Cadherin Signaling in Cancer and Autoimmune Diseases

Sisto, Margherita; Ribatti, Doménico; Lisi, Sabrina

doi:10.3390/ijms222413358

Cited by 21 publications

(18 citation statements)

References 175 publications

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“…In our study, the functional annotation of FLVCR2 revealed that cell–cell adhesion, cellular defense response, translational initiation, and ribonucleoprotein complex biogenesis were closely associated with FLVCR2 expression. Studies have shown that adhesion molecules are closely related to tumorigenesis and development ( Sisto et al, 2021 ; Ito et al, 2022 ), which is consistent with our results. The cell–cell adhesion events enriched in the high FLVCR2 expression group show that FLVCR2 plays a critical role in AML tumorigenesis.…”

Section: Discussionsupporting

confidence: 93%

The prognostic marker FLVCR2 associated with tumor progression and immune infiltration for acute myeloid leukemia

Ma²,

Bai³

et al. 2022

Front. Cell Dev. Biol.

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Acute myeloid leukemia (AML) is one of the most common hematopoietic malignancies in adults. The tumor microenvironment (TME) has a critical effect on AML occurrence, recurrence, and progression. The gene feline leukemia virus subgroup C cellular receptor family member 2 (FLVCR2) belongs to the major facilitator superfamily of transporter protein members, which is primarily involved in transporting small molecules. The potential role of FLVCR2 in the TME in AML has not been investigated. To clarify the expression and role of FLVCR2 in AML, we analyzed the Gene Expression Omnibus and The Cancer Genome Atlas databases and found that FLVCR2 mRNA expression significantly increased among patients with AML. Furthermore, based on an analysis of the Gene Expression Profiling Interactive Analysis database, FLVCR2 upregulation predicted dismal overall survival of patients with AML. Our validation analysis revealed the significant upregulation of FLVCR2 within the bone marrow of AML relative to healthy controls by western blotting and qPCR assays. Gene set enrichment analysis was conducted to explore FLVCR2’s related mechanism in AML. We found that high FLVCR2 expression was related to infiltration degrees of immune cells and immune scores among AML cases, indicating that FLVCR2 possibly had a crucial effect on AML progression through the immune response. Specifically, FLVCR2 upregulation was negatively related to the immune infiltration degrees of activated natural killer cells, activated memory CD4+ T cells, activated dendritic cells, and CD8+ T cells using CIBERSORT analysis. According to the in vitro research, FLVCR2 silencing suppressed AML cell growth and promoted their apoptosis. This study provides insights into FLVCR2’s effect on tumor immunity, indicating that it might serve as an independent prognostic biomarker and was related to immune infiltration within AML.

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Section: Discussionsupporting

confidence: 93%

The prognostic marker FLVCR2 associated with tumor progression and immune infiltration for acute myeloid leukemia

Ma²,

Bai³

et al. 2022

Front. Cell Dev. Biol.

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“…The TAZ knockdown experiment suggested that TAZ may serve an important role in the process of ADSCs delaying the progression of SS. In addition, it has been previously noted that the expression of E-cadherin will change with the progression of autoimmune diseases ( 26 , 27 ). The reason for these phenomena may be the different pathogenesis of the different autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Adipose‑derived stem cells postpone the progression of Sjögren's syndrome by upregulating the Hippo signaling pathway

Fan

et al. 2022

Exp Ther Med

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The aim of the present study was to explore the effect and mechanism of action of adipose-derived stem cells (ADSCs) on Sjögren syndrome (SS) to develop novel and more effective methods for SS treatment. ADSCs, dexamethasone or normal saline was injected into the submandibular gland (SMG) of three 12-week-old non-obese diabetic (NOD) mice. The degree of lymphocyte infiltration was considered as a criterion for judging disease progression, hematoxylin and eosin staining was performed to observe the pathological state, and the expression levels of TAZ, E-cadherin and α-catenin were assessed by western blotting. ADSC transplantation triggered an inhibitory effect on the progression of SS, which was slightly stronger compared with that of dexamethasone treatment. This was found to be related to the Hippo signaling pathway. In addition, TAZ protein expression levels decreased gradually with the progression of the disease; immunofluorescence staining showed that the expression of E-cadherin and TAZ followed similar trends. Notably, the expression of TAZ, p-TAZ, E-cadherin and α-catenin in NOD mice were lower compared with that in Control mice. Similarly, the ratio of p-TAZ/TAZ also decreased, which means that the activation level of Hippo signal pathway decreased. The results suggest that ADSCs may exert a therapeutic effect against SS and may postpone its progression by upregulating the Hippo signaling pathway.

