Nuclear β-catenin accumulation is associated with increased expression of Nanog protein and predicts poor prognosis of non-small cell lung cancer

Li, Xiqing; Yang, Xinglong; Zhang, Gong; Wu, Si-Pei; Deng, Xu-Bing; Xiao, Sheng-Jun; Liu, Qiu-Zhen; Yao, Kai-Tai; Xiao, Guang-Hui

doi:10.1186/1479-5876-11-114

Cited by 70 publications

(69 citation statements)

References 32 publications

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“…We found that IL-35 was expressed in non-tumor tissues and it was down- progression [21]. To gain further insight into the role of IL-35 in NSCLC, we examined the expression of β-catenin.…”

Section: Discussionmentioning

confidence: 99%

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Interleukin-35 Expression in Non-Small Cell Lung Cancer is Associated with Tumor Progression

Sun¹,

Zheng²,

Meng³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lung cancer continues to be the leading cause of cancer related deaths worldwide due to its high incidence, malignant behavior and lack of major advancements in treatment strategy. The occurrence and development of lung cancer is closely related to inflammation. Thus, we conducted the present study to investigate the effects of IL-35 (Interleukin 35), a newly identified anti-inflammatory factor, on non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers. Methods: We first evaluated the IL-35 expression in 384 pairs of NSCLC samples and their adjacent normal mucosa by realtime PCR, ELISA (Enzyme-linked immunoassay) and tissue microarrays. Then the role of IL-35 on patient survival rates, cancer progression and their sensitivity to chemotherapy drugs were assessed. Results: IL-35 was barely expressed in the NSCLC tissues but highly expressed in the adjacent normal tissues. The down-regulation of IL-35 was significantly correlated with the results of American Joint Committee on Cancer stage, differentiation and it was also shown to be an independent prognostic indicator of disease-free survival and overall survival for patients with NSCLC. Overexpression of IL-35 in NSCLC cells suppressed cell migration, invasion, proliferation, colony formation through suppressing β-catenin. IL-35 inhibited NSCLC formation in the mice model and sensitize the cancer cells to chemotherapy drugs. Conclusion: Our results showed that IL-35 plays an inhibitory role in NSCLC development and function as a novel prognostic indicator and a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

“…The expressions of β-catenin in A549 and SK-MES-1 cells were analyzed after treatment with 100 ng/mL rhIL-35 for 24 h, because of the important role of β-catenin in NSCLC development [21]. The mRNA and protein levels of β-catenin were suppressed by IL-35 in these two cell lines (Fig.…”

Section: Il-35 Inhibits β-Catenin Expression In Nsclc Cellsmentioning

confidence: 99%

Interleukin-35 Expression in Non-Small Cell Lung Cancer is Associated with Tumor Progression

Sun¹,

Zheng²,

Meng³

et al. 2018

Cell Physiol Biochem

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“…For the immunohistochemical detection of β-catenin, the sections were stained with a human monoclonal antibody to β-catenin (1:200, Cell Signaling Technology). Lung cancer tissues, known to widely express β-catenin, 6,23,24 were used as positive control. The immunostaining pattern in the epithelium of airways was blindly evaluated by two investigators.…”

Section: Lung Histopathology and Immunohistochemistrymentioning

confidence: 99%

WNT/β-catenin signaling regulates cigarette smoke-induced airway inflammation via the PPARδ/p38 pathway

