Journal
CANCER SCIENCE
Volume 108, Issue 4, Pages 653-662Publisher
WILEY
DOI: 10.1111/cas.13200
Keywords
Fused in sarcoma; hepatocellular carcinoma; long noncoding RNA; metastasis; SchLAH
Categories
Funding
- National Key Basic Research Program of China [2015CB553905]
- State Key Laboratory of Oncogenes and Related Genes [91-1411, 91-1502]
- National Natural Science Foundation of China [81201626, 81301759, 81402278, 81421001]
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Emerging evidence has indicated that deregulation of long non-coding RNAs (lncRNAs) can contribute to the progression and metastasis of human cancer, including hepatocellular carcinoma (HCC). However, the roles of most lncRNAs in HCC remain largely unknown. Here we found a long noncoding RNA termed SchLAH (seven chromosome locus associated with HCC; also called BC035072) was generally downregulated in HCC. Low expression of SchLAH was significantly correlated with shorter overall survival of HCC patients. In vitro and invivo assays indicated that overexpression of SchLAH inhibited the migration and lung metastasis of HCC cells. Knockdown of SchLAH by siRNA pool promoted the migration of HCC cells. RNA pull-down and RNA immunoprecipitation assays demonstrated SchLAH physically interacted with fused in sarcoma (FUS). PCR array analysis showed that RhoA and Rac1 were the downstream effector molecules of SchLAH during HCC metastasis. Knockdown of FUS rescued the mRNA levels of RhoA and Rac1 that were repressed by SchLAH. These results suggest that SchLAH may suppress the metastasis of HCC cells by interacting with FUS, which indicates potential of SchLAH for the prognosis and treatment of HCC.
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