Angiomotin like-1 is a novel component of the N-cadherin complex affecting endothelial/pericyte interaction in normal and tumor angiogenesis

Zheng, Yi; Zhang, Yuanyuan; Barutello, Giuseppina; Chiu, Kungchun; Arigoni, Maddalena; Giampietro, Costanza; Cavallo, Federica; Holmgren, Lars

doi:10.1038/srep30622

Cited by 25 publications

(18 citation statements)

References 35 publications

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“…; Zheng et al . ) mRNA levels for N‐CAD were highest in the EC from female aorta. The relative expression hierarchy (strongest to weakest) was female aorta > male aorta > female SKM > male SKM (Fig.…”

Section: Resultsmentioning

confidence: 90%

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

Huxley

Kemp

Schramm

et al. 2018

The Journal of Physiology

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Vascular endothelial cells (EC) are heterogeneous with respect to phenotype, reflecting at least the organ of origin, location within the vascular network and physical forces. As an independent influence on EC functions in health or aetiology, susceptibility, and progression of dysfunction in numerous disease states, sex has been largely ignored. The present study focussed on EC isolated from aorta (macrovascular) and skeletal muscle vessels (microvascular) of age-matched male and female rats under identical conditions of short-term (passage 4) culture. We tested the hypothesis that genomic sex would not influence endothelial growth, wound healing, morphology, lactate production, or messenger RNA and protein expression of key proteins (sex hormone receptors for androgen and oestrogens α and β; platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin mediating barrier function; α β and N-cadherin influencing matrix interactions; intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 mediating EC/white cell adhesion). The hypothesis was rejected because the EC origin (macro- vs. microvessel) and sex influenced multiple phenotypic characteristics. Statistical model analysis of EC growth demonstrated an hierarchy of variable importance, recapitulated for other phenotypic characteristics, with predictions assuming EC homogeneity < sex < vessel origin < sex and vessel origin. Furthermore, patterns of EC mRNA expression by vessel origin and by sex did not predict protein expression. Overall, the present study demonstrated that accurate assessment of sex-linked EC dysfunction first requires an understanding of EC function by position in the vascular tree and by sex. The results from a single EC tissue source/species/sex cannot provide universal insight into the mechanisms regulating in vivo endothelial function in health, and no less in disease.

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Section: Resultsmentioning

confidence: 90%

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

Huxley

Kemp

Schramm

et al. 2018

The Journal of Physiology

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“…AMOTL1 belongs to the family of angiomotins (Amots) and is known as an adaptor protein, localizing in the nuclear, cytoplasmic, or membranous fraction in a cell context-dependent manner 24 . Growing evidence has certified that AMOTL1 controls biological activities, including migration, cell polarity, tight junction formation, and angiogenesis 11 , 25 , 26 . Furthermore, previous investigations have demonstrated that AMOTL1 exhibits cancerigenic activities in malignancies, such as breast cancer and cervical cancer 12 , 15 .…”

Section: Discussionmentioning

confidence: 99%

circAMOTL1 Motivates AMOTL1 Expression to Facilitate Cervical Cancer Growth

Zhang

et al. 2020

Molecular Therapy - Nucleic Acids

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Cervical cancer is acknowledged as the most prevalent gynecological tumor and a severe public issue that threatens female health, resulting from its high incidence and fatality rate. Surging evidence have shown that circular RNAs (circRNAs) play significant roles in the initiation and progression of various malignancies. Although circAMOTL1 has been testified to execute oncogenic properties in breast cancer and prostate cancer, literature on its function and regulatory mechanism in cervical cancer development is still scanty. Using a bioinformatics analysis, we found circ_0004214 was a circular form of AMOTL1. Through qRT-PCR analysis, circAMOTL1 and its host gene AMOTL1 were both upregulated in cervical cancer tissues and closely correlated with poor prognosis of cervical cancer. Gain- or loss-of-function assays and in vivo experiments demonstrated that AMOTL1 promoted cervical cancer cell growth both in vitro and in vivo. Mechanically, circAMOTL1 served as a competing endogenous RNA (ceRNA) to prompt the expression of AMOTL1 through sponging miR-485-5p. Rescue assays revealed that miR-485-5p/AMOTL1 axis was involved in circ_AMOTL1-mediated cervical cancer progression. Our findings provide a better understanding of the molecular mechanism underlying circAMOTL1 in cervical cancer and indicated circAMOTL1/miR-485-5p/AMOTL1 as a promising novel therapeutic strategy for the treatment of this disease.

