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Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer
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Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer
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Journal Article
Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer
2018
Overview
Background
Assembling evidences suggested that aberrant expression of tissue differentiation-inducing non-protein coding RNA (TINCR) intimately associated with variety of human cancer. However, the expression pattern and involvement of TINCR in breast cancer has not been fully investigated. Here we set out to analyze expression of TINCR in breast cancer and elucidate its mechanistic involvement in tumor incidence and progression.
Methods
The expression of TINCR was determined by q-PCR. SP1 binding sites were analyzed by ChIP-qPCR. The relative transcription activity was measured with luciferase reporter assay. Cell viability was measured with CCK-8 method. Clonogenic capacity was evaluated by soft agar assay. Cell apoptosis was analyzed by Annexin V/7-AAD staining. The migration and invasion were determined by trans-well assay and wound healing. The tumor growth in vivo was evaluated in xenograft mice model. Protein expression was quantified by immunoblotting.
Results
TINCR was aberrantly up-regulated by SP1, which in turn stimulated cell proliferation, anchorage-independent growth and suppressed cell apoptosis in breast cancer. TINCR silencing significantly suppressed migration and invasion in vitro and xenograft tumor growth in vivo. Mechanistically, TINCR modulated KLF4 expression via competing with miR-7, which consequently contributed to its oncogenic potential. MiR-7 inhibition severely compromised TINCR silencing-elicited tumor repressive effects.
Conclusion
Our data uncovered a crucial role of TINCR-miR-7-KLF4 axis in human breast cancer.
Publisher
BioMed Central,BioMed Central Ltd,BMC
Subject
/ Analysis
/ Animals
/ Biomedical and Life Sciences
/ Breast Neoplasms - metabolism
/ Breast Neoplasms - pathology
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Female
/ Gene Expression Regulation, Neoplastic
/ Health Promotion and Disease Prevention
/ Humans
/ KLF4
/ Kruppel-Like Transcription Factors - metabolism
/ Male
/ miR-7
/ Oncology
/ RNA, Long Noncoding - genetics
/ Sp1 Transcription Factor - metabolism
/ TINCR
