LncRNA USP2-AS1 facilitates colorectal cancer development via upregulating PHLDA2 through recruiting IGF2BP2 and absorbing miR-134-5p

Background Colorectal cancer (CRC) is one of the most common malignant tumors and a challenging public health issue worldwide, seriously threatening human health. It is essential to explore further the molecular mechanisms involved in the occurrence and development of CRC and identify new biomarkers and therapeutic targets for CRC. Researchers have revealed that long non-coding RNAs (lncRNAs) are involved in multiple cancers development, including CRC. USP2-AS1 is a newly discovered lncRNA whose function in CRC has yet to be fully elucidated, prompting us to study further the roles and potential mechanisms of USP2-AS1 in CRC. Methods The expression of USP2-AS1 in CRC tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The biological function of USP2-AS1 in CRC was studied through Cell Counting Kit-8 (CCK-8) assays, colony formation assays, 5-Ethynyl‐2ʹ‐deoxyuridine (EdU) assays, migration assays, apoptosis assays, and animal experiments. The interaction between USP2-AS1, PHLDA2, IGF2BP2, and miR-134-5p was revealed through bioinformatics analysis, RNA sequencing, RNA stability assays, RNA Immunoprecipitation (RIP) assays, and dual-luciferase reporter assays. Results We discovered that USP2-AS1 was overexpressed in CRC tissues and cell lines, and USP2-AS1 overexpression was relevant to poor prognosis in CRC patients. Functional experiments clarified that USP2-AS1 facilitated CRC cell growth and metastasis and reduced apoptosis. Additionally, animal experiments demonstrated that USP2-AS1 could promote tumor growth in vivo. Mechanistically, on the one hand, we verified that USP2-AS1 could bind to IGF2BP2 and thus stabilize PHLDA2 mRNA. On the other hand, USP2-AS1 could absorb miR-134-5p to regulate PHLDA2 expression. Conclusions USP2-AS1 could upregulate PHLDA2 expression by recruiting IGF2BP2 and competitively binding miR-134-5p, thus facilitating CRC malignant progression. Our