Guo

Wang

et al. 2016

Laboratory Investigation

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The mechanisms of WNT/β-catenin signaling involved in airway inflammation of chronic obstructive pulmonary disease (COPD) remain unknown, although recent observations have suggested an important contribution of the pathway in pulmonary parenchymal tissue repair and airway epithelium differentiation. We investigated the role of WNT/β-catenin signaling in cigarette smoke (CS)-related airway inflammation using patient lung tissues, human bronchial epithelial cells (16HBECs), and mouse models. Reduced activity of WNT/β-catenin signaling was observed in the airway epithelium of smokers with or without COPD. The mRNA expression of WNT transcription factor TCF4 negatively correlated with the pack year. The mRNA levels of WNT receptor FZD4 negatively correlated with the mRNA levels of IL-1β. CS exposure decreased the activity of WNT/β-catenin signaling in both 16HBECs and mice. In vitro studies demonstrated the upregulation of inflammatory cytokines TNF-α and IL-1β secretion induced by CS extract (CSE) could be attenuated by β-catenin activator SB216763 and be exacerbated by β-catenin small-interfering RNA (siRNA), respectively. Furthermore, the decrease in the expression of peroxisome proliferator-activated receptor (PPARδ) induced by CSE stimulation could be rescued by SB216763. SB216763 also attenuated the upregulation of phosphorylated p38 mitogen-activated protein kinase (MAPK) stimulated by CSE. Both PPARδ agonist and p38 MAPK inhibitor could suppress the TNF-α and IL-1β release induced by CSE treatment. In addition, PPARδ activation could abolish β-catenin siRNA-mediated aggravation of phosphorylated p38 MAPK in response to CSE. Finally, SB216763 treatment significantly ameliorated peribronchial inflammatory cell infiltration, leukocyte influx, and the release of TNF-α and IL-1β in the bronchoalveolar lavage fluid of CS-exposed mice. Taken together, our findings indicate that the reduced activity of WNT/β-catenin signaling induced by CS may promote inflammatory cytokine production in airway epithelium and have an essential role in airway inflammation in COPD by PPARδ/p38 MAPK pathway.

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“…We know that the β-catenin gene is upstream of Nanog, Oct3/4, Sox2, c-Myc, and Klf4, and our previous studies have shown that there is a correlation between β-catenin and Nanog in lung cancer (31,32). Moreover, elevated β-catenin expression can promote Nanog, Oct3/4, Sox2, c-Myc, and Klf4 expression (33,34).…”

Section: Discussionmentioning

confidence: 94%

Elevated HOTAIR expression associated with cisplatin resistance in non-small cell lung cancer patients

Liu¹,

Li²,

Gao³

et al. 2016

J. Thorac. Dis.

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Background: This study investigated the mechanism of drug resistance in non-small cell lung cancer (NSCLC) patients. We specifically studied whether long noncoding RNAs influence drug resistance in NSCLC to discover new therapeutic targets to increase the survival rate of drug-resistant NSCLC patients. Methods: Tissue samples were collected from NSCLC patients, and total RNA was isolated for assessment of HOTAIR expression and drug resistance status. MTT assays, tumor sphere formation assays, and western blot were performed to cytologically determine the relationship between HOTAIR expression and cisplatin resistance, as well as to elucidate the potential molecular mechanism involved. Results: HOTAIR expression in tissues of drug-resistant NSCLC patients was higher than that of nondrug-resistant patients. HOTAIR expression was elevated in cisplatin-resistant cell strains (A549/CDDP), and reducing HOTAIR expression increased the sensitivity of A549/CDDP cells to cisplatin. In addition, overexpression of HOTAIR in A549 cells increased resistance to cisplatin. Tumor sphere formation assays showed that the volume of spheres formed by cell strains expressing elevated levels of HOTAIR was greater than that of cell strains with low expression. Western blot experiments showed that elevated expression of HOTAIR upregulated tumor stem cell-related biomarkers and HOTAIR expression was directly related to Klf4 expression.Conclusions: Elevated HOTAIR expression is associated with drug resistance in NSCLC patients and is related to Klf4 upregulation, providing a new therapeutic target for drug-resistant NSCLC patients.

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Nuclear β-catenin accumulation is associated with increased expression of Nanog protein and predicts poor prognosis of non-small cell lung cancer

Cited by 70 publications

References 32 publications

Interleukin-35 Expression in Non-Small Cell Lung Cancer is Associated with Tumor Progression

Interleukin-35 Expression in Non-Small Cell Lung Cancer is Associated with Tumor Progression

WNT/β-catenin signaling regulates cigarette smoke-induced airway inflammation via the PPARδ/p38 pathway

Elevated HOTAIR expression associated with cisplatin resistance in non-small cell lung cancer patients

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