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One of these proposed mechanisms of chronic cardiotoxicity in childhood cancer survivors is through DOX-mediated reduction of proliferation and differentiation of the progenitor cells and impairment of vascular development with decreased capillary density

in: PubMed | Google Scholar | Authorship note: NAT and BV contributed equally to this work

Reintroducing miR-199a-3p in RCC cell lines inhibited proliferation and led to the arrest ofG1 phase by negatively regulating c-Met, thus suppressing HGF/c-Met axis and it's downstream signaling such as Akt, ERK1/2 and mTOR (Huang et al., 2014)

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