FEZ Family Zinc Finger 1 Antisense RNA 1 Research Articles

LncRNA FEZF1-AS1 aggravates cell proliferation and migration in glioblastoma

ObjectivesGlioblastoma (GBM) represents the commonest malignant glioma. Long non-coding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) has been validated to play an oncogenic role in multiple human malignancies, while its function in GBM has not been largely reported. We aim to identify the regulatory mechanism of FEZF1-AS1 in GBM. Materials & MethodsThe expression pattern of FEZF1-AS1 was firstly figured out in GBM cells using RT-qPCR. Then, functional assays were conducted to examine the influence FEZF1-AS1 had on the biological properties of GBM cells. The downstream targets of FEZF1-AS1 were predicted and the underlying regulatory mechanism was determined by mechanism assays. ResultsFEZF1-AS1 possessed high expression in GBM cells. Down-regulation of FEZF1-AS1 suppressed GBM cell proliferation, migration and invasion while inducing cell apoptosis. With the help of bioinformatics prediction and mechanism assays, FEZF1-AS1 was found to bind to miR-363-3p and NOB1 was determined to be the downstream gene. Finally, results of rescue assays verified that the suppressive function of FEZF1-AS1 inhibition on GBM development were restored by miR-363-3p depletion or overexpression of NOB1. ConclusionFEZF1-AS1 had oncogenic function in the advancement of GBM by targeting miR-363-3p/NOB1, which made FEZF1-AS1 a potential biomarker for GBM treatment.

Up-Regulated LncRNA FEZF1-AS1 Promotes the Progression of Cervical Carcinoma Cells via MiR-367-3p/SLC12A5 Signal Axis

Cervical cancer (CC) is a common female malignant tumor. With the trend of younger onset, people pay more and more attention to it. Numberless evidence has been indicated that long non-coding RNAs (lncRNAs) can take part in progression of cancers and can exert the regulatory roles in assorted cancers. Nevertheless, the roles of FEZ family zinc finger 1-antisense RNA 1 (FEZF1-AS1) in CC cells are still undiscovered. Thus, the central purpose of our research was to reveal the specific functions and molecular mechanisms of FEZF1-AS1 in CC cells. RT-qPCR was utilized to test FEZF1-AS1 expression in CC cells. In addition, functional assays were conducted to evaluate cell proliferation, apoptosis, and migration as well as invasion. In addition, mechanism experiments verified relationship among FEZF1-AS1, miR-367-3p and solute carrier family 12 member 5 (SLC12A5). FEZF1-AS1 was highly expressed in CC cells. Moreover, FEZF1-AS1 depletion suppressed proliferation, migration, invasion, and induced cell apoptosis. Importantly, mechanism experiments confirmed that miR-367-3p could bissnd to FEZF1-AS1 and SLC12A5. The rescue assays determined that FEZF1-AS1 could up-regulate SLC12A5 through binding to miR-367-3p. The up-regulated FEZF1-AS1 could accelerate the malignant behaviors of CC cells by miR-367-3p/SLC12A5 signal axis.

LncRNA FEZF1-AS1 promotes colorectal cancer progression through regulating the miR-363-3p/PRRX1 pathway.

