Long noncoding RNA <i>FER1L4</i> acts as an oncogenic driver in human pan‐cancer

You, Zilong; Ge, Anqi; Pang, Da; Zhao, Yong; Xu, Shouping

doi:10.1002/jcp.29098

Cited by 15 publications

(14 citation statements)

References 33 publications

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“…Furthermore, Fer1L4 expression was an independent predictor of PFS, CSS, and OS in ccRCC patients. A recent study analyzed Fer1L4 in a pan-cancer study and demonstrated similar findings for a subset of RCC patients [17].…”

Section: Discussionmentioning

confidence: 58%

“…Additionally, siRNA-mediated knockdown of Fer1L4 decreased invasiveness of glioblastoma cells and induced apoptosis [18]. In breast cancer, upregulation of Fer1L4 is linked to promoter hypomethylation suggesting that Fer1L4 expression is epigenetically regulated [17]. Taken together, Fer1L4 expression is different in various tumor entities and may exercise as well as oncogenic and tumor suppressive effects.…”

Section: Discussionmentioning

confidence: 98%

“…It was demonstrated that Fer1L4 influences cell proliferation as a tumor suppressor by acting as a competing endogenous RNA [11][12][13]. In various tumor entities such as gastric cancer, ovarian cancer, endometrial carcinoma, lung cancer, and osteosarcoma, expression of Fer1L4 was found to be decreased [12][13][14][15][16], whereas upregulation was reported in human glioblastoma and breast cancer [17,18]. The detailed molecular and functional mechanism of its regulatory…”

Section: Introductionmentioning

confidence: 99%

“…The detailed molecular and functional mechanism of its regulatory properties is yet unclear. In the absence of any data regarding to the role of Fer1L4 in renal-cell carcinoma (RCC) [ 17 ], our study was designed to explore the expression pattern of Fer1L4 in RCC and corresponding normal tissues to investigate its influence on tumor biology and impact on patients’ survival.…”

Section: Introductionmentioning

confidence: 99%

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The lncRNA Fer1L4 is an adverse prognostic parameter in clear-cell renal-cell carcinoma

et al. 2020

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Purpose Long non-coding RNAs (lncRNA) are involved in oncogenesis and tumor progression in various tumor entities. At present, little is known about the role in tumor biology of the lncRNA Fer-1 like family member 4 (Fer1L4) in clear-cell renal-cell carcinoma (ccRCC). The aim of this study is to evaluate the expression of Fer1L4 in patients with ccRCC, its association with clinicopathological parameters, and value as prognostic biomarker. Material and methods The expression of Fer1L4 was analyzed in the TCGA ccRCC cohort (n = 603; ccRCC n = 522, normal n = 81) and subsequently validated by quantitative real-time PCR in an independent cohort (n = 103, ccRCC n = 69, normal n = 34). Expression profiles were statistically correlated with clinicopathological and survival data. Results Fer1L4 lncRNA is overexpressed in ccRCC compared to adjacent normal tissues. Increased expression significantly correlates with tumor aggressiveness: high expression levels of Fer1L4 RNA were found in higher grade, higher stage, and metastatic tumors. Furthermore, Fer1L4 overexpression is an independent prognostic factor for overall, cancer-specific, and progression-free survival of patients with ccRCC. Conclusion Fer1L4 expression significantly correlates with aspects of tumor aggressiveness. Based on this impact on tumor progression and its influence as an independent prognostic factor, Fer1L4 appears to exert properties as an oncogene in ccRCC. As a prognostic tissue biomarker, further functional investigations are warranted to investigate Fer1L4 as a potential therapeutic target.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The lncRNA Fer1L4 is an adverse prognostic parameter in clear-cell renal-cell carcinoma

et al. 2020

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“…One study found that there is a high expression of the lncRNA fer1l4 in human tumor tissues. Moreover, GO enrichment analysis also revealed that fer1l4 may be involved in processes associated with tumorigenesis [94]. Recent research shows that lncRNAs are associated with organismal aging.…”