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“…It is now widely unquestioned that the development of a fibrotic program in SS is due to the production of fibrogenic mediators by inflammatory and epithelial cells; among these mediators, a main role is played by the growth factor TGF-β1 [ 76 ]. Pioneering studies conducted by Sisto and colleagues demonstrated that TGF-β1 promotes an SG epithelial cell transition toward the mesenchymal phenotype through the activation of EMT-dependent fibrosis [ 75 , 77 , 78 ]. Experimental in vitro studies performed on human SG epithelial cells have shown that TGF-β1 induces the transition of SG epithelial cells from the classic cobblestone morphology toward a more spindle-shaped fibroblast cell type characterized by a reduction in the expression level of epithelial adherence junction proteins [ 75 , 77 , 78 ].…”

Section: New Insights Into the Regulation Of Epithelial–mesenchymal T...mentioning

confidence: 99%

“…Pioneering studies conducted by Sisto and colleagues demonstrated that TGF-β1 promotes an SG epithelial cell transition toward the mesenchymal phenotype through the activation of EMT-dependent fibrosis [ 75 , 77 , 78 ]. Experimental in vitro studies performed on human SG epithelial cells have shown that TGF-β1 induces the transition of SG epithelial cells from the classic cobblestone morphology toward a more spindle-shaped fibroblast cell type characterized by a reduction in the expression level of epithelial adherence junction proteins [ 75 , 77 , 78 ]. This was supported by the observation that SG biopsies derived from pSS patients show an elevated expression of TGF-β1 [ 77 , 78 ].…”

Section: New Insights Into the Regulation Of Epithelial–mesenchymal T...mentioning

confidence: 99%

“…Experimental in vitro studies performed on human SG epithelial cells have shown that TGF-β1 induces the transition of SG epithelial cells from the classic cobblestone morphology toward a more spindle-shaped fibroblast cell type characterized by a reduction in the expression level of epithelial adherence junction proteins [ 75 , 77 , 78 ]. This was supported by the observation that SG biopsies derived from pSS patients show an elevated expression of TGF-β1 [ 77 , 78 ]. In addition, Koski et al reported compelling evidence for the marked expression of TGF-β family member proteins, including TGF-β2, in the fibrotic area of pSS SGs [ 76 ].…”

Section: New Insights Into the Regulation Of Epithelial–mesenchymal T...mentioning

confidence: 99%

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Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren’s Syndrome: Identification of New Targets

Sisto

Ribatti

Lisi

2022

IJMS

Self Cite

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Sjögren’s syndrome (SS) is a systemic autoimmune rheumatic disorder characterized by the lymphocytic infiltration of exocrine glands and the production of autoantibodies to self-antigens. The involvement of the exocrine glands drives the pathognomonic manifestations of dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) that define sicca syndrome. To date, the molecular mechanisms mediating pathological salivary gland dysfunction in SS remain to be elucidated, despite extensive studies investigating the underlying cause of this disease, hampering the development of novel therapeutic strategies. Many researchers have identified a multifactorial pathogenesis of SS, including environmental, genetic, neuroendocrine, and immune factors. In this review, we explore the latest developments in understanding the molecular mechanisms involved in the pathogenesis of SS, which have attracted increasing interest in recent years.

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Cadherin Signaling in Cancer and Autoimmune Diseases

Cited by 21 publications

References 175 publications

The prognostic marker FLVCR2 associated with tumor progression and immune infiltration for acute myeloid leukemia

The prognostic marker FLVCR2 associated with tumor progression and immune infiltration for acute myeloid leukemia

Adipose‑derived stem cells postpone the progression of Sjögren's syndrome by upregulating the Hippo signaling pathway

Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren’s Syndrome: Identification of New Targets

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