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Figure 6 | Molecular Cancer

Figure 6

From: miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer

Figure 6

Proposed model for manipulation of miR-630 in breast cancer cells. Elevated IGF1R, HER2 and EGFR have been associated with drug resistance and cancer cell aggression. (A) Introducing miR-630 into acquired or innately resistant breast cancer cells can (1) directly inhibit the mRNA translation of IGF1R. (2) Crosstalk of IGF1R to other receptor tyrosine kinases (HER2 and EGFR) can lead to their subsequent down regulation and so (3) cause cells to become more sensitive to HER-targeting agents as well as decreasing their aggressive phenotype (in terms of motility, invasion and resistance to anoikis). (B) Conversely, inhibiting the expression of miR-630 in sensitive breast cancer cells can (1) prevent its binding to and translational suppression of target mRNA IGF1R. This causes an increase in IGF1R protein expression which in turn can (2) induce elevated HER2 and EGFR expression and as a result, (3) cells exhibit a more aggressive phenotype.

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