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“…This protein is also elevated in tumors. 51 – 53 Moreover, the potent tumorigenicity might be triggered through interactions between circ-AMOTL1 and c-myc; 49 and the alternative transcription form of the ENO1, MBP1, also interacts with c-myc P2 promoter, which explains the positive relationship between circ-AMOTL1 and ENO1 in another view. MiR-22-3p promotes cancer progression in cervical squamous carcinoma cells, 54 papillary thyroid cancer, 55 and pancreatic cancer; 56 meanwhile, it also acts as a tumor suppressor in colorectal cancer 57 and hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

<p>The circ-AMOTL1/ENO1 Axis Implicated in the Tumorigenesis of OLP-Associated Oral Squamous Cell Carcinoma</p>

Liu¹,

Yang²,

Sun³

et al. 2020

CMAR

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Background: Oral squamous cell carcinoma (OSCC) may develop from a variety of oral potentially malignant disorders, but the mechanism of malignant transformation is still unknown. Among them, oral lichen planus (OLP) has a high prevalence. Previous studies have shown that α-enolase (ENO1) can promote cell proliferation and play an important role in tumorigenesis. In this study, we aim to explore the mechanism of ENO1 regulation in the process of OSCC tumorigenesis from OLP. Methods: ENO1 expression in tissues was determined by real-time quantitative PCR and immunohistochemistry. ENO1 was knocked down in cal-27 to observe the change in cell proliferation. Then, RNA-seq and bioinformatics analyses were conducted between OLP and OSCC samples. The expression of circ-AMOTL1, miRNA-22-3p, and miRNA-1294 was assessed using the real-time quantitative PCR. With knockdown and overexpression of circ-AMOTL1 in vitro, the change of ENO1 in the mRNA level was also assessed. Results: ENO1 was enhanced in the OSCC samples in comparison with OLP. Immunohistochemistry and real-time quantitative PCR results showed that ENO1 was significantly higher in OSCC tissue than in the OLP group, with a statistically significant difference (p<0.05). When ENO1 was knocked down in cal-27, cell proliferation was inhibited (p<0.05). The expression of miR-22-3p and miR-1294 was decreased in OSCC tissues, whereas ENO1 and circ-AMOTL1 increased. In an in vitro study, knockdown of circ-AMOTL1 resulted in a decrease of ENO1, while overexpression of circ-AMOTL1 led to an increase of ENO1 in the mRNA level. Conclusion: We confirmed that ENO1 expression was elevated in OSCC and increased cell proliferation. In an in vitro study, ENO1 expression was promoted by circ-AMOTL1. ENO1 may play a role as a tumor-promoting gene in OSCC through the circ-AMOTL1/miR-22-3p/ miR-1294 network. These novel findings may shed further light on the pathogenesis from OLP to OSCC and the potential precursor markers.

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Angiomotin like-1 is a novel component of the N-cadherin complex affecting endothelial/pericyte interaction in normal and tumor angiogenesis

Cited by 25 publications

References 35 publications

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

circAMOTL1 Motivates AMOTL1 Expression to Facilitate Cervical Cancer Growth

<p>The circ-AMOTL1/ENO1 Axis Implicated in the Tumorigenesis of OLP-Associated Oral Squamous Cell Carcinoma</p>

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