LncRNA REG1CP promotes tumorigenesis through an enhancer complex to recruit FANCJ helicase for REG3A transcription

Yari, Hamed; Jin, Lei; Teng, Liu; Wang, Yufang; Wu, Yongyan; Liu, Guang Zhi; Gao, Wei; Jin, Liang; Xi, Yanfeng; Feng, Yu Chen; Zhang, Chunming; Tabatabaee, Hessam; La, Ting; Yang, Rui; Wang, Fu Hua; Yan, Xu Guang; Farrelly, Margaret; Scott, Rodney J.; Liu, Tao; Thorne, Rick F.; Guo, Su; Zhang, Xu Dong

doi:10.1038/s41467-019-13313-z

Cited by 53 publications

(46 citation statements)

References 41 publications

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“…After discarding the supernatant, the cell pellet was resuspended in 0.5 ml PBS containing 10 μg/mL RNase A and 20 μg/mL PI stock solution and incubate at room temperature (RT) in the dark for 30 min. Cells were then subjected to analysis using a flow cytometer (FACSCanto, BD Biosciences) 70 . The gate strategy is shown in Supplementary Fig.…”

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confidence: 99%

c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis

et al. 2020

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The functions of the proto-oncoprotein c-Myc and the tumor suppressor p53 in controlling cell survival and proliferation are inextricably linked as “Yin and Yang” partners in normal cells to maintain tissue homeostasis: c-Myc induces the expression of ARF tumor suppressor (p14ARF in human and p19ARF in mouse) that binds to and inhibits mouse double minute 2 homolog (MDM2) leading to p53 activation, whereas p53 suppresses c-Myc through a combination of mechanisms involving transcriptional inactivation and microRNA-mediated repression. Nonetheless, the regulatory interactions between c-Myc and p53 are not retained by cancer cells as is evident from the often-imbalanced expression of c-Myc over wildtype p53. Although p53 repression in cancer cells is frequently associated with the loss of ARF, we disclose here an alternate mechanism whereby c-Myc inactivates p53 through the actions of the c-Myc-Inducible Long noncoding RNA Inactivating P53 (MILIP). MILIP functions to promote p53 polyubiquitination and turnover by reducing p53 SUMOylation through suppressing tripartite-motif family-like 2 (TRIML2). MILIP upregulation is observed amongst diverse cancer types and is shown to support cell survival, division and tumourigenicity. Thus our results uncover an inhibitory axis targeting p53 through a pan-cancer expressed RNA accomplice that links c-Myc to suppression of p53.

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c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis

et al. 2020

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“…Studies have confirmed that lncRNAs can combine with different functional proteins to exhibit various effects. For instance, lncRNAs can enhance protein recruitment toward the associated target ( Chen et al, 2019 ; Yari et al, 2019 ) or can strengthen/weaken the binding force of proteins and their targets ( Liu et al, 2018 ; Wang et al, 2020 ). In this research, we demonstrated for the first time the role of GAS5 in RNA NMD of BMSCs via UPF1.…”

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confidence: 99%

GAS5 protects against osteoporosis by targeting UPF1/SMAD7 axis in osteoblast differentiation

Xie

et al. 2020

eLife

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Osteoporosis is a common systemic skeletal disorder resulting in bone fragility and increased fracture risk. It is still necessary to explore its detailed mechanisms and identify novel targets for the treatment of osteoporosis. Previously, we found that a lncRNA named GAS5 in human could negatively regulate the lipoblast/adipocyte differentiation. However, it is still unclear whether GAS5 affects osteoblast differentiation and whether GAS5 is associated with osteoporosis. Our current research found that GAS5 was decreased in the bones and BMSCs, a major origin of osteoblast, of osteoporosis patients. Mechanistically, GAS5 promotes the osteoblast differentiation by interacting with UPF1 to degrade SMAD7 mRNA. Moreover, a decreased bone mass and impaired bone repair ability were observed in Gas5 heterozygous mice, manifesting in osteoporosis. The systemic supplement of Gas5-overexpressing adenoviruses significantly ameliorated bone loss in an osteoporosis mouse model. In conclusion, GAS5 promotes osteoblast differentiation by targeting the UPF1/SMAD7 axis and protects against osteoporosis.

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“…For example, a HOX transcript antisense RNA, lncRNA HOTAIR, was found to correlate with poor prognosis of lung cancer and promote tumor progression [18]. LncRNA REG1CP was shown to promote the development and progression of tumor [19]. For ESCC, several lncRNAs have been detected to associate with short survival, such as lncRNA H19 [20], lncRNA CASC9 [21] and lncRNA LUCAT1 [22].…”

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confidence: 99%

Prognostic value of a five-lncRNA signature in esophageal squamous cell carcinoma

Zhang

Liu

et al. 2020

Cancer Cell Int

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Background: The aim of this study was to identify prognostic long non-coding RNAs (lncRNAs) and develop a multi-lncRNA signature for suvival prediction in esophageal squamous cell carcinoma (ESCC). Methods: The clinical and gene expression data from Gene Expression Omnibus database (GSE53624, n = 119) were obtianed as training set. A total of 98 paired ESCC tumor and normal tissues were detected by RNA sequencing and used as test set. Another 84 ESCC tissues were used for real-time quantitative PCR(qRT-PCR) and as an independent validation cohort. Survival analysis, Cox regression and Kaplan-Meier analysis were performed. Results: We screened a prognostic marker of ESCC from the GSE53624 dataset and named it as the five-lncRNA signature including AC007179.1, MORF4L2-AS1, RP11-488I20.9, RP13-30A9.2, RP4-735C1.6, which could classify patients into high-and low-risk groups with significantly different survival(median survival: 1.75 years vs. 4.01 years, log rank P < 0.05). Then test dataset and validation dataset confirmed that the five-lncRNA signature can determine the prognosis of ESCC patients. Predictive independence of the prognostic marker was proved by multivariable Cox regression analyses in the three datasets (P < 0.05). In addition, the signature was found to be better than TNM stage in terms of prognosis. Conclusion: The five-lncRNA signature could be a good prognostic biomarker for ESCC patients and has important clinical value.

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LncRNA REG1CP promotes tumorigenesis through an enhancer complex to recruit FANCJ helicase for REG3A transcription

Cited by 53 publications

References 41 publications

c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis

c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis

GAS5 protects against osteoporosis by targeting UPF1/SMAD7 axis in osteoblast differentiation

Prognostic value of a five-lncRNA signature in esophageal squamous cell carcinoma

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