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The novel lnc RNA CALIC upregulates AXL to promote colon cancer metastasis
Author(s) -
Kawasaki Yoshihiro,
Miyamoto Masaya,
Oda Takeaki,
Matsumura Kosuke,
Negishi Lumi,
Nakato Ryuichiro,
Suda Sakiko,
Yokota Naoko,
Shirahige Katsuhiko,
Akiyama Tetsu
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201847052
Subject(s) - small hairpin rna , gene knockdown , metastasis , cancer research , downregulation and upregulation , long non coding rna , colorectal cancer , receptor tyrosine kinase , rna interference , cancer , biology , rna , microbiology and biotechnology , signal transduction , cell culture , gene , genetics
Long non‐coding RNA s (lnc RNA s) are aberrantly expressed in many disease conditions, including cancer. Accumulating evidence indicates that some lnc RNA s may play critical roles in cancer progression and metastasis. Here, we identify a set of lnc RNA s that are upregulated in metastatic subpopulations isolated from colon cancer HCT 116 cells in vivo and show that one of these lnc RNA s, which we name CALIC , is required for the metastatic activity of colon cancer cells. We show that CALIC associates with the RNA ‐binding protein hn RNP ‐L and imparts specificity to hn RNP ‐L‐mediated gene expression. Furthermore, we demonstrate that the CALIC /hnRNP‐L complex upregulates the tyrosine kinase receptor AXL and that knockdown of CALIC or AXL using sh RNA in colon cancer cells attenuates their ability to form metastases in mice. These results suggest that the CALIC /hn RNP ‐L complex enhances the metastatic potential of colon cancer cells.