Characteristics of Selected Adipokines in Ascites and Blood of Ovarian Cancer Patients

Wróblewski, Marcin; Szewczyk-Golec, Karolina; Hołyńska-Iwan, Iga; Wróblewska, Joanna; Woźniak, Alina

doi:10.3390/cancers13184702

Cited by 8 publications

(4 citation statements)

References 77 publications

(195 reference statements)

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“…19 IL-8, otherwise called CXCL8, is a critical cytokine that positively regulates neutrophil chemotaxis and inflammation. 20,21 It is secreted by numerous cells, namely, neutrophils, monocytes, endothelial cells and tumour cells. Emerging evidences suggested that the circulating IL-8 levels in tumour patients is strongly associated with worse patient outcome and chemoresistance.…”

Section: Discussionmentioning

confidence: 99%

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IL‐8 from CD248‐expressing cancer‐associated fibroblasts generates cisplatin resistance in non‐small cell lung cancer

Wu,

Zhang,

et al. 2024

J Cellular Molecular Medi

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Chemotherapy‐resistant non‐small cell lung cancer (NSCLC) presents a substantial barrier to effective care. It is still unclear how cancer‐associated fibroblasts (CAFs) contribute to NSCLC resistance to chemotherapy. Here, we found that CD248+CAFs released IL‐8 in NSCLC, which, in turn, enhanced the cisplatin (CDDP) IC50 in A549 and NCI‐H460 while decreasing the apoptotic percentage of A549 and NCI‐H460 in vitro. The CD248+CAFs‐based IL‐8 secretion induced NSCLC chemoresistance by stimulating nuclear factor kappa B (NF‐κB) and elevating ATP‐binding cassette transporter B1 (ABCB1). We also revealed that the CD248+CAFs‐based IL‐8 release enhanced cisplatin chemoresistance in NSCLC mouse models in vivo. Relative to wild‐type control mice, the CD248 conditional knockout mice exhibited significant reduction of IL‐8 secretion, which, in turn, enhanced the therapeutic efficacy of cisplatin in vivo. In summary, our study identified CD248 activates the NF‐κB axis, which, consecutively induces the CAFs‐based secretion of IL‐8, which promotes NSCLC chemoresistance. This report highlights a potential new approach to enhancing the chemotherapeutic potential of NSCLC‐treating cisplatin.

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Section: Discussionmentioning

confidence: 99%

“…IL‐8, otherwise called CXCL8, is a critical cytokine that positively regulates neutrophil chemotaxis and inflammation 20,21 . It is secreted by numerous cells, namely, neutrophils, monocytes, endothelial cells and tumour cells.…”

Section: Discussionmentioning

confidence: 99%

IL‐8 from CD248‐expressing cancer‐associated fibroblasts generates cisplatin resistance in non‐small cell lung cancer

Wu,

Zhang,

et al. 2024

J Cellular Molecular Medi

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“…In addition to adipocytes, there are also stromal vascular fraction, adipose-derived stem cells, preadipocytes, macrophages, lymphocytes, eosinophils, mast cells, fibroblasts, and nerve cells [ 27 , 30 , 31 ]. There are four types of AT differentiated by histological structure and function: white adipose tissue (WAT), brown adipose tissue (BAT), beige adipose tissue, and pink adipose tissue [ 27 , 32 ]. WAT, one of the largest organs, is the main energy store of the organism, which captures and accumulates lipids [ 33 ].…”

Section: Characteristics Of Adipose Tissuementioning

confidence: 99%

The Role of Oxidative Stress Enhanced by Adiposity in Cardiometabolic Diseases

Świątkiewicz

Wróblewski

Nuszkiewicz

et al. 2023

IJMS

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Cardiometabolic diseases (CMDs), including cardiovascular disease (CVD), metabolic syndrome (MetS), and type 2 diabetes (T2D), are associated with increased morbidity and mortality. The growing prevalence of CVD is mostly attributed to the aging population and common occurrence of risk factors, such as high systolic blood pressure, elevated plasma glucose, and increased body mass index, which led to a global epidemic of obesity, MetS, and T2D. Oxidant–antioxidant balance disorders largely contribute to the pathogenesis and outcomes of CMDs, such as systemic essential hypertension, coronary artery disease, stroke, and MetS. Enhanced and disturbed generation of reactive oxygen species in excess adipose tissue during obesity may lead to increased oxidative stress. Understanding the interplay between adiposity, oxidative stress, and cardiometabolic risks can have translational impacts, leading to the identification of novel effective strategies for reducing the CMDs burden. The present review article is based on extant results from basic and clinical studies and specifically addresses the various aspects associated with oxidant–antioxidant balance disorders in the course of CMDs in subjects with excess adipose tissue accumulation. We aim at giving a comprehensive overview of existing knowledge, knowledge gaps, and future perspectives for further basic and clinical research. We provide insights into both the mechanisms and clinical implications of effects related to the interplay between adiposity and oxidative stress for treating and preventing CMDs. Future basic research and clinical trials are needed to further examine the mechanisms of adiposity-enhanced oxidative stress in CMDs and the efficacy of antioxidant therapies for reducing risk and improving outcome of patients with CMDs.

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“…Thus, it led to an extra effect on tissue invasion [38]. On the other hand, another pro-inflammatory cytokine is IL-8, which has numerous activities such as the migration of neutrophils, monocytes, tumor cell proliferation, and metastasis [32,39]. Additionally, it is known as an important cytokine involved in the angiogenesis process [40].…”

Section: Interplay Hgf/c-met With Cytokinesmentioning

confidence: 99%

Anti-cancer therapeutic strategies based on HGF/MET, EpCAM, and tumor-stromal cross talk

et al. 2022

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As an intelligent disease, tumors apply several pathways to evade the immune system. It can use alternative routes to bypass intracellular signaling pathways, such as nuclear factor-κB (NF-κB), Wnt, and mitogen-activated protein (MAP)/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR). Therefore, these mechanisms lead to therapeutic resistance in cancer. Also, these pathways play important roles in the proliferation, survival, migration, and invasion of cells. In most cancers, these signaling pathways are overactivated, caused by mutation, overexpression, etc. Since numerous molecules share these signaling pathways, the identification of key molecules is crucial to achieve favorable consequences in cancer therapy. One of the key molecules is the mesenchymal-epithelial transition factor (MET; c-Met) and its ligand hepatocyte growth factor (HGF). Another molecule is the epithelial cell adhesion molecule (EpCAM), which its binding is hemophilic. Although both of them are involved in many physiologic processes (especially in embryonic stages), in some cancers, they are overexpressed on epithelial cells. Since they share intracellular pathways, targeting them simultaneously may inhibit substitute pathways that tumor uses to evade the immune system and resistant to therapeutic agents.

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Characteristics of Selected Adipokines in Ascites and Blood of Ovarian Cancer Patients

Cited by 8 publications

References 77 publications

IL‐8 from CD248‐expressing cancer‐associated fibroblasts generates cisplatin resistance in non‐small cell lung cancer

IL‐8 from CD248‐expressing cancer‐associated fibroblasts generates cisplatin resistance in non‐small cell lung cancer

The Role of Oxidative Stress Enhanced by Adiposity in Cardiometabolic Diseases

Anti-cancer therapeutic strategies based on HGF/MET, EpCAM, and tumor-stromal cross talk

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