Associations of potentially functional variants in IL-6, JAKs and STAT3 with gastric cancer risk in an eastern Chinese population

Zhou, Fei; Cheng, Lei; Qiu, Li Xin; Wang, Mengyun; Li, Jin; Sun, Meng; Yang, Ya; Wang, Jiu Cun; Jin, Li; Wang, Ya Nong; Wei, Qing

doi:10.18632/oncotarget.8492

Cited by 21 publications

(30 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, Helicobacter pylori infection is linked to an increased risk of developing gastric cancer due to alteration the expression level of IL-6 (41, 42). Furthermore, some studies have also showed that gastric cancer patients with liver metastases have higher levels of IL-6 compared to the healthy controls and high serum IL-6 level is associated with tumor invasion, tumor size and lymph node metastasis and IL-6 mediated STAT3 activation plays a crucial role in increasing tumor size and proliferation of gastric cancer (43)(44)(45)(46)(47)(48). Our results demonstrated that IL-6 and STAT3 expression level were considerably higher in cachectic gastric cancer patients levels compared to the non-cachectic and healthy control group (p < 0.01).…”

Section: Discussionmentioning

confidence: 99%

IL-6 mediated JAK/STAT3 signaling pathway in cancer patients with cachexia

Eskiler¹,

Bezdegümeli²,

Özman³

et al. 2019

BLL

View full text Add to dashboard Cite

OBJECTIVES: We investigated the changes in the IL-6 and STAT3 expression levels in cachectic and noncachectic patients with gastric, lung and breast cancer and evaluated the association between IL-6 and STAT3 levels and cancer types in terms of cachexia condition. BACKGROUND: Cancer-associated cachexia, observed in nearly 50-80 % of cancer patients, has drawn attention in advanced patients. IL-6/JAK/STAT pathway plays an essential role in the progression of cancer cachexia through the regulation of the infl ammatory response. METHODS: This study consisted of 48 gastric, breast and lung cancer patients (18 cachectic and 30 noncachectic) and healthy individuals. Total RNA isolation and cDNA synthesis was performed after the collection of blood samples. IL-6 and STAT3 expression levels were analyzed by RT-PCR analysis. RESULTS: Our fi ndings demonstrated that IL-6 mRNA levels considerably increased 19.89 ± 8.25, 5.18 ± 2.81 and 15.33±9.54-fold in gastric, lung and breast cancer patients with cachexia, respectively. Additionally, a 16.67±7.13, 14.21 ± 11.72 and 8.85 ± 3.89-fold increase in the STAT3 expression level was detected in cachectic gastric, lung and breast cancer patients, respectively (p < 0.01). CONCLUSION: STAT3 may be considered as a therapeutic target for cachectic patients with gastric, lung and breast cancer. Furthermore, IL-6 mediates STAT3 activation in cachectic gastric and breast cancer patients (Tab. 5, Fig. 2, Ref. 62).

show abstract

Section: Discussionmentioning

confidence: 99%

IL-6 mediated JAK/STAT3 signaling pathway in cancer patients with cachexia

Eskiler¹,

Bezdegümeli²,

Özman³

et al. 2019

BLL

View full text Add to dashboard Cite

show abstract

“…in the cytoplasm, where it can be phosphorylated at Tyr705 via Janus kinase (JAK)-mediated tyrosine phosphorylation when stimulated by cytokines. The phosphorylated STAT3 translocates into the nucleus, combines with DNA sites, and regulates various cellular processes, including cell apoptosis and proliferation (11,12). Persistent activation of STAT3 has been observed in >70% of solid and hematological tumors, which may be one of the most notable differences between normal and malignant cells (13).…”

Section: Gallic Acid Has Anticancer Activity and Enhances The Anticanmentioning

confidence: 99%

Gallic acid has anticancer activity and enhances the anticancer effects of cisplatin in non‑small cell lung cancer A549 cells via the JAK/STAT3 signaling pathway

Zhang¹,

Ma²,

Wu³

et al. 2019

Oncol Rep

View full text Add to dashboard Cite

Gallic acid (3,4,5-trihydroxybenzoic acid; GA), a plant-derived natural phenolic compound, has been reported to prevent the development and progression of various types of cancers. However, there has been little elaboration of the anticancer effects and underlying mechanisms of GA alone and/or in combination with cisplatin in non-small cell lung cancer (NSCLC). The aim of the present study was to investigate the anticancer effects of GA on NSCLC A549 cells and its auxiliary effects on the anticancer activity of cisplatin. The results revealed that GA inhibited the proliferation and induced the apoptosis of NSCLC A549 cells in dose-and time-dependent manners, which was associated with upregulated B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) and downregulated Bcl-2. Notably, the results also indicated that GA enhanced the anticancer effects of cisplatin in the inhibition of cancer cell proliferation and the induction of cell apoptosis following elevated Bax expression and suppressed Bcl-2 expression. Furthermore, the results of the present study also demonstrated that GA exerted independent anticancer effects on NSCLC A549 cells, and facilitated the anticancer effects of cisplatin by modulating the JAK/STAT3 signaling pathway and downstream apoptotic molecules. These results may serve as a rationale for further basic studies and preclinical investigations on the anticancer effects of GA and its auxiliary effects on cisplatin function in human NSCLC.

show abstract

“…Available evidence suggests that the abnormal expression of related genes plays a pivotal role in the development of gastric cancer, including tumor initiation, promotion, progression and metastasis. For example, IL‐6 and IL‐11 are important regulatory factors in the process of inflammation leading to cancer development, and they may promote tumor aggressiveness correlating with patients’ survival time . STAT3 and NF‐κB activation, which causes gastric cancer progression and leads to enhanced cellular proliferation, is also correlated with poor survival .…”

Section: Introductionmentioning

confidence: 99%