Long non-coding RNAs (lncRNAs) are involved in the development of many cancers, including colorectal cancer (CRC). FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) is a key lncRNA in the regulation of CRC progression, but its potential molecular mechanisms need to be further explored. To investigate the mechanism of lncRNA FEZF1-AS1 in the progression of CRC. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure FEZF1-AS1 and miR-363-3p expression. Cell proliferation, migration and invasion were analyzed using Cell Counting Kit-8 (CCK-8) and transwell assays. Protein expression of epithelial-mesenchymal transformation (EMT)-related markers and paired-related homeobox 1 (PRRX1) were determined using western blot analysis. The interactions among FEZF1-AS1, miR-363-3p and PRRX1 were verified with dual-luciferase reporter assay. A xenograft model was constructed in vivo to confirm the role of FEZF1-AS1 in CRC tumor growth. We demonstrated that FEZF1-AS1 expression was upregulated in CRC, and its silencing reduced CRC cell proliferation, migration, invasion, and EMT. MiR-363-3p could be inhibited by FEZF1-AS1, which inhibitor could reverse the suppressive effect of FEZF1-AS1 silencing on CRC progression. Paired-related homeobox 1 could be targeted by miR-363-3p, and the inhibitory effect of FEZF1-AS1 knockdown on CRC progression could also be eliminated by PRRX1 overexpression. Furthermore, interference of FEZF1-AS1 reduced the tumor growth of CRC in vivo. Our data demonstrate that FEZF1-AS1 regulated PRRX1 expression to promote CRC progression via inhibition of miR-363-3p.

Long non‑coding RNA FEZF1‑AS1 facilitates non‑small cell lung cancer progression via the ITGA11/miR‑516b‑5p axis.

Long non-coding RNAs (lncRNAs) have emerged as key players in the development and progression of cancer. FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) is a novel lncRNA that is involved in the development of cancer and acts as a potential biomarker for cancer. However, the clinical significance and molecular mechanism of FEZF1-AS1 in non-small cell lung cancer (NSCLC) remains uncertain. In the present study, FEZF1-AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC. Loss-of-function assays revealed that FEZF1-AS1 inhibition decreased cell proliferation and migration, and arrested cells at the G2/M cell cycle phase. Mechanistically, FEZF1-AS1 expression was influenced by N6-methyladenosine (m6A) modification. Since FEZF1-AS1 was mainly located in the cytoplasmic fraction of NSCLC cells, it was hypothesized that it may be involved in competing endogenous RNA regulatory network to impact the prognosis of NSCLC. Via integrating Arraystar Human mRNA microarray data and miRNA bioinformatics analysis, it was revealed that ITGA11 expression was decreased with loss of FEZF1-AS1 and increased with gain of FEZF1-AS1 expression, and microRNA (miR)-516b-5p inhibited the expression levels of both FEZF1-AS and ITGA11. RNA-binding protein immunoprecipitation and RNA pulldown assays further demonstrated that FEZF1-AS1 could bind to miR-516b-5p and that ITGA11 was a direct target of miR-516b-5p by luciferase reporter assay. Overall, the present findings demonstrated that FEZF1-AS1 was upregulated and acted as an oncogene in NSCLC by regulating the ITGA11/miR-516b-5p axis, suggesting that FEZF1-AS1 may be a potential prognostic biomarker and therapeutic target for NSCLC.

LncRNA FEZF1‑AS1 promotes migration, invasion and epithelial‑mesenchymal transition of retinoblastoma cells by targeting miR‑1236‑3p.

Long non-coding RNAs (lncRNAs) and microRNAs (miRs) have been reported to regulate disease progression in numerous types of disease, including retinoblastoma (Rb). Therefore, the present study aimed to investigate the effects of the lncRNA FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) on Rb and to determine its possible mechanism of action. Reverse transcription-quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit-8, wound healing and transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. The potential association between FEZF1-AS1 and miR-1236-3p in Y79 cells was measured via dual-luciferase reporter assay. The results of the present study revealed that the levels of FEZF1-AS1 were significantly upregulated in different Rb cell lines, with the most prominent upregulation observed in Y79 cells. In addition, the cell viability, invasive and migratory abilities, and the ability to undergo epithelial-mesenchymal transition (EMT), were significantly inhibited following the transfection of short hairpin RNA (shRNA)-FEZF1-AS1 into Y79 cells. Further experimental validation confirmed that miR-1236-3p may be a direct target of FEZF1-AS1. Notably, the miR-1236-3p inhibitor was discovered to reverse the inhibitory effects of shRNA-FEZF1-AS1 on cell viability, invasion, migration and EMT. In conclusion, the findings of the present study suggested that lncRNA-FEZF1-AS1 may promote the viability, migration, invasion and EMT of Rb cells by modulating miR-1236-3p.

