The novel lncRNA CALIC upregulates AXL to promote colon cancer metastasis.
Yoshihiro KawasakiMasaya MiyamotoTakeaki OdaKosuke MatsumuraLumi NegishiRyuichiro NakatoSakiko SudaNaoko YokotaKatsuhiko ShirahigeTetsu AkiyamaPublished in: EMBO reports (2019)
Long non-coding RNAs (lncRNAs) are aberrantly expressed in many disease conditions, including cancer. Accumulating evidence indicates that some lncRNAs may play critical roles in cancer progression and metastasis. Here, we identify a set of lncRNAs that are upregulated in metastatic subpopulations isolated from colon cancer HCT116 cells in vivo and show that one of these lncRNAs, which we name CALIC, is required for the metastatic activity of colon cancer cells. We show that CALIC associates with the RNA-binding protein hnRNP-L and imparts specificity to hnRNP-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 shRNA in colon cancer cells attenuates their ability to form metastases in mice. These results suggest that the CALIC/hnRNP-L complex enhances the metastatic potential of colon cancer cells.
Keyphrases
- tyrosine kinase
- long non coding rna
- epidermal growth factor receptor
- gene expression
- papillary thyroid
- squamous cell carcinoma
- small cell lung cancer
- binding protein
- network analysis
- squamous cell
- poor prognosis
- induced apoptosis
- cell cycle arrest
- genome wide analysis
- genome wide identification
- dna methylation
- type diabetes
- cell proliferation
- insulin resistance
- endoplasmic reticulum stress