The role of long non-coding RNAs in angiogenesis and anti-angiogenic therapy resistance in cancer

Liu, Junxia; Zhang, Qinqiu; Yang, Dongxue; Xie, Fei; Wang, Zhaoxia

doi:10.1016/j.omtn.2022.03.012

Cited by 20 publications

(9 citation statements)

References 130 publications

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“…The ever-increasing evidence indicated that tumor-related stromal cells and immune in ltration cells in the microenvironment of cancers had inseparable associations with tumorigenesis [41][42][43]. We are convinced that the tumor-related angiogenesis and broblast in the microenvironment seriously accelerated the growth and metastasis of LUAD, and the results in Fig.…”

Section: Discussionmentioning

confidence: 75%

WITHDRAWN: Upregulated HMGB3 resulting in the poor prognosis of lung adenocarcinoma by activating stromal angiogenesis through immune microenvironment

Feng

Bai

2022

Preprint

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HMGB3 belongs to the high mobility group box (HMGB) family and the abnormally increased HMGB3 is associated with various types of malignancy progression. However, there is exiguous well clarified research to illustrate the correlation between HMGB3 and lung cancer. The expression profile data of lung adenocarcinoma (LUAD) were obtained from GEO and TCGA databases. The differential expression, prognostic survival, clinical characters, functional enrichment and immune infiltration were analyzed through R software, Kaplan–Meier (KM) plotter, ClusterProfiler package and ssGSEA algorithm. Besides, further research on HMGB3 expression level was confirmed using xenograft mice through immunohistochemistry and western blot assays. Results showed that HMGB3 was highly expressed in LUAD samples compared with adjacent normal samples. The T stage, pathologic stage, smoker and angiogenesis within the LUAD patients were positively correlated with HMGB3 expression. Functional enrichment analysis indicated that the correlative genes of HMGB3 are most related to the cell cycle process. HMGB3 is weakly related to the immune infiltration cells in LUAD stromal. However, increased existence of HMGB3 induced active angiogenesis in LUAD stromal and possibly accelerated the tumor progression through immune microenvironment. In conclusion, we confirmed that HMGB3 is a biomarker of poor prognosis for LUAD. The operative mechanism of which is activating tumor angiogenesis through immune infiltration cells. Further study will focus on exploring the related pathways in angiogenesis and immune microenvironment.

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Section: Discussionmentioning

confidence: 75%

WITHDRAWN: Upregulated HMGB3 resulting in the poor prognosis of lung adenocarcinoma by activating stromal angiogenesis through immune microenvironment

Feng

Bai

2022

Preprint

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“…GAS5), scaffold (HOTAIR), regulating splicing (MALAT1) etc [35]. Some specific lncRNAs have been identified as regulators of endothelial biology and angiogenesis [38, 39]. For instance, Tee et al showed that MALAT1 promotes tumor angiogenesis in response to hypoxia in part by inducing the secretion of FGF-2 [40].…”

Section: Discussionmentioning

confidence: 99%

DNA damage-induced lncRNA MEG9 impacts angiogenesis

Fraile-Bethencourt

Khou

Wilson

et al. 2022

Preprint

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Endothelial cells are highly responsive to environmental changes that allow them to adapt to intrinsic and extrinsic stimuli and switch their transcriptome accordingly to go back to vascular homeostasis. Our previous data demonstrated that small non-coding-RNAs respond quickly to genotoxic stressors and determined endothelial cell fate and DNA damage response. To further understand the contribution of non-coding-RNAs, we profiled differentially expressed long non-coding RNAs in response to genotoxic stress and compared them to pro-angiogenic growth factor signaling. We identified the Maternally expressed gene 9 (MEG9) as a cytoprotective lncRNA in the endothelium. Gain and Loss-of-function studies indicate that MEG9 prevents endothelial cells from cell death, suggesting that MEG9 responses to genotoxic stress can be an adaptive and protective mechanism. Consistent with this phenotype, the knockdown of MEG9 decreases growth factor-dependent angiogenesis in a 3D fibrin gel angiogenesis assay. Deletion of the MEG9 ortholog, Mirg, in mice results in increased vascular leak in Matrigel plugs and a sex and age-dependent decrease in platelets. Mechanistically, we observed that both MEG9 knockdown in vitro and Mirg-deleted mice in vivo activated common pathways, including apoptosis, clotting, and inflammation. Indeed, the proinflammatory adhesion molecule ICAM1 was significantly increased in human and mouse endothelial cells in a MEG9-dependent manner, supporting the increased vascular permeability observed on MEG9 deficient cells. Taken together, our findings illustrate how genotoxic stress responses through dynamic modulation of lncRNAs, such as MEG9, trigger adaptive mechanisms to maintain endothelial function, while loss of these molecules contributes to maladaptive responses and endothelial cell dysfunction.

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“…The chromatin epigenetic regulation of proangiogenic genes has also been attributed to different lncRNA packaged in EVs, although the mechanism is not fully elucidated [ 101 , 102 , 103 ] ( Figure 2 ). LncRNAs can work as molecular scaffold, assembling several chromatin regulator proteins and reshaping the DNA structure in the nucleus and thus favoring the transcription or silencing of target genes [ 104 ]. In other cases, lncRNAs can act as ceRNAs or sponges, sequestering endogenous miRNAs and inhibiting their action on target.…”

Section: Basic Mechanisms and Epigenetic Role Of Evs In Tumor Vascula...mentioning

confidence: 99%

Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage

Schiano

Balbi²,

Nigris

et al. 2023

IJMS

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Both progression from the early pathogenic events to clinically manifest cardiovascular diseases (CVD) and cancer impact the integrity of the vascular system. Pathological vascular modifications are affected by interplay between endothelial cells and their microenvironment. Soluble factors, extracellular matrix molecules and extracellular vesicles (EVs) are emerging determinants of this network that trigger specific signals in target cells. EVs have gained attention as package of molecules with epigenetic reversible activity causing functional vascular changes, but their mechanisms are not well understood. Valuable insights have been provided by recent clinical studies, including the investigation of EVs as potential biomarkers of these diseases. In this paper, we review the role and the mechanism of exosomal epigenetic molecules during the vascular remodeling in coronary heart disease as well as in cancer-associated neoangiogenesis.

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The role of long non-coding RNAs in angiogenesis and anti-angiogenic therapy resistance in cancer

Cited by 20 publications

References 130 publications

WITHDRAWN: Upregulated HMGB3 resulting in the poor prognosis of lung adenocarcinoma by activating stromal angiogenesis through immune microenvironment

WITHDRAWN: Upregulated HMGB3 resulting in the poor prognosis of lung adenocarcinoma by activating stromal angiogenesis through immune microenvironment

DNA damage-induced lncRNA MEG9 impacts angiogenesis

Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage

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