Plasma lncRNA FEZF1-AS1 as a potential biomarker for diagnosis of non-small-cell lung carcinoma.

Diagnosis of numerous cancers has been closely linked to the expression of certain long non-coding RNAs. This study aimed to evaluate levels of plasma FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) relative to non-small-cell lung carcinoma (NSCLC) diagnosis.The level of FEZF1-AS1 in the blood plasma of 126 NSCLC patients and 62 healthy controls was examined by quantitative real-time polymerase chain reaction.Plasma FEZF1-AS1 of the NSCLC group was increased compared with that in the control group (P < .0001). Plasma FEZF1-AS1 could distinguish patients with NSCLC from healthy individuals via the area under the ROC curve (AUC) of 0.855 (95% CI = 0.800–0.909; P = .000). FEZF1-AS1 combined with neuron-specific enolase increased the area under the (ROC) curve to 0.932 (95% CI = 0.897–0.968; P = .018). A high expression level of plasma FEZF1-AS1 was associated with some clinical features of NSCLC. Increased expression of FEZF1-AS1 greatly improved the risk of NSCLC (adjusted OR = 2.42; 95% CI = 1.23–4.76). A significant concentration–dependent relationship was noted between risk of NSCLC and higher FEZF1-AS1 expression (P for trend <.001).Plasma FEZF1-AS1 could potentially be used as a biomarker for NSCLC diagnosis.

Progress in Role of FEZF1-AS1 in Non-small Cell Lung Cancer

现如今越来越多的证据表明，长非编码RNA（long non-coding RNA, lncRNA）在肿瘤发生及发展中起着重要的作用。作为一种新发现的lncRNA，FEZ家族锌指1反义RNA1（FEZ family zinc finger 1-antisense RNA 1, FEZF1-AS1）在非小细胞肺癌（non-small cell lung cancer, NSCLC）等恶性肿瘤中表达上调，且FEZF1-AS1的异常表达与NSCLC患者的临床特征及预后有关。此外，FEZF1-AS1可以通过多种机制调节肺癌细胞增殖、迁移和侵袭等生物学过程，可能是潜在的NSCLC治疗新靶点。本文就FEZF1-AS1在NSCLC中的最新研究进展进行阐述。

LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Gastric cancer (GC) is a leading cause of cancer-related death with poor prognosis. Growing evidence has shown that long noncoding ribonucleic acid (lncRNA) FEZ family zinc finger 1 antisense RNA 1(FEZF1-AS1), an “oncogene,” regulates tumor progression and supports cancer stem cell. However, the tumorigenic mechanism of FEZF1-AS1 on gastric cancer stem cell (GCSC) is yet to be investigated. Here, we discovered that FEZF1-AS1 was upregulated in GC tissues and cell lines. Knockdown of FEZF1-AS1 inhibited sphere formation and decreased expression of stem factors and markers. Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. MiR-363-3p is used as a target of FEZF1-AS1, because its expression was suppressed by FEZF1-AS1 in GCSCs. FEZF1-AS1 could sponge miR-363-3p and increased the expression of high-mobility group AT-hook 2 (HMGA2). The expression of FEZF1-AS1 and miR-363-3p, as well as that of miR-363-3p and HMGA2, was negatively correlated in GC tissues. Finally, FEZF1-AS1 contributed to promotion of GCSCs progression partially through inhibition of miR-363-3p. Subcutaneous xenotransplanted tumor model revealed that silence of FEZF1-AS1 suppressed in vivo tumorigenic ability of GSCS via downregulation of HMGA2. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.

