FALEC

Gene Summary

Gene:FALEC; focally amplified long non-coding RNA in epithelial cancer
Aliases: FAL1, ncRNA-a1, LINC00568
Location:1q21.2
Summary:-
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Source:NCBIAccessed: 01 September, 2019

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 01 September 2019 using data from PubMed using criteria.

Literature Analysis

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Tag cloud generated 01 September, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (1)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications: FALEC (cancer-related)

Wu K, Zhang N, Ma J, et al.
Long noncoding RNA FAL1 promotes proliferation and inhibits apoptosis of human colon cancer cells.
IUBMB Life. 2018; 70(11):1093-1100 [PubMed] Related Publications
Aberrant expression of long non-coding RNAs (lncRNAs) has been associated with a variety of malignancies including colon cancer. In this study, we aimed to characterize the biological mechanisms of focally amplified lncRNA on chromosome 1 (FAL1) in colon cancers. Here, our results indicate that FAL1 expression was remarkably up-regulated in colon tumor tissues as compared to corresponding tumor-adjacent normal tissues. Importantly, the cumulative survival rate of patients with high levels of FAL1 in tumor tissues was considerably lower than those with low FAL1 levels in tumor tissues. Cox regression analysis showed that lncRNA FAL1 could act as an independent prognostic factor in CRC. Knockdown of FAL1 in HT29 cells attenuated cell proliferation and stimulated cell apoptosis. In contrast, overmetastasis-related molecules Bcl-2, TGF-β1, p65, and PCNA at the mRNA and protein levels. Mechanistically, FAL1 was found to interact with STAT3 at 200 to 400 bp and promote phosphorylation of STAT3. In addition, we found that knockdown of STAT3 in HT29 cells abolished the effects of FAL1 on cell proliferation as well as the expression of TGF-β1 and Bcl-2. Based on these findings, we concluded that FAL1 might be a potential oncogene for the progression of colon cancer. © 2018 IUBMB Life, 70(11):1093-1100, 2018.

Li B, Mao R, Liu C, et al.
LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells.
Life Sci. 2018; 197:122-129 [PubMed] Related Publications
BACKGROUND: Long non-coding RNAs (LncRNAs) have been demonstrated to play crucial role in tumor growth and metastasis for hepatocellular carcinoma (HCC). LncRNA FAL1 has been indicated to promote the progression of various cancers. However, the role of lncRNA FAL1 in HCC was poorly understood.
METHODS: The expression levels of lncRNA FAL1 in HCC tissues and cells were determined by RT-qPCR. The roles of lncRNA FAL1 on HCC cells were investigated by MTT, colony formation, transwell, RT-qPCR, and Western blotting. The miRNA binding sites of lncRNA FAL1 was predicted using RegRNA 2.0 and miR-1236 was validated to target lncRNA FAL1 by luciferase reporter assays and RT-qPCR. Finally, the expression levels of lncRNA FAL1 in serum exosome of HCC patients was also investigated and the role of exosome-mediated lncRNA FAL1 was further investigated by co-culturing with HCC cells.
RESULTS: This study first showed that lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC. LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover, lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migration.
CONCLUSIONS: Taken together, this study indicated that lncRNA FAL1 functions as an oncogenic in HCC and may be a novel diagnostic biomarker or a novel target for the treatment of HCC in future.

Ni N, Song H, Wang X, et al.
Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21.
Biomed Pharmacother. 2017; 96:1371-1379 [PubMed] Related Publications
Accumulating evidences have suggested that focally amplified lncRNA on chromosome 1 (FALEC) serves as an oncogenic long non-coding RNA (lncRNA) and has been identified to be dysregulated in various tumors. However, the expression, clinical values, and biological function of FALEC in melanoma are still unknown. In this study we detected the expression level of FALEC in tumor tissues and cell lines and measured the prognostic value of FALEC for melanoma patients and the biological effects of FALEC on melanoma cell proliferation, cell cycle, and apoptosis. Our results indicated that FALEC was more highly expressed in melanoma tissues and cell lines than in non-neoplastic nevi tissues and normal cell lines. Moreover, functional assays showed that silenced FALEC suppressed the proliferation of melanoma cells, resulted in cell cycle arrest, and induced apoptosis. Mechanically, we discovered that FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21. Generally, our results suggested that FALEC acted as an oncogene in melanoma and had the potential to be a prognostic biomarker and therapeutic target for melanoma.

Murugan AK, Munirajan AK, Alzahrani AS
Long noncoding RNAs: emerging players in thyroid cancer pathogenesis.
Endocr Relat Cancer. 2018; 25(2):R59-R82 [PubMed] Related Publications
Thyroid cancer continues to be the most common malignancy of endocrine glands. The incidence of thyroid cancer has risen significantly over the past 4 decades and has emerged as a major health issue. In recent years, significant progress has been achieved in our understanding of the molecular mechanisms of thyroid carcinogenesis, resulting in significant diagnostic, prognostic and therapeutic implications; yet, it has not reached a satisfactory level. Identifying novel molecular therapeutic targets and molecules for diagnosis and prognosis is expected to advance the overall management of this common malignancy. Long noncoding RNAs (lncRNAs) are implicated in the regulation of various key cellular genes involved in cell differentiation, proliferation, cell cycle, apoptosis, migration and invasion mainly through modulation of gene expression. Recent studies have established that lncRNAs are deregulated in thyroid cancer. In this review, we discuss extensively the tumor-suppressive (for example, LINC00271, MEG3, NAMA, PTCSC1/2/3, etc.) and oncogenic (for example, ANRIL, FAL1, H19, PVT1, etc.) roles of various lncRNAs and their possible disease associations implicated in thyroid carcinogenesis. We briefly summarize the strategies and mechanisms of lncRNA-targeting agents. We also describe the potential role of lncRNAs as prospective novel therapeutic targets, and diagnostic and prognostic markers in thyroid cancer.

