IκB kinase ɛ (IKKɛ): A therapeutic target in inflammation and cancer

Verhelst, Kelly; Verstrepen, Lynn; Carpentier, Isabelle; Beyaert, Rudi

doi:10.1016/j.bcp.2013.01.007

Cited by 95 publications

(66 citation statements)

References 91 publications

(129 reference statements)

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“…The mutual interplay between NF-κB and proinflammatory cytokines such as TNFα and IL1β might stimulate cancer cell proliferation during chronic inflammation [70]. Inhibition of NF-κB with IKK inhibitors, siRNA, or IkappaB super suppressor downregulated lung cancer cell survival and proliferation [70,71].…”

Section: Roles Of Inflammation In Bio-behaviors Of Lung Cancer Cellsmentioning

confidence: 99%

“…Inhibition of NF-κB with IKK inhibitors, siRNA, or IkappaB super suppressor downregulated lung cancer cell survival and proliferation [70,71]. IL6 is considered as a key growth-promoting and anti-apoptotic factor to promote cell proliferation in primary squamous cell carcinomas, adenocarcinomas, or tumor cell lines [72].…”

Section: Roles Of Inflammation In Bio-behaviors Of Lung Cancer Cellsmentioning

confidence: 99%

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Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Shi

Wang

Hou

et al. 2015

Cancer Metastasis Rev

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Inflammatory cells and mediators are essential components in tumor microenvironment and play decisive roles in the initiation, proliferation, survival, promotion, invasion, or metastasis of lung cancer. Clinical and epidemiologic studies suggested a strong association between inflammation and lung cancer and an influence of immune surveillances and tumor responses to chemotherapeutic drugs, although roles of inflammation in lung cancer remain unclear. The present review outlined roles of inflammation in lung cancer, with particular focus on inflammatory components, types, biomarkers, or principal mechanisms by which the inflammation contributes to the development of lung cancer. The cancer-associated inflammatory cells (CICs) should be furthermore defined and include cancer-specific and interacted cells with inflammatory or inflammation-like characteristics, e.g., innate or adaptive immune cells and cancer tissue cells. We also discuss targeting potentials of inflammation in the prevention and treatment of lung cancer. The diversity of cancer-related inflammatory microenvironment is instrumental to design novel therapeutic approaches for lung cancer.

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Section: Roles Of Inflammation In Bio-behaviors Of Lung Cancer Cellsmentioning

confidence: 99%

Section: Roles Of Inflammation In Bio-behaviors Of Lung Cancer Cellsmentioning

confidence: 99%

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Shi

Wang

Hou

et al. 2015

Cancer Metastasis Rev

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“…Activation of this transcription factor is a very important step in the development of DN [26]; therefore, the pharmacological modulation of this process is the main objective in the design of new therapies for DN. In this work, we analyzed the effects of the natural compound parthenolide, which is an NF-κB inhibitor, and found that it reduces IκB degradation, preventing NF-κB activation and subsequent MCP-1 mRNA and protein expression.…”

Section: Discussionmentioning

confidence: 99%

AOPPs Induce MCP-1 Expression by Increasing ROS-Mediated Activation of the NF-κB Pathway in Rat Mesangial Cells: Inhibition by Sesquiterpene Lactones

Wang

Zhao

Chen

et al. 2013

Cell Physiol Biochem

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Background: Monocyte chemoattractant protein-1 (MCP-1) plays an important role in extracellular matrix accumulation through macrophage recruitment and activation in the development and progression of diabetic nephropathy. Therefore, this study examined whether advanced oxidation protein products (AOPPs) are involved in nuclear factor-κB (NF-κB) activation and MCP-1 mRNA and protein expression in mesangial cells (MCs) and evaluated the effects of derivatives of sesquiterpene lactones (SLs) on AOPP-induced renal damage. Methods: MCP-1 mRNA and protein expression in MCs were determined by quantitative real-time PCR and ELISA, respectively. The level of intracellular reactive oxygen species (ROS) was determined by flow cytometry. The protein expression of tubulin, P47, NF-κB p65, phospho-NF-κB p65, IκB, phospho-IκB, IKKß and phospho-IKKß was evaluated by Western blot. Results: AOPPs caused oxidative stress in MCs and activated the NF-κB pathway by inducing IκBa phosphorylation and degradation. Inhibition of ROS by SOD (ROS inhibitor) blocked the AOPP-mediated NF-κB pathway. Moreover, the inhibition of AOPP-induced overproduction of MCP-1 mRNA and protein was associated with inhibition of IκBa degradation by SLs. Conclusion: AOPPs induce MCP-1 expression by activating the ROS/NF-κB pathway and can be inhibited by SLs. These findings may provide a novel approach to treat inflammatory and immune renal diseases, including diabetic nephropathy.

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“…Despite extensive basic and clinical research over the past 40 years, little progress has been made in treating SCLC [64]. The innate immune system forms our first line of defense against invading pathogens and relies for a major part on the activation of two transcription factors, NF-κB and interferon regulatory factor 3 (IRF3) [65]. NF-κB-dependent cell survival genes play an important antiapoptotic role [66].…”

Section: Smoking and Copdmentioning

confidence: 99%

Smoking, inflammation and small cell lung cancer: recent developments

Hamilton

Rath

2015

Wien Med Wochenschr

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Small cell lung cancer (SCLC) accounts for 15 % of all lung tumors and represents an invasive neuroendocrine malignancy with poor survival rates. This cancer is highly prevalent in smokers and characterized by inactivation of p53 and retinoblastoma. First in vitro expansion of circulating tumor cells (CTCs) of SCLC patients allowed for investigation of the cell biology of tumor dissemination. In the suggested CTC SCLC model, the primary tumor attracts and educates tumor-promoting and immunosuppressive macrophages which in turn arm CTCs to spread and generate distal lesions. Preexisting inflammatory processes associated with chronic obstructive pulmonary disease (COPD) seem to potentiate the subsequent activity of tumor-associated macrophages (TAM). Activation of signal transducer and activator of transcription 3 (STAT3) and expression of chitinase-3-like 1/YKL-40 in SCLC CTCs seems to be associated with drug resistance. In conclusion, inflammation-associated generation of invasive and chemoresistant CTCs most likely explains the characteristic features of SCLC, namely early dissemination and rapid failure of chemotherapy.

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IκB kinase ɛ (IKKɛ): A therapeutic target in inflammation and cancer

Cited by 95 publications

References 91 publications

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

AOPPs Induce MCP-1 Expression by Increasing ROS-Mediated Activation of the NF-κB Pathway in Rat Mesangial Cells: Inhibition by Sesquiterpene Lactones

Smoking, inflammation and small cell lung cancer: recent developments

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IκB kinase ɛ (IKKɛ): A therapeutic target in inflammation and cancer

Cited by 95 publications

References 91 publications

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

AOPPs Induce MCP-1 Expression by Increasing ROS-Mediated Activation of the NF-&#954;B Pathway in Rat Mesangial Cells: Inhibition by Sesquiterpene Lactones

Smoking, inflammation and small cell lung cancer: recent developments

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AOPPs Induce MCP-1 Expression by Increasing ROS-Mediated Activation of the NF-κB Pathway in Rat Mesangial Cells: Inhibition by Sesquiterpene Lactones