miR-181d stabilized c-myc through directly targeting the 3'-UTRs of CRY2 and FBXL3
First-pass extracted concept
c-myc
Candidate: toolkit item1 source documents6 linked claims
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Aliases
MYC
Evidence Snippets
Supporting Sources
Linked Claims
Activation of c-myc signaling directly induces miR-181d expression.
Quoted textsource-backed
miR-181d expression could be directly induced by an activation of c-myc signaling
miR-181d stabilizes c-myc by directly targeting the 3'-UTRs of CRY2 and FBXL3.
Quoted textsource-backed
miR-181d stabilized c-myc through directly targeting the 3'-UTRs of CRY2 and FBXL3
miR-181d-mediated stabilization of c-myc increases glucose consumption and lactate production.
Quoted textsource-backed
which subsequently increased the glucose consumption and the lactate production
Inhibition of c-myc abolishes the oncogenic effects of miR-181d on colorectal cancer cell growth and metastasis.
Quoted textsource-backed
Inhibition of c-myc via siRNA or small molecular inhibitor abolished the oncogenic effects of miR-181d on the growth and metastasis of CRC cells.
The miR-181d/CRY2/FBXL3/c-myc feedback loop might be a therapeutic target for patients with colorectal cancer.
Quoted textsource-backed
miR-181d/CRY2/FBXL3/c-myc feedback loop might be a therapeutic target for patients with CRC
A c-myc/HDAC3 transcriptional suppressor complex co-localizes on the CRY2 and FBXL3 promoters and epigenetically inhibits their transcription in colorectal cancer cells.
Quoted textsource-backed
c-myc/HDAC3 transcriptional suppressor complex was found to co-localize on the CRY2 and FBXL3 promoters, epigenetically inhibit their transcription, and finally induce their downregulation in CRC cells