Zhao R, Sun F, Bei X, et al.
Upregulation of the long non-coding RNA FALEC promotes proliferation and migration of prostate cancer cell lines and predicts prognosis of PCa patients.
Prostate. 2017; 77(10):1107-1117 [PubMed] Related Publications
BACKGROUND: LncRNAs are aberrantly expressed in various cancer types and were found to be a responsible prognosis biomarker and therapeutic target of many human cancers.
METHODS: In this study, we characterized the expression profile of FALEC in prostate cancer and paired histologically normal tissues. Additionally, biological function of FALEC in prostate cancer cell lines was determined by in vitro and in vivo assays.
RESULTS: In a total of 85 patients, FALEC expression was significantly increased in clinical PCa tissues compared to adjacent normal tissues, and can be considered as an independent prognostic factor in patients with PCa. Downregulation of FALEC could inhibit cell proliferation, migration and invasion in vitro. In vivo tumorigenesis study and orthotopic bioluminescence image also support the evidence that FALEC may promote the progression of prostate cancer. We also find FALEC is a potential hypoxia induced lncRNA and can be induced by the hypoxia master regulator HIF-1α.
CONCLUSIONS: These findings suggested that FALEC may be a potential diagnostic and therapeutic target in patients with prostate cancer.

Jeong S, Lee J, Kim D, et al.
Relationship of Focally Amplified Long Noncoding on Chromosome 1 (FAL1) lncRNA with E2F Transcription Factors in Thyroid Cancer.
Medicine (Baltimore). 2016; 95(4):e2592 [PubMed] Free Access to Full Article Related Publications
Recent functional genomic studies revealed that the oncogenic activity of focally amplified lncRNA on chromosome 1 (FAL1, ENSG00000228126) contributes to tumor growth by p21 repression in human cancers. However, the expression of FAL1 was not investigated in papillary thyroid cancer (PTC). We aimed to determine if FAL1 was up-regulated in PTC compared to paired contralateral normal thyroid tissues, and to investigate the potential targets of this lncRNA and its clinicopathological significance in PTC. We analyzed FAL1 and p21 expression levels in 100 PTC samples and matched normal thyroid tissue by qRT-PCR. Using lncRNA microarray data from the Gene Expression Omnibus (accession no. GSE61763), we explored potential targets of FAL1 by Gene Set Enrichment Analysis, followed by verification by qRT-PCR in our PTC samples. A cross-sectional observational study was conducted to investigate the relationship between patients' clinicopathological features and FAL1 expression. FAL1 expression was significantly higher in PTC than in paired normal thyroid tissues (paired t test, P < 0.001). p21 mRNA expression was also increased, not decreased, in PTC, and had no correlation with FAL1 expression (r = 0.0897, P = 0.4002). Gene Set Enrichment Analysis, using publicly available microarray data, indicated that a gene set related to the cell cycle, including E2F transcription factors 1 and 2, and cyclin D1, was coordinately enriched among samples with high FAL1 expression. A volcano plot showed that E2F1, E2F2, and VEGFA mRNAs were increased in the high FAL1 samples. In clinicopathological analyses, multifocality was more frequently observed in PTC patients with high FAL1 (P = 0.018). Multivariate analysis showed that high FAL1 expression increased the risk of multifocality (after adjustment for clinical variables, OR = 4.019, CI = 1.041-11.020, P = 0.043). FAL1 may have a role in cell-cycle progression and may be associated with aggressive tumor behavior in PTC.

Hu X, Feng Y, Zhang D, et al.
A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer.
Cancer Cell. 2014; 26(3):344-357 [PubMed] Free Access to Full Article Related Publications
In a genome-wide survey on somatic copy-number alterations (SCNAs) of long noncoding RNA (lncRNA) in 2,394 tumor specimens from 12 cancer types, we found that about 21.8% of lncRNA genes were located in regions with focal SCNAs. By integrating bioinformatics analyses of lncRNA SCNAs and expression with functional screening assays, we identified an oncogene, focally amplified lncRNA on chromosome 1 (FAL1), whose copy number and expression are correlated with outcomes in ovarian cancer. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo.

Athie A, Huarte M
FAL1ing inside an amplicon.
Cancer Cell. 2014; 26(3):303-304 [PubMed] Related Publications
Frequently amplified regions of the cancer genome contain well-known oncogenes. In this issue of Cancer Cell, Hu and colleagues discover that FAL1, a long noncoding RNA is encoded in one of these regions. FAL1 acts as an oncogene by stabilizing BMI1, which results in the repression of CDKN1A expression.

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Cite this page: Cotterill SJ. FALEC, Cancer Genetics Web: http://www.cancer-genetics.org/FALEC.htm Accessed:

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