Interleukin-32 contributes to invasion and metastasis of primary lung adenocarcinoma via NF-kappaB induced matrix metalloproteinases 2 and 9 expression

Zeng, Qingli; Li, Shaoli; Zhou, Yan; Ou, Weijun; Cai, Xingdong; Zhang, Longjuan; Huang, Wenwei; Huang, Lixia; Wang, Qinqin

doi:10.1016/j.cyto.2013.09.017

Cited by 63 publications

(66 citation statements)

References 32 publications

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“…IL-32 overexpression has been described in head and neck squamous cell carcinoma and has been related to shorter survival, possibly due to the potential role of IL-32 in the metastatic process [23]. IL-32 has also been proposed as a lung adenocarcinoma prognostic biomarker, in which high IL-32 expression was associated with high grade disease and metastasis incidence [24,25]. In clear cell renal cell carcinoma patients, IL-32 overexpression was associated with disease progression and poor overall survival, indicating that IL-32 may be a novel prognostic factor for predicting outcomes in this disease [26].…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, IL-32 has been reported as a poor prognostic marker for gastric cancer [27,28]. Using the lung cancer A549 cell line, IL-32 inhibition reduced cell viability, migration and invasion, whereas IL-32 overexpression increased migration and invasion, indicating that this protein participates in the malignant phenotype of lung cancer cells [24].…”

Section: Discussionmentioning

confidence: 99%

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IL32 expression in peripheral blood CD3+ cells from myelodysplastic syndromes patients

et al. 2017

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Background: Myelodysplastic syndromes (MDS) are a heterogeneous group of disorders characterized by ineffective hematopoiesis and risk of leukemia transformation. There is evidence to suggest the participation of immune system deregulation in MDS pathogenesis. Interleukin-32 (IL-32) is a newly described multifunctional cytokine reported as an important mediator in autoimmune and inflammatory disorders. In the present study, we reported the expression of IL32 and IL32 transcript variants (α, β, γ and δ) in peripheral blood CD3 + cells from healthy controls and MDS patients. Methods: CD3 + cells were isolated by immunomagnetic cell sorting from thirty-nine untreated MDS patients and twenty-nine healthy donors. Gene expression was evaluated by quantitative PCR. For statistical analysis, Mann-Whitney test, Kruskal-Wallis test with Dunns post test and Log-rank (Mantel-Cox) were used, as appropriate. A p value <0.05 was considered statistically significant.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

IL32 expression in peripheral blood CD3+ cells from myelodysplastic syndromes patients

et al. 2017

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“…In vitro studies showed that this protein induces migration and invasion of cancer cells. Overexpression of IL-32 contributes to invasion and metastasis in primary lung adenocarcinoma, induced by increased expression of MMPs 2 and 9 via NF-kappaB activation (70). IL-32α exhibits more migratory ability to melanoma cells, through downregulation of E-cadherin expression (71).…”

Section: Role In Cancer Biologymentioning

confidence: 99%

Interleukin-32 in Infection, Inflammation and Cancer Biology

Pavlovic

Jovanović

Arsenijević

2020

Serbian Journal of Experimental and Clinical Research

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“…On the other hand, IL-32 expression is distinctly altered in lung cancer cells and closely associated with increased lung cancer invasiveness, metastasis and poor prognosis [48,49]. Recent reports show that IL-32 also is involved in the invasion and metastasis of primary lung adenocarcinoma via NF-κB induced MMP-2 and MMP-9 expression [2,49,50]. Because LL-37 can significantly suppress IL-32-induced production of pro-inflammatory cytokines and IL-32-mediated phosphorylation of Fyn (Y420) Src kinase [48], it was proposed that LL-37 can affect the carcinogenesis of lung cancer by suppressing the biological activity of IL-32 ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Roles and Mechanisms of Human Cathelicidin LL-37 in Cancer

Chen

Zou

et al. 2018

Cell Physiol Biochem

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LL-37, the C-terminal peptide of human cathelicidin antimicrobial peptide (CAMP, hCAP18), reportedly increases resistance to microbial invasion and exerts important physiological functions in chemotaxis, promotion of wound closure, and angiogenesis. Accumulating evidence indicates that LL-37 also plays a significant role in human cancer. LL-37 induces tumorigenic effects in cancers of the ovary, lung, breast, prostate, pancreas, as well as in malignant melanoma and skin squamous cell carcinoma. In contrast, LL-37 displays an anti-cancer effect in colon cancer, gastric cancer, hematologic malignancy and oral squamous cell carcinoma. Mechanistically, LL-37-induced activation of membrane receptors and subsequent signaling pathways lead to alteration of cellular functions. Different membrane receptors on various cancer cells appear to be responsible for the tissue-specific effects of LL-37. Meanwhile, the findings that vitamin D-dependent induction of cathelicidin in human macrophages activates the anti-cancer activity of tumor-associated macrophages (TAMs) and enhances antibody-dependent cellular cytotoxicity (ADCC) support critical roles of vitamin D-dependent induction of cathelicidin in cancer progression. This review describes novel advances involving the roles and mechanisms of human cathelicidin LL-37 in cancer.

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Interleukin-32 contributes to invasion and metastasis of primary lung adenocarcinoma via NF-kappaB induced matrix metalloproteinases 2 and 9 expression

Cited by 63 publications

References 32 publications

IL32 expression in peripheral blood CD3+ cells from myelodysplastic syndromes patients

IL32 expression in peripheral blood CD3+ cells from myelodysplastic syndromes patients

Interleukin-32 in Infection, Inflammation and Cancer Biology

Roles and Mechanisms of Human Cathelicidin LL-37 in Cancer

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