Co-inhibition of Notch and NF-κB Signaling Pathway Decreases Proliferation through Downregulating IκB-α and Hes-1 Expression in Human Ovarian Cancer OVCAR-3 Cells

Majidinia, Maryam; Yousefi, Bahman; Akbarzadeh, Maryam; Mihanfar, Aynaz; Rahmati-Yamchi, Mohammad; Zarghami, Nosratollah

doi:10.1055/s-0042-115405

Cited by 21 publications

(24 citation statements)

References 26 publications

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“…A number of NF‐κB regulated lncRNAs have been reported, which can impact cellular processes. The abnormal regulation of NF‐κB and its downstream targets often leads to inflammation, drug resistance, and metastasis in breast cancer (Majidinia et al, 2017; Yousefi et al, 2017). Several studies have exposed the role of NF‐κB interaction with lncRNA (NKILA) in the NF‐κB signaling pathway (Figure 1).…”

Section: Crosstalk Between Various Signaling Pathways and Lncrnasmentioning

confidence: 99%

Critical roles of long noncoding RNAs in breast cancer

Abolghasemi

Tehrani

Yousefi

et al. 2020

Journal Cellular Physiology

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Breast cancer is a major clinical challenge that affects a wide range of the female population and heavily burdens the health system. In the past few decades, attempts have been made to understand the etiology of breast cancer, possible environmental risk factors, and the genetic predispositions, pathogenesis, and molecular aberrations involved in the process. Studies have shown that breast cancer is a heterogeneous entity; each subtype has its specific set of aberrations in different cell signaling pathways, such as Notch, Wnt/β‐catenin, transforming growth factor‐β, and mitogen‐activated protein kinase pathways. One novel group of molecules that have been shown to be inducted in the regulation of multiple cell signaling pathways is the long noncoding RNAs (lncRNAs). These molecules have important implications in the regulation of multiple signaling pathways by interacting with various genes, affecting the transcription process, and finally, playing roles in posttranslational control of these genes. There is growing evidence that lncRNAs are involved in the process of breast cancer formation by effecting the aforementioned signaling pathways, and that this involvement can have significant diagnostic and prognostic values in clinical contexts. The present review aims to elicit the significance of lncRNAs in the regulation of cell signaling pathways, and the resulting changes in cell survival, proliferation, and invasion, which are the hallmarks of breast cancer.

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Section: Crosstalk Between Various Signaling Pathways and Lncrnasmentioning

confidence: 99%

Critical roles of long noncoding RNAs in breast cancer

Abolghasemi

Tehrani

Yousefi

et al. 2020

Journal Cellular Physiology

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“…FAK inhibition in a murine model resulted in decreased proliferation and migration of tumor-associated Mϕ [51]. Notch signaling plays context-dependent roles in differentiation, proliferation, and apoptosis, and has been implicated in cancer progression through influencing both the FAK and NFκB activity [52,53]. In the context of Mϕ, our results in this study show that along with an increase in Notch1 expression, FAK level was also increased in splenic Mϕ of Chagas mice and in Mϕ in vitro infected with T. cruzi, and treatment with SRT1720 inhibited the expression as well as phosphorylation of FAK ( Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Origin of Monocytes/Macrophages Contributing to Chronic Inflammation in Chagas Disease: SIRT1 Inhibition of FAK-NFκB-Dependent Proliferation and Proinflammatory Activation of Macrophages

