Abstract
Emerging evidence has confirmed that long noncoding RNAs (lncRNAs) are strongly involved in tumor initiation and development. LncRNA ZFPM2 antisense RNA 1 (ZFPM2-AS1) has been identified as a tumor facilitator in some cancers; nevertheless, its functional significance and regulatory mechanism remain greatly unclear in esophageal squamous cell carcinoma (ESCC). Here, we detected ZFPM2-AS1 expression in ESCC cell lines using qRT-PCR. ZFPM2-AS1 knockdown models were established for investigating the biological function of ZFPM2-AS1 in ESCC cells. The association between miR-3612 and ZFPM2-AS1 or TRAF4 was assessed by RNA pull-down and luciferase reporter assays. The present study indicated that ZFPM2-AS1 was significantly up-regulated in ESCC cells. Functional assays manifested that ZFPM2-AS1 knockdown restrained cell proliferation, migration and invasion, and facilitated cell apoptosis in ESCC. Mechanistically, ZFPM2-AS1 promoted ESCC cell growth and up-regulated TRAF4 to trigger NF-κB pathway by sequestering miR-3612. Besides, miR-3612 was confirmed to be a tumor inhibitor in ESCC. Through restoration experiments, we observed that TRAF4 overexpression could recover the suppressive effect of ZFPM2-AS1 on ESCC cell growth. Collectively, all the results suggested that ZFPM2-AS1 was an oncogene in ESCC cell growth by up-regulating TRAF4 and activating NF-κB pathway.
Highlights
Esophageal cancer, a commonly occurred cancer, causes the increasing deaths that related to cancers worldwide [1]
These findings suggested that ZFPM2-AS1 (NR 125796.1 but not NR 125797.1) is overexpressed in Esophageal squamous cell carcinoma (ESCC) and promotes ESCC cell growth
Accumulating studies have uncovered the aberrant expression of long noncoding RNA (lncRNA) in ESCC [22]
Summary
Esophageal cancer, a commonly occurred cancer, causes the increasing deaths that related to cancers worldwide [1]. It is of great importance to explore the novel biomarkers and mechanisms underlying ESCC progression for identifying attractive therapeutic strategies. LncRNA functions as a regulator in gene expression via multiple mechanisms, such as chromatin modifications, miRNA competition, protein amounts and genomic interactions [6,7]. LncRNA ZEB1-AS1 acts as an oncogene in glioma and promotes cancer progression [10]. LncRNA HULC promotes cell proliferation and invasion and activates PI3K/AKT pathway in pancreatic cancer [11]. SNHG6 [13] and LINC01980 [14] are up-regulated in ESCC and function as tumor promoter in ESCC progression. GAS5 [15] and FER1L4 [16] are down-regulated in ESCC and suppress the cancer progression.
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