrupts let-7 binding to the mRNA transcript and prevents let-7 mediated suppression, resulting in increased KRAS protein expression. By a still undefined mechanism, the variant allele is also associated with decreased let-7 levels.25 It is hypothesized that KRAS may induce Lin-28, a negative regulator of let-7. Both increased KRAS and decreased let-7 are associated with tumorigenesis. Let-7 is involved in a feedback loop such that low let-7 induces IL-6 expression, which activates the transcription factor STAT3, leading to tumorigenesis.27