Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer.

摘要: Assembling evidences suggested that aberrant expression of tissue differentiation-inducing non-protein coding RNA (TINCR) intimately associated with variety human cancer. However, the pattern and involvement TINCR in breast cancer has not been fully investigated. Here we set out to analyze elucidate its mechanistic tumor incidence progression. The was determined by q-PCR. SP1 binding sites were analyzed ChIP-qPCR. relative transcription activity measured luciferase reporter assay. Cell viability CCK-8 method. Clonogenic capacity evaluated soft agar apoptosis Annexin V/7-AAD staining. migration invasion trans-well assay wound healing. growth vivo xenograft mice model. Protein quantified immunoblotting. aberrantly up-regulated SP1, which turn stimulated cell proliferation, anchorage-independent suppressed silencing significantly vitro vivo. Mechanistically, modulated KLF4 via competing miR-7, consequently contributed oncogenic potential. MiR-7 inhibition severely compromised silencing-elicited repressive effects. Our data uncovered a crucial role TINCR-miR-7-KLF4 axis