scholarly journals Targeting HMGB1 in the Treatment of Non-Small Cell Lung Adenocarcinoma

Onco ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 25-37
Author(s):  
Brady Anderson ◽  
Mary Vue ◽  
Nya Gayluak ◽  
Sarah Jane Brown ◽  
Lynne T. Bemis ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Posttranslational Modification ◽  
Nuclear Protein ◽  
Small Cell ◽  
Small Cell Lung ◽  
Inflammatory Signaling ◽  
Molecular Pattern ◽  
Damage Repair ◽  
Disease Systemic Lupus Erythematosus ◽  
Molecular Group

Evidence of immunogenic cell death as a predictor of response to cancer therapy has increased interest in the high molecular group box 1 protein (HMGB1). HMGB1 is a nuclear protein associated with chromatin organization and DNA damage repair. HMGB1 is also a damage-associated molecular pattern (DAMP) protein and promotes proinflammatory signaling in a paracrine and autocrine manner. Extracellular HMGB1 can promote activation of NF-kB and is associated with several chronic inflammatory and autoimmune diseases, including sepsis, rheumatoid arthritis, atherosclerosis, chronic kidney disease, systemic lupus erythematosus (SLE), as well as cancer. In this review, we describe studies that demonstrate the use of deacetylase inhibitors and HMGB1 inhibitors to alter the expression and localization of HMGB1 in cancer cells, with a focus on lung cancer. The drugs described herein are well established and frequently used in human and small mammal studies. The main objective of this review is to summarize the potential benefit of targeting posttranslational modification of HMGB1 to decrease inflammatory signaling in the tumor microenvironment, and perhaps lead to improved response to current immunotherapeutic approaches.

scholarly journals Nab-paclitaxel-associated photosensitivity: report in a woman with non-small cell lung cancer and review of taxane-related photodermatoses

2015 ◽  
pp. 121-124
Author(s):  
Bryce D. Beutler ◽  
Philip R. Cohen
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Sun Exposure ◽  
Skin Lesions ◽  
Small Cell ◽  
Small Cell Lung ◽  
Oral Corticosteroids

Background: Taxanes [paclitaxel, nab-paclitaxel (Abraxane, Celgene Corp, USA), and docetaxel]—used in the treatment of lung, breast, and head and neck cancers—have been associated with cutaneous adverse effects, including photodermatoses. Purpose: We describe a woman with non-small cell lung cancer who developed a photodistributed dermatitis associated with her nab-paclitaxel therapy and review photodermatoses in patients receiving taxanes. Materials and methods: The features of a woman with a nab-paclitaxel-associated photodistributed dermatitis are presented and the literature on nab-paclitaxel-associated photosensitivity is reviewed. Results: Our patient developed nab-paclitaxel-associated photodistributed dermatitis on the sun-exposed surfaces of her upper extremities, which was exacerbated with each course of nab-paclitaxel. Biopsies revealed an interface dermatitis and laboratory studies were negative for lupus erythematosus and dermatomyositis. Her condition improved following topical corticosteroid cream application and strict avoidance of sunlight. Conclusion: Chemotherapy can be associated with adverse mucocutaneous events, including dermatoses on sun-exposed areas of the skin. Paclitaxel and nab-paclitaxel have both been associated with photodermatoses, including dermatitis, erythema multiforme, onycholysis, and subacute cutaneous lupus erythematosus. Strict avoidance of sun exposure, topical or oral corticosteroids, and/or discontinuation of the drug results in improvement with progressive resolution of symptoms and skin lesions. Development of photodermatoses is not an absolute contraindication to continuing chemotherapy, provided that the cutaneous condition resolves with dermatosis-directed treatment and the patient avoids sun exposure.

MMP10 involved in Radiosensitivity in Non-Small Cell Lung Cancer via DNA damage repair pathway

2020 ◽  
Author(s):  
Xiao Lei ◽  
Yuanyuan Chen ◽  
Na Ma ◽  
Pei Zhang ◽  
Yanan Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Small Cell Lung Cancer ◽  
Clonogenic Assay ◽  
Dna Damage Repair ◽  
Small Cell ◽  
Repair Pathway ◽  
Small Cell Lung ◽  
Damage Repair ◽  
Apoptosis Assay

Abstract Background Non-small cell lung cancer (NSCLC) is an aggressive subtype of lung cancer with high mortality and morbidity. Our purpose in this study is to investigate the effect of MMP10 in NSCLC during radiotherapy and its mechanism. Materials and methods We analyzed MMP10 expression and overall survival rate of patients via UALCAN analysis. Western blot analysis was used to test the protein expression. We applied clonogenic assay and apoptosis assay to detect radioresistance in vitro. The level of DNA damage and the DNA damage repair were disclosed via comet assay and γH2AX foci assay. Results Our results showed that high MMP10 expression in Lung Adenocarcinoma specimens is associated with poor outcomes of patients. Knockdown MMP10 induced radiosensitization in A549 cells via clonogenic assay and apoptosis assay. Furthermore, we found MMP10 siRNA enhanced DNA damage of NSCLC cells and MMP10 involved in DNA damage repair after IR. Conclusion Our data highlighted that MMP10 plays a crucial role in NSCLC after radiation via DNA damage repair pathway, and the regulating effect of MMP10 on radiosensitivity in NSCLC might confer to therapeutic implications to NSCLC radiotherapy.

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