LINC01134 promotes the progression of colorectal cancer through enhancing SLC1A5 mRNA stability

Abstract

Abstract Colorectal cancer (CRC) is one of the most common malignant tumors with a poor prognosis. Long noncoding RNAs (lncRNAs) were reported to play a vital role in regulating the progression of cancers and had been become the focus of intense research in cancer biology. Meanwhile, LINC01134 functions as an oncogene in many cancers, but the possible roles and mechanisms in the occurrence and development of CRC are still unclear. This study aimed to explore the biological mechanism of LINC01134 in the progression of CRC. First, we found LINC01134 was highly expressed in CRC tissues and associated with worse clinical stages and poor prognosis, which was in line with that in CRC cell lines. Functional experiments indicated that silencing of LINC01134 attenuated CRC cells proliferation and induced the apoptosis both in vitro and in vivo. Mechanistically, weighted gene co-expression analysis identified that LINC01134 was positively related to SLC1A5, which was also upregulated and associated with poor prognosis in CRC. Going further, RNA–RNA interaction in vitro analysis and analysis of mRNA stability indicated that LINC01134 could directly bind to SLC1A5 mRNA and enhance SLC1A5 mRNA stability. Notably, silencing of SLC1A5 could partly reverse the promotion effect of LINC01134 overexpression on proliferation and the inhibitory effect on cells apoptosis in CRC cells. Our findings showed that LINC01134 acted as an oncogene in CRC via directly binding to SLC1A5 mRNA and enhancing SLC1A5 mRNA stability, which suggested that LINC01134 might act as a promising therapeutic target for CRC.