Dermokine contributes to epithelial–mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer

Huang, Chenlu; Xiang, Yukai; Chen, Shengchuan; Yu, Huajun; Wen, Zhengde; Ye, Tingting; Sun, Hongwei; Kong, Heng; Li, Dapei; Yu, Dinglai; Chen, Bicheng; Zhou, Mengtao

doi:10.1111/cas.13347

Cited by 21 publications

(29 citation statements)

References 44 publications

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“…These results demonstrate that the inhibition of NF-κB signaling cascade could be a promising approach to overcome cancer cells resistance to the therapeutic agents (de Castro Barbosa et al, 2017). Baicalein from Scutellaria baicalensis has been identified as an inhibitor of NF-κB activation, which suppressed TNF-α- | 8209 (C. Huang et al, 2017) cancers and so increased cancer cells survival and proliferation. Interleukin (IL) 6 that has a major role in STAT3 activation is one of the crucial cytokines in the tumor microenvironment that is detected at extraordinary concentrations in cancer.…”

Section: Inhibition Of Nuclear Factor-κb (Nf-κb) Signal Transducer and Activator Of Transcription 3 (Stat3) And Src Kinases Signaling Patmentioning

confidence: 82%

Leukemia therapy by flavonoids: Future and involved mechanisms

Saraei

Marofi

Naimi

et al. 2018

Journal Cellular Physiology

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Flavonoids are a varied family of phytonutrients (plant chemicals) usually are detected in fruits and vegetables. In this big family, there exist more than 10,000 members that is separated into six chief subtypes: isoflavonols, flavonoenes, flavones, flavonols, anthocyanins, and chalcones. The natural compounds, such as fruits, have visible positive effects in regulating of survival involved signaling pathways that performance as the regulator of cell survival, growth, and proliferation. Researchers have established that commonly consumption up flavonoids decreases incidence and development risk of certain cancers, especially leukemia. Flavonoids have been able to induce apoptosis and stimulate cell cycle arrest in cancer cells via different pathways. Similarly, they have antiangiogenesis and antimetastasis capability, which were shown in wide ranges of cancer cells, particularly, leukemia. It seems that flavonoid because of their widespread approval, evident safety and low rate of side effects, have hopeful anticarcinogenic potential for leukemia therapy. Based on the last decade reports, the most important acting mechanisms of these natural compounds in leukemia cells are stimulating of apoptosis pathways by upregulation of caspase 3, 8, 9 and poly ADP‐ribose polymerase (PARP) and proapoptotic proteins, particularly Bax activation. As well, they can induce cell cycle arrest in target cells not only via increasing of activated levels of p21 and p53 but also by inhibition of cyclins and cyclin‐dependent kinases. Furthermore, attenuation of neclear factor‐κB and signal transducer and activator of transcription 3 activation, suppression of signaling pathway and downregulation of intracellular antiapoptotic proteins are other significant antileukemic function mechanism of flavonoids. Overall, it appears that flavonoids are promising and effective compounds in the field of leukemia therapy. In this review, we tried to accumulate and revise most promising flavonoids and finally declared their major working mechanisms in leukemia cells.

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Section: Inhibition Of Nuclear Factor-κb (Nf-κb) Signal Transducer and Activator Of Transcription 3 (Stat3) And Src Kinases Signaling Patmentioning

confidence: 82%

Leukemia therapy by flavonoids: Future and involved mechanisms

Saraei

Marofi

Naimi

et al. 2018

Journal Cellular Physiology

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“…Expression of these genes suggests that the E12.5 mesothelial population may be primed for migration and differentiation. In contrast, the E17.5 mesothelial population expressed genes related to barrier or immune function, such as dermokine ( Dmkn ) 60 , 61 , bone marrow stromal antigen 2 ( Bst2 ), and retinoic acid receptor responder 2 ( Rarres2 ) 62 . These results suggest stage-dependent roles for the mesothelium throughout development.…”

