miRNA and lncRNA Expression Networks Modulate Cell Cycle and DNA Repair Inhibition in Senescent Prostate Cells

Silveira, Willian A. da; Renaud, Ludivine; Hazard, E. Starr; Hardiman, Gary

doi:10.3390/genes13020208

Cited by 10 publications

(6 citation statements)

References 117 publications

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“…This same microRNA is predicted from the miRTarBase to target ZNF365. We can speculate that the observed reduction in ZNF365 expression following doxorubicin treatment in our study could result from the same miRNA (senescence-associated miRNA [ 30 ]) or, since both molecules physically interact, they could work through feedback loops.…”

Section: Discussionmentioning

confidence: 99%

Lack of ZNF365 Drives Senescence and Exacerbates Experimental Lung Fibrosis

Urista

Maldonado

Toscano-Marquez

et al. 2022

Cells

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Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant activation of the alveolar epithelium, the expansion of the fibroblast population, and the accumulation of extracellular matrix. Global gene expression of human lung fibroblasts stimulated with TGFβ-1, a strong fibrotic mediator revealed the overexpression of ZNF365, a zinc finger protein implicated in cell cycle control and telomere stabilization. We evaluated the expression and localization of ZNF365 in IPF lungs and in the fibrotic response induced by bleomycin in WT and deficient mice of the orthologous gene Zfp365. In IPF, ZNF365 was overexpressed and localized in fibroblasts/myofibroblasts and alveolar epithelium. Bleomycin-induced lung fibrosis showed an upregulation of Zfp365 localized in lung epithelium and stromal cell populations. Zfp365 KO mice developed a significantly higher fibrotic response compared with WT mice by morphology and hydroxyproline content. Silencing ZNF365 in human lung fibroblasts and alveolar epithelial cells induced a significant reduction of growth rate and increased senescence markers, including Senescence Associated β Galactosidase activity, p53, p21, and the histone variant γH2AX. Our findings demonstrate that ZNF365 is upregulated in IPF and experimental lung fibrosis and suggest a protective role since its absence increases experimental lung fibrosis mechanistically associated with the induction of cell senescence.

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Section: Discussionmentioning

confidence: 99%

Lack of ZNF365 Drives Senescence and Exacerbates Experimental Lung Fibrosis

Urista

Maldonado

Toscano-Marquez

et al. 2022

Cells

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“…An increasing number of studies indicate that lncRNAs play integral roles in the occurrence and development of diverse tumors 16 , 17 . Additionally, lncRNAs are involved in mechanisms linked with aging including proliferation, differentiation, and apoptosis 18 . Recent studies have revealed that lncRNAs are directly linked to senescence.…”

Section: Introductionmentioning

confidence: 99%

A novel aging-associated lncRNA signature for predicting prognosis in osteosarcoma

He,

Huang,

et al. 2024

Sci Rep

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Osteosarcoma (OS) is one of the most prevalent bone tumors in adolescents, and the correlation between aging and OS remains unclear. Currently, few accurate and reliable biomarkers have been determined for OS prognosis. To address this issue, we carried out a detailed bioinformatics analysis based on OS with data from the Cancer Genome Atlas data portal and Human Aging Genomic Resources database, as well as in vitro experiments. A total of 88 OS samples with gene expression profiles and corresponding clinical characteristics were obtained. Through univariate Cox regression analysis and survival analysis, 10 aging-associated survival lncRNAs (AASRs) were identified to be associated with the overall survival of OS patients. Based on the expression levels of the 10 AASRs, the OS patients were classified into two clusters (Cluster A and Cluster B). Cluster A had a worse prognosis, while Cluster B had a better prognosis. Then, 5 AASRs were ultimately included in the signature through least absolute shrinkage and selection operator-Cox regression analysis. Kaplan‒Meier survival analysis verified that the high-risk group exhibited a worse prognosis than the low-risk group. Furthermore, univariate and multivariate Cox regression analyses confirmed that the riskScore was an independent prognostic factor for OS patients. Subsequently, we discovered that the risk signature was correlated with the properties of the tumor microenvironment and immune cell infiltration. Specifically, there was a positive association between the risk model and naïve B cells, resting dendritic cells and gamma delta T cells, while it was negatively related to CD8+ T cells. Finally, in vitro experiments, we found that UNC5B-AS1 inhibited OS cells from undergoing cellular senescence and apoptosis, thereby promoting OS cells proliferation. In conclusion, we constructed and verified a 5 AASR-based signature, that exhibited excellent performance in evaluating the overall survival of OS patients. In addition, we found that UNC5B-AS1 might inhibit the senescence process, thus leading to the development and progression of OS. Our findings may provide novel insights into the treatment of OS patients.

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“…The lncRNAs regulate many key cellular activities, including cell proliferation, apoptosis, differentiation, and metabolism [ 12 ]. In addition, lncRNAs regulate physiological and pathological processes such as cell cycle and DNA damage repair, whose disruption can result in the progression of malignant tumors [ 13 , 14 ]. Furthermore, lncRNAs can control the pathogenesis of CRC from a variety of angles, primarily involving the tumor microenvironment (TME) that includes inflammation, immune evasion and exosome secretion, epithelial-mesenchymal transition (EMT), stemness maintenance, and angiogenesis of tumor, thus allowing them to control the occurrence, development, and treatment of CRC [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Long Non-Coding RNAs Induced by the Gut Microbiome on Regulating the Development of Colorectal Cancer

Fan

Xing

Jiang

et al. 2022

Cancers

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Although an imbalanced gut microbiome is closely associated with colorectal cancer (CRC), how the gut microbiome affects CRC is not known. Long non-coding RNAs (lncRNAs) can affect important cellular functions such as cell division, proliferation, and apoptosis. The abnormal expression of lncRNAs can promote CRC cell growth, proliferation, and metastasis, mediating the effects of the gut microbiome on CRC. Generally, the gut microbiome regulates the lncRNAs expression, which subsequently impacts the host transcriptome to change the expression of downstream target molecules, ultimately resulting in the development and progression of CRC. We focused on the important role of the microbiome in CRC and their effects on CRC-related lncRNAs. We also reviewed the impact of the two main pathogenic bacteria, Fusobacterium nucleatum and enterotoxigenic Bacteroides fragilis, and metabolites of the gut microbiome, butyrate, and lipopolysaccharide, on lncRNAs. Finally, available therapies that target the gut microbiome and lncRNAs to prevent and treat CRC were proposed.

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miRNA and lncRNA Expression Networks Modulate Cell Cycle and DNA Repair Inhibition in Senescent Prostate Cells

Cited by 10 publications

References 117 publications

Lack of ZNF365 Drives Senescence and Exacerbates Experimental Lung Fibrosis

Lack of ZNF365 Drives Senescence and Exacerbates Experimental Lung Fibrosis

A novel aging-associated lncRNA signature for predicting prognosis in osteosarcoma

Effects of Long Non-Coding RNAs Induced by the Gut Microbiome on Regulating the Development of Colorectal Cancer

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