LINC00667 Sponges miR-4319 to Promote the Development of Nasopharyngeal Carcinoma by Increasing FOXQ1 Expression

Abstract

Accumulating evidence has indicated that lncRNAs regulate various biological and pathological processes in diverse malignant tumors. The roles of LINC00667 in cancer development have been explored in glioma, hepatocellular carcinoma and non-small cell lung cancer, but not in nasopharyngeal carcinoma (NPC). In the present study, we characterize the role and molecular mechanism of LINC00667 in NPC progression. It was found that LINC00667 was overexpressed in NPC cells compared to normal cells. Silencing LINC00667 suppressed the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) in NPC cells. In addition, bioinformatics analysis revealed that LINC00667 acted as a ceRNA to absorb miR-4319. Further investigations illustrated that miR-4319 had low expression in NPC cells and functioned as a tumor suppressor in the progression of NPC. Mechanistic study identified forkhead box Q1 (FOXQ1) as a functional target of miR-4319. The effect of LINC00667 in NPC development was mediated by the miR-4319/FOXQ1 axis. Analysis on tumorxenograft mouse model demonstrated that knockdown of LINC00667 repressed NPC tumor growth in vivo and confirmed the in vitro results. Our present study suggested that LINC00667 promoted the malignant phenotypes of NPC cells by competitively binding to miR-4319 to up-regulate FOXQ1 expression. Our results reveled that LINC00667 could be a diagnostic and therapeutic target for NPC patients.

Long intergenic non-protein coding RNA 02570 promotes nasopharyngeal carcinoma progression by adsorbing microRNA miR-4649-3p thereby upregulating both sterol regulatory element binding protein 1, and fatty acid synthase

“…Mechanistically, lncRNAs mainly regulate target gene expression by adsorbing miRNAs. For instance, LINC00667 promotes NPC progression by adsorbing miR-4319, increasing levels of forkhead box Q1 (FOXQ1) [ 18 ]. MSC antisense RNA 1 (MSC-AS1) exacerbated NPC progression by adsorbing miR-524-5p to upregulate nuclear receptor subfamily 4 group A member 2 (NR4A2) [ 19 ].…”

LncRNA LINC00667 gets involved in clear cell renal cell carcinoma development and chemoresistance by regulating the miR-143-3p/ZEB1 axis

“…For instance, LINC00667 stimulates migration, invasion, and proliferation in cells pertaining to esophageal cancer by mediating the sponge axis miR-200b-3p/SLC2A3 [ 19 ]. LINC00667 up-regulates FOXQ1 by combining with miR-4319 in a competitive manner, hence facilitating the malignant phenotype of nasopharyngeal carcinoma cells [ 20 ]. It was found that LINC00667 silencing restrained the proliferation, migration and angiogenesis of non-small cell lung cancer cells ex vivo .…”

LncRNA LINC00667 aggravates the progression of hepatocellular carcinoma by regulating androgen receptor expression as a miRNA-130a-3p sponge

“…For example, lncRNA AY promoted HCC metastasis by inducing ITGAV transcription [ 37 ], and lncRNA-PDPK2P promoted the progression of HCC via PDK1/AKT/caspase 3 axis [ 38 ]. It has been reported that LncRNA LINC00667 is upregulated in many kinds of cancers such as colorectal cancer [ 39 ] and lung cancer [ 40 ] as well as nasopharyngeal carcinoma [ 41 ]. However, the roles of LINC00667 in HCC remain largely unclear.…”