Circulatinglong non-coding RNA FEZF1-AS1 and AFAP1-AS1 serve as potential diagnostic biomarkers for gastric cancer

BackgroundGrowing evidence indicates that two long non-coding RNAs (lncRNAs), FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) and Actin filament associated protein 1 antisenseRNA1 (AFAP1-AS1), are highly expressed in different cancers, including gastric cancer (GC). However, the expression pattern and clinical utility of these two lncRNAs are still unknown. MethodsSerum expression levels of FEZF1-AS1 andAFAP1-AS1 were measured by quantitative real-time polymerase chain reaction (qRT-PCR). CEA and CA19-9 were detected by ARCHITET I2000 SR. Analyses were all performed using SPSS software version 20.0 (SPSS Inc., Chicago, USA). P < 0.05 was considered statistically significant. ResultsDetection of serum FEZF1-AS1 and AFAP1-AS1 showed both of them were up-regulated in GC patients compared with the normal controls (p < 0.0001), and high serum expression levels were correlated with tumor size, tumor-node-metastasis (TNM) stage and lymph node metastasis. Besides, the area under the ROC curve (AUC) demonstrated the two lncRNAs had higher diagnostic utility than CEA and CA19-9. Furthermore, when combined the two lncRNAs as a model, it yielded an AUC of 0.866, and the combination of the model, CEA and CA19-9 could observably improve diagnostic sensitivity to 95.5 %. What’s more, circulating FEZF1-AS1 and AFAP1-AS1 were significantly decreased after the GC patients underwent the operation (both p < 0.001). ConclusionOur study indicated that serum FEZF1-AS1 and AFAP1-AS1 had better sensitivity and efficiency for the diagnosis of GC and the combination of the two lncRNAs might be used as a potential prognostic indicator in GC.

FEZF1-AS1: a novel vital oncogenic lncRNA in multiple human malignancies.

Long noncoding RNAs (LncRNAs) refer to the RNA with a length of >200 nucleotides, which lack or have no open reading coding frame and have higher tissue and organ specificity compared with the protein coding genes. A surging number of studies have shown that lncRNA is involved in numerous essential regulatory processes, such as X chromosome silencing, genomic imprinting, chromatin modification, transcriptional activation, transcriptional interference and nuclear transport, which are closely related to the occurrence and development of human malignancies. FEZ family Zinc Finger 1-Antisense RNA 1 (FEZF1-AS1) of FEZ family is a recently discovered lncRNA. FEZF1-AS1 is highly expressed in pancreatic cancer, colorectal cancer, lung adenocarcinoma and other human malignancies, and is associated with poor prognosis. As an oncogene, it plays crucial role in the proliferation, migration, invasion and Warburg effect of various tumor cells. In addition, FEZF1-AS1 is also involved in the regulation of multiple signal pathways such as epithelial–mesenchymal transition (EMT), signal transducer and activator of transcription 3 (STAT3) and Wnt/ β-catenin. In this paper, the recent research progress of FEZF1-AS1 in tumorigenesis and development is reviewed systematically.

LncRNA FEZF1-AS1 Promotes TGF-β2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04.

Posterior capsule opacification (PCO) is a common complication after cataract surgery attributed to the proliferation and migration of postoperative residual lens epithelial cells (LECs). The long noncoding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) promotes the proliferation and migration of multiple types of cancer cells. Here, we discovered that FEZF1-AS1 is markedly upregulated in TGF-β2-treated SRA01/04 cells. In addition, the proliferation and migration of SRA01/04 cells were enhanced following TGF-β2 treatment. FEZF1-AS1 knockdown inhibited the TGF-β2-induced proliferation and migration of SRA01/04 cells. Accordingly, FEZF1-AS1 overexpression promoted the TGF-β2-induced proliferation and migration of SRA01/04 cells. Finally, FEZF1-AS1 upregulated TGF-β2-induced SRA01/04 cell proliferation and migration via boosting FEZF1 protein levels. Our findings indicate that the dysregulation of FEZF1-AS1 participates in the TGF-β2-induced proliferation and migration of human lens epithelial cells (HLECs), which might be achieved, at least in part, through the induction of FEZF1 expression.