Section: Non-coding Rnas In Invertebrates During Agingmentioning

confidence: 99%

The Epigenetics of Aging in Invertebrates

Gao

et al. 2019

IJMS

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Aging is an unstoppable process coupled to the loss of physiological function and increased susceptibility to diseases. Epigenetic alteration is one of the hallmarks of aging, which involves changes in DNA methylation patterns, post-translational modification of histones, chromatin remodeling and non-coding RNA interference. Invertebrate model organisms, such as Drosophila melanogaster and Caenorhabditis elegans, have been used to investigate the biological mechanisms of aging because they show, evolutionarily, the conservation of many aspects of aging. In this review, we focus on recent advances in the epigenetic changes of aging with invertebrate models, providing insight into the relationship between epigenetic dynamics and aging. conserved in both insects and mammals, where it regulates the rate of aging [11]. Therefore, this review will summarize recent advances in the roles of epigenetic changes in aging in these two invertebrates. DNA Methylation in Invertebrate AgingDNA methylation is a covalent chemical modification, which usually occurs at 5-methyl cytosine (5mC) and which is enriched in cytosine phosphate guanine (CpG) dinucleotides [12]. CpG methylation within promoters leads to transcriptional repression through the formation of compact chromatin structures such as heterochromatin. Conversely, promoters of genes that are highly expressed are devoid of DNA methylation, hence their name-CpG islands [13]. The dynamic changes in DNA methylation can impact aging and health. The local methylation level increases while the global methylation level decreases with aging [14]. Age-related DNA methylation changes are also correlated with human age-related diseases, such as cancer and sarcopenia [15,16]. Cytosine methylation is catalyzed by three DNA methyltransferases (DNMTs): DNMT1, DNMT3a, and DNMT3b. Three ten-eleven translocation (TET) proteins initiate the specific demethylation of 5mC residues in DNA: TET1, TET2, and TET3 [17]. The schematic diagram of DNA methylation and demethylation is shown in Figure 1. Worms do not encode a conventional DNA methyltransferase to silence DNA repeats, which led to the prevailing view that DNA methylation does not occur in C. elegans [18]. Similarly, in adult D. melanogaster, only a low level of DNA methylation was confirmed [19,20]. In Drosophila, overexpression of the DNA methyltransferase gene, dDnmt2, extends lifespan in a small heat shock protein-dependent way [21]. However, although 5mC methylation is rare, methylation on N6 adenine (6mA) is prevalent in C. elegans and D. melanogaster [22,23]. Recent studies have confirmed that NMAD-1 (MT-A70 family) and DMAD (DNA 6mA demethylase, TET ortholog) are 6mA demethylases in C. elegans and D. melanogaster, respectively. DAMT-1 (AlKB family) is likely a 6mA methyltransferase in C. elegans [24]. NMAD-1 and DAMT-1 can regulate 6mA levels and control the epigenetic inheritance of phenotypes associated with the loss of the H3K4me2 demethylase spr-5 [22]. The worm mutant of spr-5 displayed a transgenerational increase in H3K4me...

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Effects of FER1L4-miR-106a-5p/miR-372-5p-E2F1 regulatory axis on drug resistance in liver cancer chemotherapy

Chen

Dong

et al. 2021

Molecular Therapy - Nucleic Acids

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Liver cancer presents a challenge in today’s healthcare system. This study aimed at investigating the effects of Fer-1 like family member 4 (FER1L4) on chemotherapy resistance and liver cancer development by using clinically collected liver cancer tissues and commercially purchased human liver cancer cisplatin-resistant cell line HUH-7/DDP. Bioinformatics analysis, dual luciferase reporter gene assay, and RNA pull-down were applied to predict and verify the possible binding relationships. The expressions of FER1L4, E2F transcription factor 1 (E2F1), microRNA-106a-5p (miR-106a-5p), or miR-372-5p were altered in the cells, followed by flow cytometry, Cell Counting Kit-8 (CCK-8), and Transwell assays to evaluate apoptotic, proliferative, and invasive abilities in vitro and nude mice xenografts to observe tumor growth in vivo . FER1L4 was highly expressed and miR-106-5p and miR-372-5p were poorly expressed in tumor cells and tissues. FER1L4 knockdown or the overexpression of miR-106-5p and miR-372-5p inhibited the cancerous cell proliferation and invasion while promoting apoptosis. FERIL4 silencing increased the miR-106-5p/miR-372-5p expression to inhibit the E2F1-activated nuclear factor κB (NF-κB) pathway. Besides, overexpressing FER1L4 led to an increased tumor growth in nude mice, which was reversed by the NF-κB inhibitor pyrollidine dithiocarbamate (PDTC). In conclusion, the results indicated that FER1L4 could inhibit the expression of miR-106a-5p/miR-372-5p, to activate E2F1-mediated NF-κB pathway, leading to drug resistance in liver cancer.

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Long noncoding RNA FER1L4 acts as an oncogenic driver in human pan‐cancer

Cited by 15 publications

References 33 publications

The lncRNA Fer1L4 is an adverse prognostic parameter in clear-cell renal-cell carcinoma

The lncRNA Fer1L4 is an adverse prognostic parameter in clear-cell renal-cell carcinoma

The Epigenetics of Aging in Invertebrates

Effects of FER1L4-miR-106a-5p/miR-372-5p-E2F1 regulatory axis on drug resistance in liver cancer chemotherapy

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