LINC00022 acts as an oncogene in colorectal cancer progression via sponging miR-375-3p to regulate FOXF1 expression

• Published in: BMC cancer 2022-04, Vol.22 (1), p.453-453, Article 453
• Main Authors: Xu, Lingling, He, Hongmei, Shang, Yu, Qu, Xiaona, Sun, Jinghua
• Format: Article
• Language: English
• Subjects: Analysis; Apoptosis; Binding sites; c-Myc protein; Cancer; Care and treatment; Caspase-3; Cell cycle; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell Proliferation; Cloning; Colorectal cancer; Colorectal carcinoma; Colorectal Neoplasms - pathology; Cyclin D1; Diagnosis; Down-regulation; Endothelial cells; Endothelial growth factors; Esophageal cancer; Forkhead protein; Forkhead Transcription Factors - genetics; Forkhead Transcription Factors - metabolism; FOXF1; Gelatinase B; Gene expression; Gene Expression Regulation, Neoplastic; Genetic aspects; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Laryngeal cancer; lncRNA LINC00022; Matrix metalloproteinase; Medical prognosis; Metalloproteinase; MicroRNA; MicroRNAs - metabolism; miR-375-3p; Myc protein; Oncogenes; Poly(ADP-ribose); Poly(ADP-ribose) polymerase; Proteins; Ribose; Risk factors; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Tumors; Umbilical vein; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - metabolism; Wound healing
• ISSN: 1471-2407; 1471-2407
• DOI: 10.1186/s12885-022-09566-5

Abnormal expression of long non-coding RNAs (lncRNAs) has been shown to be associated with the pathogenesis of cancers, including colorectal cancer (CRC). It has been reported that LINC00022 is highly expressed in some typs of cancer and its overexpression indicates poor prognosis. The function of LINC00022 in CRC progression remains unclear and is mainly investigated in the present study. LINC00022 expression in CRC tissues was analyzed by using the TNMplot software. LINC00022 expression in CRC cells was measured by quantitative real-time PCR. The effects of LINC00022 on the malignant behaviors of CRC cells were detected by a series of in vitro and in vivo experiments. Dual-luciferase assays were used to verify the targeting relationship between LINC00022 and miR-375-3p and between miR-375-3p and Forkhead box F1 (FOXF1), followed by the rescue experiment. LINC00022 was highly expressed in CRC tissues compared with paired para-carcinoma tissues (n = 41). CRC cells with LINC00022 knockdown exhibited decreased cell proliferation, migration, and invasion abilities but increased apoptosis accompanied by decreased protein levels of c-Myc, cyclin D1, cleaved caspase 3, cleaved poly(ADP-ribose) polymerase, matrix metalloproteinase (MMP) 2, and MMP9. Additionally, LINC00022 downregulation in CRC cells suppressed the tube formation of human umbilical vein endothelial cells (HUVECs) as evidenced by decreased vascular endothelial growth factor A levels in LINC00022-silenced cells. The inhibitory effect of LINC00022 knockdown on tumor growth was also observed in an in vivo model. Conversely, LINC00022 overexpression showed that opposite effect. We further demonsrtaed that LINC00022 could upregulate FOXF1 expression through sponging miR-375-3p. Moreover, miR-375-3p knockdown reversed the effects of LINC00022 down-regulation. LINC00022 may up-regulate FOXF1 expression via competitively binding miR-375-3p, thereby promoting the development of CRC.