Interleukin-23 promotes the migration and invasion of gastric cancer cells by inducing epithelial-to-mesenchymal transition via the STAT3 pathway

Xu, Xiang; Yang, Changdong; Liu, Junyan; Li, Pingang; Shi, Yan; Yu, Ping

doi:10.1016/j.bbrc.2018.03.144

Cited by 21 publications

(14 citation statements)

References 23 publications

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“…Other pro-inflammatory cytokines, IL-32β and IL-23, are highly expressed in cancers. STAT3 activation by IL-23/IL23R and via IL-32β-induced VEGF leads to increased migration and invasion of breast cancer (BC) and gastric cancer (GC) cells [40,41]. Additionally, the FAM3 family of created cytokines, ILEI-induced PDGF-C/PDGF-Rβ [42], or PDGF-Rα activation [43], enhance EMT and aggressiveness by increasing p-STAT3 via Src activation.…”

Section: Critical Modulators Of the Jak2/stat3 Signaling Pathway In Emtmentioning

confidence: 99%

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Jin

2020

Cells

304

193

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The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts as a critical regulator in the progression of cancer and is involved in regulating invasion, spread, and survival. Furthermore, accumulating evidence indicates the failure of conventional therapies due to the acquisition of CSC properties. In this review, we summarize the effects of JAK/STAT3 activation on EMT and the generation of CSCs. Moreover, we discuss cutting-edge data on the link between EMT and CSCs in the tumor microenvironment that involves a previously unknown function of miRNAs, and also discuss new regulators of the JAK/STAT3 signaling pathway.

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Section: Critical Modulators Of the Jak2/stat3 Signaling Pathway In Emtmentioning

confidence: 99%

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Jin

2020

Cells

304

193

View full text Add to dashboard Cite

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“…Elucidation of possible mechanism of IL-23’s direct effect in GC tumorigenesis is still rare. Through in vitro experiment, Liu et al showed co-cultured cell lines SGC-7901 and MKN45 with human recombinant IL-23A and H. pylori lysate induced IL-17A/IL-17RA/NF-κB activation [ 108 ], while Xu et al demonstrated IL-23 promoting tumor cell migration via STAT3 in BGC-823 GC cell line [ 109 ].…”

Section: Il-17 Il-21 and Il-23 Role In Gc Developmentmentioning

confidence: 99%

The Roles of IL-17, IL-21, and IL-23 in the Helicobacter pylori Infection and Gastrointestinal Inflammation: A Review

Dewayani

Fauzia

Alfaray

et al. 2021

Toxins

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Although millions of people have been infected by Helicobacter pylori (H. pylori), only a small proportion of infected individuals will develop adverse outcomes, ranging from chronic gastritis to gastric cancer. Advanced development of the disease has been well-linked with chronic inflammation, which is significantly impacted by the adaptive and humoral immunity response. From the perspective of cellular immunity, this review aims to clarify the intricate axis between IL-17, IL-21, and IL-23 in H. pylori-related diseases and the pathogenesis of inflammatory gastrointestinal diseases. CD4+ helper T (Th)-17 cells, with the hallmark pleiotropic cytokine IL-17, can affect antimicrobial activity and the pathogenic immune response in the gut environment. These circumstances cannot be separated, as the existence of affiliated cytokines, including IL-21 and IL-23, help maintain Th17 and accommodate humoral immune cells. Comprehensive understanding of the dynamic interaction between molecular host responses in H. pylori-related diseases and the inflammation process may facilitate further development of immune-based therapy.

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“…Increasing evidence shows that chronic inflammation can remarkably promote the progression and malignancy of cancer cells [259,260]. IL-23 is one of the pro-inflammatory cytokines and it has been reported that IL-23 induces the EMT mechanism through STAT3 upregulation to ensure the migration and metastasis of GC cells [261].…”

Section: Other Molecular Signaling Pathways Regulate Stat3mentioning

confidence: 99%

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Biology

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Molecular signaling pathways play a significant role in the regulation of biological mechanisms, and their abnormal expression can provide the conditions for cancer development. The signal transducer and activator of transcription 3 (STAT3) is a key member of the STAT proteins and its oncogene role in cancer has been shown. STAT3 is able to promote the proliferation and invasion of cancer cells and induces chemoresistance. Different downstream targets of STAT3 have been identified in cancer and it has also been shown that microRNA (miR), long non-coding RNA (lncRNA) and other molecular pathways are able to function as upstream mediators of STAT3 in cancer. In the present review, we focus on the role and regulation of STAT3 in gastric cancer (GC). miRs and lncRNAs are considered as potential upstream mediators of STAT3 and they are able to affect STAT3 expression in exerting their oncogene or onco-suppressor role in GC cells. Anti-tumor compounds suppress the STAT3 signaling pathway to restrict the proliferation and malignant behavior of GC cells. Other molecular pathways, such as sirtuin, stathmin and so on, can act as upstream mediators of STAT3 in GC. Notably, the components of the tumor microenvironment that are capable of targeting STAT3 in GC, such as fibroblasts and macrophages, are discussed in this review. Finally, we demonstrate that STAT3 can target oncogene factors to enhance the proliferation and metastasis of GC cells.

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Interleukin-23 promotes the migration and invasion of gastric cancer cells by inducing epithelial-to-mesenchymal transition via the STAT3 pathway

Cited by 21 publications

References 23 publications

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

The Roles of IL-17, IL-21, and IL-23 in the Helicobacter pylori Infection and Gastrointestinal Inflammation: A Review

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

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