Long non-coding RNA LINC01133 inhibits epithelial–mesenchymal transition and metastasis in colorectal cancer by interacting with SRSF6

Highlights • LINC01133 is a repressor of the epithelial–mesenchymal transition (EMT) process in colorectal cancer and is associated with colorectal cancer metastasis. • LINC01133 directly binds to splicing factor SRSF6 and blocks its function of inducing the EMT in colorectal cancer. • LINC01133 is...

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Bibliographic Details
Published in:Cancer letters 2016-10, Vol.380 (2), p.476-484
Main Authors: Kong, Jianlu, Sun, Wenjie, Li, Chen, Wan, Ledong, Wang, Shuo, Wu, Yihua, Xu, Enping, Zhang, Honghe, Lai, Maode
Format: Article
Language:English
Subjects:
Alternative splicing
Animals
Antigens, CD
Cadherins - metabolism
Cell Movement
Colorectal cancer
Colorectal carcinoma
Colorectal Neoplasms - genetics
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
E-cadherin
EMT
Epithelial-Mesenchymal Transition
Gene expression
HCT116 Cells
Hematology, Oncology and Palliative Medicine
HT29 Cells
Humans
lncRNA
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - secondary
Lymphatic Metastasis
Mesenchyme
Metastases
Metastasis
Mice, Inbred NOD
Mice, SCID
Non-coding RNA
Phosphoproteins - genetics
Phosphoproteins - metabolism
Phosphorylation
Proteins
RNA Interference
RNA polymerase
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Roles
Serine-Arginine Splicing Factors - genetics
Serine-Arginine Splicing Factors - metabolism
Signal Transduction
Splicing factors
SRSF6
Studies
Time Factors
Transfection
Tumor Burden
Tumors
Vimentin
Vimentin - metabolism
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Summary:Highlights • LINC01133 is a repressor of the epithelial–mesenchymal transition (EMT) process in colorectal cancer and is associated with colorectal cancer metastasis. • LINC01133 directly binds to splicing factor SRSF6 and blocks its function of inducing the EMT in colorectal cancer. • LINC01133 is downregulated in colorectal cancer, and its overexpression is correlated with good survival.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2016.07.015