Prognostic value of lncRNA FEZF1 antisense RNA 1 over-expression in oncologic outcomes of patients with solid tumors

Background:FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1), as a novel lncRNA, was reported to be up-regulated in various cancers and involved in tumor progression. This study systematically assessed the prognostic value of FEZF1-AS1 in solid tumors.Methods:Web of Science, PubMed, EMBASE, Chinese National Knowledge Infrastructure, and Wanfang databases were searched for eligible studies that evaluated the prognostic role of FEZF1-AS1 expression in cancer patients. Pooled hazard ratios (HRs) and combined odds ratios (ORs) with their 95% confidence intervals (CIs) were calculated. The meta-analysis was conducted using Stata/SE 14.1.Results:Fifteen original studies involving 1378 patients were enrolled. Pooled results showed that increased expression of FEZF1-AS1 significantly correlated with shorter overall survival (OS) in cancer patients (HR 2.04, 95% CI 1.60–2.47), and also shorter disease-free survival (DFS) (HR 2.08, 95% CI 1.27–2.89). Additionally, the combined ORs indicated that increased FEZF1-AS1 expression was significantly associated with lymph node metastasis (OR 3.35, 95% CI 1.98–5.67), distant metastasis (OR 3.10, 95% CI 1.86–5.15), poor tumor differentiation (OR 2.90, 95% CI 1.45–5.80), high depth of tumor invasion (OR 2.72, 95% CI 1.36–5.43), and advanced clinical stage (OR 2.76, 95% CI 1.75–4.35). Expression analysis using the Gene Expression Profiling Interactive Analysis database indicated that the expression of FEZF1-AS1 was higher in tumor tissues than that in the corresponding normal tissues. The results of survival analysis revealed that increased FEZF1-AS1 expression was correlated with poor OS and DFS in cancer patients.Conclusions:LncRNA FEZF1-AS1 may serve as a valuable prognostic biomarker for clinical outcomes in various solid tumors.

&lt;p&gt;Long noncoding RNA FEZF1-AS1 promotes the motility of esophageal squamous cell carcinoma through Wnt/β-catenin pathway&lt;/p&gt;

Background: Long noncoding RNAs (lncRNAs), a class of noncoding RNA nucleotides >200 bp, has been demonstrated to play vital role in the development of cancer. FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) has been reported as an lncRNA which acts as a tumor-promoting effect in some cancers. However, the role of it in esophageal squamous cell carcinoma (ESCC) and its potential regulatory mechanism was unclear now.Methods: qRT-PCR was used to detect the levels of FEZF1-AS1 and mRNA CTNNB1 (β-catenin) in ESCC tissues and cells. Cell transfection experiments were used to knock down or overexpress the level of FEZF1-AS1 in EC1 and EC9706 cell lines. WST-1 assays, cell cycle assays, scratch wound assays, migration, and invasion assays were used to evaluate the function of FEZF1-AS1 in ESCC progression.Results: FEZF1-AS1 was remarkably upregulated in ESCC tissues and cell lines. Silencing of FEZF1-AS1 significantly inhibited the migration and invasion of ESCC cells, while overexpression of FEZF1-AS1 notably accelerated ESCC migration and invasion. Meanwhile, the levels of FEZF1-AS1 had no effect on ESCC cell proliferation and cell cycle. We also found that β-catenin was upregulated in ESCC tissues, and the level of it was positively correlated with the expression of FEZF1-AS1. Silencing of FEZF1-AS1 could decrease the mRNA and protein level of β-catenin, while overexpression FEZF1-AS1 could lead to the contrary.Conclusion: Our results suggested that the expression of lncRNA FEZF1-AS1 played an important role in ESCC progression, especially the motility of the tumor. FEZF1-AS1 may provide us with a new sight for ESCC treatment.