Wan

Chowdhury

Jie

et al. 2019

Cells

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Background: Trypanosoma cruzi (Tc) causes Chagas disease (CD) that is the most frequent cause of heart failure in Latin America. TNF-α + monocytes/macrophages (Mo/Mϕ) are associated with inflammatory pathology in chronic CD. In this study, we determined the progenitor lineage of Mo/Mϕ contributing to inflammation and examined the regulatory role of SIRT1 in modulating the Mo/Mϕ response in Chagas disease. Methods and Results: C57BL/6 mice were infected with Tc, treated with SIRT1 agonist (SRT1720) after control of acute parasitemia, and monitored during chronic phase (150 days post-infection). Flow cytometry studies showed an increase in maturation of bone marrow hematopoietic stem cell (HSC)-derived Mo of proinflammatory and anti-inflammatory phenotype in acutely-and chronically-infected mice; however, these cells were not increased in splenic compartment of infected mice. Instead, yolk-sac-derived CD11b + F4/80 + Mo/Mϕ were increased in sinusoidal compartment of Chagas mice. The splenic CD11b + F4/80 + Mo/Mϕ of Chagas (vs. control) mice exhibited increased mRNA, protein, and surface expression of markers of proinflammatory phenotype (CD80 + /CD64 + > CD200 + /CD206 + ) associated with proinflammatory cytokines response (IL-6+TNF-α >> Arg-1+IL-10), and these were also detected in the myocardium of chronically infected mice. Infected mice treated with SRT1720 (vs. infected/untreated) exhibited decreased splenic expansion and myocardial infiltration of proinflammatory Mo/Mϕ. SRT1720 did not alter the inherent capability of splenic Mo/Mϕ of Chagas mice to respond to pathogen stimulus. Instead, SRT1720 dampened the Tc-induced increase in the expression and/or phosphorylation of focal adhesion kinase (FAK) and downstream transcription factors (Pu.1, c-Myb, and Runx1) involved in Mϕ proliferation and migration and Notch1 involved in functional activation. Studies in cultured Mϕ confirmed the agonistic effects of SIRT1 in controlling the Tc-induced, FAK-dependent increase in the expression of transcription factors and showed that SIRT1 agonist and FAK inhibitor abrogated the NF-κB transcriptional activity and inflammatory cytokine gene expression in Tc-infected Mϕ. Conclusions: The proinflammatory Mo/Mϕ of yolk sac origin drive the splenic and tissue inflammatory response in chronic CD. SRT1720 reprogrammed the Tc-induced FAK-dependent transcription factors involved in Mϕ proliferation and proinflammatory activation in Chagas disease.

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“…The Notch signaling pathway was conserved. The Notch pathway, which regulates biological development through interaction between cells, plays an important role in cell proliferation, differentiation, development and homeostasis [44]. The Notch pathway can interact with many growth factors and cytokines, such as VEGF [45], Wnt/β-catenin [46], TGF-β [47,48] and so on.…”

Section: Plos Onementioning

confidence: 99%

Integrative analysis of long non-coding RNA and mRNA in broilers with valgus-varus deformity

et al. 2020

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Background Bone abnormality and leg disease in commercial broiler flocks are increasingly prominent, causing serious economic losses to the broiler breeding industry. Valgus-varus deformity (VVD) is a common deformity of the long bone in broilers that manifests as an outward or inward deviation of the tibiotarsus or tarsometatarsus. There is a paucity of studies on the molecular mechanisms of VVD. Results In this study, 6 cDNA libraries were constructed from spleen samples from VVD birds and normal birds. A total of 1951 annotated lncRNAs, 7943 novel lncRNAs and 30252 mRNAs were identified by RNA-sequencing. In addition, 420 differentially expressed (DE) mRNAs and 124 differentially expressed lncRNAs (adjusted P-value < 0.05) were obtained. A total of 16 dysregulated genes were confirmed by qPCR to be consistent with the results of the RNA-Seq. The functional lncRNA-mRNA co-expression network was constructed using differentially expressed mRNAs and target genes of the differentially expressed lncRNAs. 11 DE genes were obtained from the analysis. In order to gain insight into the interactions of genes, lncRNAs and pathways associated with VVD, we focused on the following pathways, which are involved in immunity and bone development: the Jak-stat signaling pathway, Tolllike receptor signaling pathway, Wnt-signaling pathway, mTOR signaling pathway, VEGF signaling pathway, Notch signaling pathway, TGF-beta signaling pathway and Fanconi anemia pathway. All together, 30 candidate DE genes were obtained from these pathways. We then analyzed the interaction between the DE genes and their corresponding lncRNAs. From these interaction network analyses we found that GARS, NFIC, PIK3R1, BMP6, NOTCH1, ACTB and CREBBP were the key core nodes of these networks. Conclusion This study showed that differentially expressed genes and signaling pathways were related to immunity or bone development. These results increase the understanding of the PLOS ONE

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Co-inhibition of Notch and NF-κB Signaling Pathway Decreases Proliferation through Downregulating IκB-α and Hes-1 Expression in Human Ovarian Cancer OVCAR-3 Cells

Cited by 21 publications

References 26 publications

Critical roles of long noncoding RNAs in breast cancer

Critical roles of long noncoding RNAs in breast cancer

Origin of Monocytes/Macrophages Contributing to Chronic Inflammation in Chagas Disease: SIRT1 Inhibition of FAK-NFκB-Dependent Proliferation and Proinflammatory Activation of Macrophages

Integrative analysis of long non-coding RNA and mRNA in broilers with valgus-varus deformity

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