Long noncoding RNA FOXD3‐AS1 promotes colon adenocarcinoma progression and functions as a competing endogenous RNA to regulate SIRT1 by sponging miR‐135a‐5p

More and more documents have proved that the abnormal expression of long noncoding RNAs (lncRNAs) are correlated with the initiation and progression of colorectal cancer (CRC). lncRNA FOXD3‐AS1 has been reported in glioma for its oncogenic property. According to the survival analysis of The Cancer Genome Atlas database, FOXD3‐AS1 upregulation implied lower survival rate of patients with CRC. Quantitative real‐time polymerase chain reaction showed the overexpression of FOXD3‐AS1 in both CRC tissues and cells. The Kaplan–Meier method demonstrated the prognostic value of FOXD3‐AS1 for patients with CRC. To explore the effect of FOXD3‐AS1 on CRC progression, loss‐of‐function experiments were carried out, whose results indicated that knockdown of FOXD3‐AS1 suppressed cell proliferation, migration, and invasion, inhibited cell cycle and promoted cell apoptosis in vitro. In vivo experiments affirmed that FOXD3‐AS1 affected tumor growth. FOXD3‐AS1 expression was enriched in the cytoplasm of CRC cells. Mechanism experiments revealed that FOXD3‐AS1 served as a competing endogenous RNA to upregulate SIRT1 by sponging miR‐135a‐5p. In addition, SIRT1 silencing also restrained cell proliferation and motility. Rescue assays revealed the biological function of FOXD3‐AS1/miR‐135a‐5p/SIRT1 axis in CRC progression. In conclusion, FOXD3‐AS1 promotes CRC progression by regulating miR‐135a‐5p/SIRT1 axis, shedding lights on the way to CRC treatments. Upregulation of FOXD3‐AS1 predicts unfavorable prognosis for patients with colorectal cancer (CRC). FOXD3‐AS1 promotes tumor growth of CRC in vitro and in vivo. FOXD3‐AS1 acts as a competing endogenous RNA by sponging miR‐135a‐5p to upregulate SIRT1. FOXD3‐AS1/miR‐135a‐5p/SIRT1 axis functions in CRC progression.