Section: Discussionmentioning

confidence: 97%

Lineage dynamics of murine pancreatic development at single-cell resolution

et al. 2018

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Organogenesis requires the complex interactions of multiple cell lineages that coordinate their expansion, differentiation, and maturation over time. Here, we profile the cell types within the epithelial and mesenchymal compartments of the murine pancreas across developmental time using a combination of single-cell RNA sequencing, immunofluorescence, in situ hybridization, and genetic lineage tracing. We identify previously underappreciated cellular heterogeneity of the developing mesenchyme and reconstruct potential lineage relationships among the pancreatic mesothelium and mesenchymal cell types. Within the epithelium, we find a previously undescribed endocrine progenitor population, as well as an analogous population in both human fetal tissue and human embryonic stem cells differentiating toward a pancreatic beta cell fate. Further, we identify candidate transcriptional regulators along the differentiation trajectory of this population toward the alpha or beta cell lineages. This work establishes a roadmap of pancreatic development and demonstrates the broad utility of this approach for understanding lineage dynamics in developing organs.

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“…The DMKN gene is located on human chromosome 19q13.12 and encodes 10 putative dermokine (DMKN) transcriptional subtypes in normal epidermis [ 39 ]. Studies have confirmed that the abnormal expression of DMKN is related to skin cancer [ 40 ], pancreatic cancer [ 41 ], colorectal cancer [ 42 ], and other cancers, but no study has shown its role in nervous system tumors. However, a report showing that DMKN can affect the activation of STAT3 and down-stream molecular proteins of the MAPK and PI3K signaling pathways suggests that DMKN may play a role in nervous system tumors through this pathway [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of key methylation differentially expressed genes in posterior fossa ependymoma based on epigenomic and transcriptome analysis

Wang

Jia

et al. 2021

J Transl Med

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Background Posterior fossa ependymoma (EPN-PF) can be classified into Group A posterior fossa ependymoma (EPN-PFA) and Group B posterior fossa ependymoma (EPN-PFB) according to DNA CpG island methylation profile status and gene expression. EPN-PFA usually occurs in children younger than 5 years and has a poor prognosis. Methods Using epigenome and transcriptome microarray data, a multi-component weighted gene co-expression network analysis (WGCNA) was used to systematically identify the hub genes of EPN-PF. We downloaded two microarray datasets (GSE66354 and GSE114523) from the Gene Expression Omnibus (GEO) database. The Limma R package was used to identify differentially expressed genes (DEGs), and ChAMP R was used to analyze the differential methylation genes (DMGs) between EPN-PFA and EPN-PFB. GO and KEGG enrichment analyses were performed using the Metascape database. Results GO analysis showed that enriched genes were significantly enriched in the extracellular matrix organization, adaptive immune response, membrane raft, focal adhesion, NF-kappa B pathway, and axon guidance, as suggested by KEGG analysis. Through WGCNA, we found that MEblue had a significant correlation with EPN-PF (R = 0.69, P = 1 × 10–08) and selected the 180 hub genes in the blue module. By comparing the DEGs, DMGs, and hub genes in the co-expression network, we identified five hypermethylated, lower expressed genes in EPN-PFA (ATP4B, CCDC151, DMKN, SCN4B, and TUBA4B), and three of them were confirmed by IHC. Conclusion ssGSEA and GSVA analysis indicated that these five hub genes could lead to poor prognosis by inducing hypoxia, PI3K-Akt-mTOR, and TNFα-NFKB pathways. Further study of these dysmethylated hub genes in EPN-PF and the pathways they participate in may provides new ideas for EPN-PF treatment.

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Dermokine contributes to epithelial–mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer

Cited by 21 publications

References 44 publications

Leukemia therapy by flavonoids: Future and involved mechanisms

Leukemia therapy by flavonoids: Future and involved mechanisms

Lineage dynamics of murine pancreatic development at single-cell resolution

Identification of key methylation differentially expressed genes in posterior fossa ependymoma based on epigenomic and transcriptome analysis

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