DC-SIGN mediates gastric cancer progression by regulating the JAK2/STAT3 signaling pathway and affecting LncRNA RP11-181G12.2 expression

Li, Yongming; Na, Heya; Xu, Lijie; Zhang, Xinsheng; Feng, Zhen; Xu, Zhou; Cui, Jingyi; Zhang, Jingbo; Lin, Fang; Yang, Shu; Yue, Fangxia; Mousa, Haithm; Zuo, Yongchun

doi:10.1016/j.biopha.2019.109644

Cited by 12 publications

(8 citation statements)

References 40 publications

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“…Published literature has confirmed the contribution of LSECtin members DC-SIGN and DC-SIGNR to GC carcinogenesis through upregulation of STAT family molecules [ 9 , 10 ]. We inferred that LSECtin can also regulate STAT family members STAT1, STAT3, and STAT5A, which have been reported to be closely related with cancer [ 19 ].…”

Section: Resultsmentioning

confidence: 99%

“…In serum from colon cancer patients, the expression of LSECtin and DC-SIGNR was found to be elevated, and in cases of liver metastasis, the expression was further increased [ 7 , 8 ], as was that of DC-SIGNR in GC [ 9 ]. DC-SIGN and DC-SIGNR can affect the expression of long noncoding RNA (lncRNA) by upregulating STAT3 and STAT5A expression to promote the progression and metastasis of GC [ 9 , 10 ]. In summary, it is reasonable to hypothesize that LSECtin participates in tumor progression.…”

Section: Introductionmentioning

confidence: 99%

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Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

Zhang

Feng

et al. 2022

Cell Death Dis

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Liver and lymph node sinusoidal endothelial cell C-type lectin (LSECtin) plays an important regulatory role in a variety of diseases, including tumors. However, the underlying mechanism of LSECtin in gastric cancer (GC) remains largely unknown. In our research, LSECtin promoted the adhesion and invasion of GC cells, and was involved in lymphatic metastasis of GC cells. Mechanistically, LSECtin promoted the adhesion, proliferation and migration of GC cells by downregulating STAT1 expression. The circular RNA circFBXL4, which is regulated by LSECtin, sponges the microRNA miR-146a-5p to regulate STAT1 expression. The promotion of GC cell proliferation, migration and invasion mediated by LSECtin was largely inhibited by circFBXL4 overexpression or miR-146a-5p silencing. Moreover, in its role as a transcription factor, STAT1 modulated the expression of FN1 and CHD4. In conclusion, LSECtin might be involved in the lymphatic metastasis of GC by upregulating the expression of FN1 and CHD4 via the circFBXL4/miR-146a-5p/STAT1 axis, possibly indicating a newly discovered pathogenic mechanism.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

Zhang

Feng

et al. 2022

Cell Death Dis

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“…This report proposed that RP11-181G12.2 may impart a growth-inhibitory effect by negatively modulating DC-SIGN associated JAK/STAT3 pathway in GC cells. 373 Some mRNAs are stabilized by the interaction with lncRNAs which results in their enhanced expression.…”

Section: Gastric Cancermentioning

confidence: 99%

Noncoding RNAs as regulators of STAT3 pathway in gastrointestinal cancers: Roles in cancer progression and therapeutic response

Ashrafizadeh

Mohan

Rangappa

et al. 2023

Medicinal Research Reviews

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Gastrointestinal (GI) tumors (cancers of the esophagus, gastric, liver, pancreas, colon, and rectum) contribute to a large number of deaths worldwide. STAT3 is an oncogenic transcription factor that promotes the transcription of genes associated with proliferation, antiapoptosis, survival, and metastasis. STAT3 is overactivated in many human malignancies including GI tumors which accelerates tumor progression, metastasis, and drug resistance. Research in recent years demonstrated that noncoding RNAs (ncRNAs) play a major role in the regulation of many signaling pathways including the STAT3 pathway. The major types of endogenous ncRNAs that are being extensively studied in oncology are microRNAs, long noncoding RNAs, and circular RNAs. These ncRNAs can either be tumor‐promoters or tumor‐suppressors and each one of them imparts their activity via different mechanisms. The STAT3 pathway is also tightly modulated by ncRNAs. In this article, we have elaborated on the tumor‐promoting role of STAT3 signaling in GI tumors. Subsequently, we have comprehensively discussed the oncogenic as well as tumor suppressor functions and mechanism of action of ncRNAs that are known to modulate STAT3 signaling in GI cancers.

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“…In addition, it can mediate cell migration and adhesion of dendritic cells, and in cancer, it can mediate immune escape of tumor cells. Expression of DC-SIGN is normally low in gastric tissue, being overexpressed in gastric cancer (Domínguez-Soto et al, 2011), where it promotes proliferation, cell cycle progression, migration and invasion of GC cells in vitro (Li et al, 2020). In children, DC-SIGN is overexpressed in gastric tissue of H. pylori infected children, which has been directly correlated with the magnitude of inflammation (Wu et al, 2014); this correlates with in vitro results, showing that H. pylori induces DC-SIGN expression in gastric epithelial cells and a Th1 immune response (Wu et al, 2014).…”

Section: Cell-adhesion Proteinsmentioning

confidence: 99%

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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Helicobacter pylori (H. pylori) is well-known to be involved in gastric carcinogenesis, associated with deregulation of cell proliferation and epigenetic changes in cancerrelated genes. H. pylori infection is largely acquired during childhood, persisting long-term in about half of infected individuals, a subset of whom will go on to develop peptic ulcer disease and eventually gastric cancer, however, the sequence of events leading to disease is not completely understood. Knowledge on carcinogenesis and gastric damage-related biomarkers is abundant in adult populations, but scarce in children. We performed an extensive literature review focusing on gastric cancer related biomarkers identified in adult populations, which have been detected in children infected with H. pylori. Biomarkers were related to expression levels (RNA or protein) and/or methylation levels (DNA) in gastric tissue or blood of infected children as compared to non-infected controls. In this review, we identified 37 biomarkers of which 24 are over expressed, three are under expressed, and ten genes are significantly hypermethylated in H. pylori-infected children compared to healthy controls in at least 1 study. Only four of these biomarkers (pepsinogen I, pepsinogen II, gastrin, and SLC5A8) have been studied in asymptomatically infected children. Importantly, 13 of these biomarkers (β-catenin, C-MYC, GATA-4, DAPK1, CXCL13, DC-SIGN, TIMP3, EGFR, GRIN2B, PIM2, SLC5A8, CDH1, and VCAM-1.) are consistently deregulated in infected children and in adults with gastric cancer. Future studies should be designed to determine the clinical significance of these changes in infection-associated biomarkers in children and their persistence over time. The effect of eradication therapy over these biomarkers in children if proven significant, could lead to modifications in treatment guidelines for younger populations, and eventually promote the development of preventive strategies, such as vaccination, in the near future.

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DC-SIGN mediates gastric cancer progression by regulating the JAK2/STAT3 signaling pathway and affecting LncRNA RP11-181G12.2 expression

Cited by 12 publications

References 40 publications

Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

Novel roles of LSECtin in gastric cancer cell adhesion, migration, invasion, and lymphatic metastasis

Noncoding RNAs as regulators of STAT3 pathway in gastrointestinal cancers: Roles in cancer progression and therapeutic response

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

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