Revisiting the multiple roles of T-cadherin in health and disease

Рубина, К. А.; Semina, Ekaterina V.; Калинина, Н.И.; Sysoeva, Veronika; Balatsky, Alexander V.; Ткачук, В. А.

doi:10.1016/j.ejcb.2021.151183

Cited by 21 publications

(14 citation statements)

References 111 publications

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“…3A, B). Several studies have shown that CDH13 inhibits cancer cells 23 . Co-administration of cytotoxic drugs that work through different mechanisms may improve their synergistic effects.…”

Section: Discussionmentioning

confidence: 99%

Small RNA activation of CDH13 expression overcome BCR-ABL1-independent imatinib-resistance and their signaling pathway studies in chronic myeloid leukemia

Fei,

Su,

Wang

et al. 2024

Preprint

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BCR-ABL1-independent resistance to imatinib has no effective treatment due to its complexity and diversity. We previously reported that the CDH13 oncogene was expressed at low levels in BCR-ABL1-independent resistant CML cell lines. However, its effects on CML resistant cells and mechanisms remain unknown. This study investigated the effects of saRNA-based CDH13 activation on BCR-ABL1-independent imatinib resistance in CML and its underlying mechanism, and proposes a unique treatment method to overcome imatinib resistance. Specifically, this study demonstrated that using the DSIR (Designer of Small Interfering RNA) website tool, saRNAs targeting the CDH13 promoter region were generated and validated using qPCR and western blotting. Among the predicted sequences, C2 and C3 efficiently elevated CDH13 mRNA and protein expression, as well as inhibited the relative vitality of cells and the ability to form clones. After promoting CDH13 expression in K562-IMR cells, it inhabited the NF-κB signaling pathway and induced apoptosis in imatinib-resistant CML cells. LNP-saRNA (C3) was also observed to limit the growth of K562-IMR cells in vivo. From the above, the activation of CDH13 expression by saRNA promotes cell apoptosis by inhibiting the NF-κB signaling pathway to overcome to BCR-ABL1-independent resistance to imatinib in patients with CML.

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“…3A, B). Several studies have shown that CDH13 inhibits cancer cells 23 . Co-administration of cytotoxic drugs that work through different mechanisms may improve their synergistic effects.…”

Section: Discussionmentioning

confidence: 99%

Small RNA activation of CDH13 expression overcome BCR-ABL1-independent imatinib-resistance and their signaling pathway studies in chronic myeloid leukemia

Fei,

Su,

Wang

et al. 2024

Preprint

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“…Finally, the nine SNPs on chromosome 16, intronic to the CDH13 gene, were eQTLs of this gene, which encodes the T-cadherin protein, a regulator of vascular permeability, but also receptor of adiponectin and LDL. It is involved in lung function, and reportedly associated with several metabolic disorders as atherosclerosis, dyslipidemia, obesity, and also diabetes (as reviewed in 43 ).…”

Section: Discussionmentioning

confidence: 99%

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

Minnai,

Biscarini,

Esposito

et al. 2024

Sci Rep

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The clinical manifestations of SARS-CoV-2 infection vary widely among patients, from asymptomatic to life-threatening. Host genetics is one of the factors that contributes to this variability as previously reported by the COVID-19 Host Genetics Initiative (HGI), which identified sixteen loci associated with COVID-19 severity. Herein, we investigated the genetic determinants of COVID-19 mortality, by performing a case-only genome-wide survival analysis, 60 days after infection, of 3904 COVID-19 patients from the GEN-COVID and other European series (EGAS00001005304 study of the COVID-19 HGI). Using imputed genotype data, we carried out a survival analysis using the Cox model adjusted for age, age2, sex, series, time of infection, and the first ten principal components. We observed a genome-wide significant (P-value < 5.0 × 10−8) association of the rs117011822 variant, on chromosome 11, of rs7208524 on chromosome 17, approaching the genome-wide threshold (P-value = 5.19 × 10−8). A total of 113 variants were associated with survival at P-value < 1.0 × 10−5 and most of them regulated the expression of genes involved in immune response (e.g., CD300 and KLR genes), or in lung repair and function (e.g., FGF19 and CDH13). Overall, our results suggest that germline variants may modulate COVID-19 risk of death, possibly through the regulation of gene expression in immune response and lung function pathways.

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“…Once recognition and binding have occurred, Acrp30 promotes the recruitment of adaptor protein APPL1, which in turn activates AMPactivated protein kinase (AMPK) and peroxisome proliferator-activated receptor α (PPARα) [35] . Besides regulating energy homeostasis, Acrp30-related intracellular targets are actively engaged in controlling several signaling pathways that, depending on cell specialization, may lead to opposite effects [49] . The third receptor in order of discovery is a calcium-dependent adhesion molecule, also referred to as T-cadherin, whereby a lack of its intracellular domain may serve as Acrp30 co-receptor for unknown signaling [50] .…”

Section: Across the Controversial Relationship Between Adiponectin An...mentioning

confidence: 99%

“…Besides regulating energy homeostasis, Acrp30-related intracellular targets are actively engaged in controlling several signaling pathways that, depending on cell specialization, may lead to opposite effects [ 49 ] . The third receptor in order of discovery is a calcium-dependent adhesion molecule, also referred to as T-cadherin, whereby a lack of its intracellular domain may serve as Acrp30 co-receptor for unknown signaling [ 50 ] .…”

Section: Introductionmentioning

confidence: 99%

AdipoRon and Pancreatic Ductal Adenocarcinoma: a future perspective in overcoming chemotherapy-induced resistance?

et al. 2022

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The latest scientific knowledge has provided additional insights accountable for the worst prognosis for pancreatic ductal adenocarcinoma (PDAC). Among the causative factors, the aptitude to develop resistance towards approved medications denotes the master key for understanding the lack of improvement in PDAC survival over the years. Even though several compounds have achieved encouraging results at preclinical stage, no new adjuvant agents have reached the bedside of PDAC patients lately. The adiponectin receptor agonist AdipoRon is emerging as a promising anticancer drug in different cancer models, particularly in PDAC. Building on the existing findings, we recently reinforced its candidacy in PDAC cells, proposing AdipoRon either as a suitable partner in gemcitabine-based treatment or as an effective drug in resistant cells. Crossing the current state-of-the-art, herein we provide a critical perspective on AdipoRon to figure out whether this receptor agonist can potentially be considered a future therapeutic choice in overcoming chemotherapy-induced resistance, expressly in PDAC.

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Revisiting the multiple roles of T-cadherin in health and disease

Cited by 21 publications

References 111 publications

Small RNA activation of CDH13 expression overcome BCR-ABL1-independent imatinib-resistance and their signaling pathway studies in chronic myeloid leukemia

Small RNA activation of CDH13 expression overcome BCR-ABL1-independent imatinib-resistance and their signaling pathway studies in chronic myeloid leukemia

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

AdipoRon and Pancreatic Ductal Adenocarcinoma: a future perspective in overcoming chemotherapy-induced resistance?

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