Research progress in the role and mechanism of Cadherin-11 in different diseases

Chen, Xinyi; Xiang, Hongjiao; Yu, Shiyu; Lü, Yifei; Wu, Tao

doi:10.7150/jca.52720

Cited by 24 publications

(20 citation statements)

References 86 publications

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“…The loss of SETD2 is involved in the occurrence and development of HCC ( 47 ). The loss of CDH11 function will change the adhesion status resulting in the invasion and metastasis of HCC ( 48 ). The profiles of TP53, TSC2, CDH11, SETD2, and CTNNB1 mutation sites are shown in Figure 5D .…”

Section: Resultsmentioning

confidence: 99%

A Novel hepatocellular carcinoma specific hypoxic related signature for predicting prognosis and therapeutic responses

et al. 2022

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Hypoxia is an important feature of the tumor microenvironment(TME) and is closely associated with cancer metastasis, immune evasion, and drug resistance. However, the precise role of hypoxia in hepatocellular carcinoma(HCC), as well as its influence on the TME, and drug sensitivity remains unclear. We found the excellent survival prediction value of Hypoxia_DEGs_Score model. In hypoxic HCC, somatic mutation, copy number variation, and DNA methylation were closely related to hypoxic changes and affected tumorigenesis, progression, metastasis, and drug resistance. In HCC, aggravated hypoxic stress was found to be accompanied by an immune exclusion phenotype and increased infiltration of immunosuppressive cells. In the validation cohort, patients with high Hypoxia_DEGs_Score were found to have worse immunotherapeutic outcomes and prognoses, and may benefit from drugs against cell cycle signaling pathways rather than those inhibiting the PI3K/mTOR pathway. Hypoxia_DEGs_Score has an excellent predictive capability of changes in the TME, the efficacy of immunotherapy, and the response of drugs. Therefore, Hypoxia_DEGs_Score can help develop personalized immunotherapy regimens and improve the prognosis of HCC patients.

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Section: Resultsmentioning

confidence: 99%

A Novel hepatocellular carcinoma specific hypoxic related signature for predicting prognosis and therapeutic responses

et al. 2022

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“…N-cadherin (CDH2), on the other hand, is abundantly expressed in FHL124 cells but does not alter with age and has only a mild TGFβ2-mediated response. Interestingly, cadherin 11 (CDH11), an emerging gene marker and a top-ranked EMT gene [32,[50][51][52], is moderately expressed in young FHL124 cells and demonstrates an age-related decline in FHL124 cells. Along with the positive TGFβ2-mediated response, we believe CDH11 may be used as a sensitive EMT marker for LECs.…”

Section: Discussionmentioning

confidence: 99%

Aged Lens Epithelial Cells Suppress Proliferation and Epithelial–Mesenchymal Transition-Relevance for Posterior Capsule Opacification

Wei

Gordon

Hao

et al. 2022

Cells

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Posterior capsule opacification (PCO) is a frequent complication after cataract surgery, and advanced PCO requires YAG laser (Nd: YAG) capsulotomy, which often gives rise to more complications. Lens epithelial cell (LEC) proliferation and transformation (i.e., epithelial–mesenchymal transition (EMT)) are two critical elements in PCO initiation and progression pathogenesis. While PCO marginally impacts aged cataract surgery patients, PCO incidences are exceptionally high in infants and children undergoing cataract surgery. The gene expression of lens epithelial cell aging and its role in the discrepancy of PCO prevalence between young and older people have not been fully studied. Here, we conducted a comprehensive differentially expressed gene (DEG) analysis of a cell aging model by comparing the early and late passage FHL124 lens epithelial cells (LECs). In vitro, TGFβ2, cell treatment, and in vivo mouse cataract surgical models were used to validate our findings. We found that aged LECs decelerated rates of cell proliferation accompanied by dysregulation of cellular immune response and cell stress response. Surprisingly, we found that LECs systematically downregulated epithelial–mesenchymal transition (EMT)-promoting genes. The protein expression of several EMT hallmark genes, e.g., fibronectin, αSMA, and cadherin 11, were gradually decreased during LECs aging. We then confirmed these findings in vitro and found that aged LECs markedly alleviated TGFβ2-mediated EMT. Importantly, we explicitly confirmed the in vitro findings from the in vivo mouse cataract surgery studies. We propose that both the high proliferation rate and EMT-enriched young LECs phenotypic characteristics contribute to unusually high PCO incidence in infants and children.

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“…The porcine valvular endothelium had a more chondrogenicoriented transcription profile when compared to the aortic endothelium (Butcher et al, 2006). Cadherin 11, which is linked to epithelial-mesenchymal transitions (Chen et al, 2021), was expressed in the VECs but not in the aortic ECs. However, BMP4 was expressed in both the aortic endothelium and the fibrosa side of the valve (Butcher et al, 2006), suggesting that BMP4 was in locations where it could trigger EndMTs.…”

Section: Role Of the Valve Endothelium In Calcific Aortic Valve Calcificationmentioning

confidence: 94%

Contributions of the Endothelium to Vascular Calcification

Zhang

Yao

et al. 2021

Front. Cell Dev. Biol.

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Vascular calcification (VC) increases morbidity and mortality and constitutes a significant obstacle during percutaneous interventions and surgeries. On a cellular and molecular level, VC is a highly regulated process that involves abnormal cell transitions and osteogenic differentiation, re-purposing of signaling pathways normally used in bone, and even formation of osteoclast-like cells. Endothelial cells have been shown to contribute to VC through a variety of means. This includes direct contributions of osteoprogenitor cells generated through endothelial-mesenchymal transitions in activated endothelium, with subsequent migration into the vessel wall. The endothelium also secretes pro-osteogenic growth factors, such as bone morphogenetic proteins, inflammatory mediators and cytokines in conditions like hyperlipidemia, diabetes, and renal failure. High phosphate levels caused by renal disease have deleterious effects on the endothelium, and induction of tissue non-specific alkaline phosphatase adds to the calcific process. Furthermore, endothelial activation promotes proteolytic destruction of the internal elastic lamina that serves, among other things, as a stabilizer of the endothelium. Appropriate bone mineralization is highly dependent on active angiogenesis, but it is unclear whether the same relationship exists in VC. Through its location facing the vascular lumen, the endothelium is the first to encounter circulating factor and bone marrow-derived cells that might contribute to osteoclast-like versus osteoblast-like cells in the vascular wall. In the same way, the endothelium may be the easiest target to reach with treatments aimed at limiting calcification. This review provides a brief summary of the contributions of the endothelium to VC as we currently know them.

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Research progress in the role and mechanism of Cadherin-11 in different diseases

Cited by 24 publications

References 86 publications

A Novel hepatocellular carcinoma specific hypoxic related signature for predicting prognosis and therapeutic responses

A Novel hepatocellular carcinoma specific hypoxic related signature for predicting prognosis and therapeutic responses

Aged Lens Epithelial Cells Suppress Proliferation and Epithelial–Mesenchymal Transition-Relevance for Posterior Capsule Opacification

Contributions of the Endothelium to Vascular Calcification

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