scholarly journals Modulating redox homeostasis and cellular reprogramming through inhibited methylenetetrahydrofolate dehydrogenase 2 enzymatic activities in lung cancer

Aging ◽  
2020 ◽  
Vol 12 (18) ◽  
pp. 17930-17947
Author(s):  
Chun-Hao Chan ◽  
Chia-Yu Wu ◽  
Navneet Kumar Dubey ◽  
Hong-Jian Wei ◽  
Jui-Hua Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Redox Homeostasis ◽  
Enzymatic Activities ◽  
Cellular Reprogramming ◽  
Methylenetetrahydrofolate Dehydrogenase

scholarly journals LKB1 and Tumor Metabolism: The Interplay of Immune and Angiogenic Microenvironment in Lung Cancer

2019 ◽  
Vol 20 (8) ◽  
pp. 1874 ◽  
Author(s):  
Laura Bonanno ◽  
Elisabetta Zulato ◽  
Alberto Pavan ◽  
Ilaria Attili ◽  
Giulia Pasello ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Redox Homeostasis ◽  
Suppressor Gene ◽  
Response To Treatment ◽  
Primary Resistance ◽  
Potential Applications ◽  
Liver Kinase B1 ◽  
Immunosuppressive Microenvironment ◽  
Tumor Types

Liver kinase B1 (LKB1) is a tumor suppressor gene whose inactivation is frequent in different tumor types, especially in lung adenocarcinoma (about 30% of cases). LKB1 has an essential role in the control of cellular redox homeostasis by regulating ROS production and detoxification. Loss of LKB1 makes the tumor cell more sensitive to oxidative stress and consequently to stress-inducing treatments, such as chemotherapy and radiotherapy. LKB1 loss triggers complex changes in tumor microenvironment, supporting a role in the regulation of angiogenesis and suggesting a potential role in the response to anti-angiogenic treatment. On the other hand, LKB1 deficiency can promote an immunosuppressive microenvironment and may be involved in primary resistance to anti-PD-1/anti-PD-L1, as it has been reported in lung cancer. The aim of this review is to discuss interactions of LKB1 with the tumor microenvironment and the potential applications of this knowledge in predicting response to treatment in lung cancer.

scholarly journals Glutamine Addiction and Therapeutic Strategies in Lung Cancer

2019 ◽  
Vol 20 (2) ◽  
pp. 252 ◽  
Author(s):  
Karolien Vanhove ◽  
Elien Derveaux ◽  
Geert-Jan Graulus ◽  
Liesbet Mesotten ◽  
Michiel Thomeer ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tricarboxylic Acid Cycle ◽  
Treatment Options ◽  
Redox Homeostasis ◽  
Glutamine Metabolism ◽  
Lung Cancer Cells ◽  
Production Networks ◽  
Tricarboxylic Acid Cycle Intermediates

Lung cancer cells are well-documented to rewire their metabolism and energy production networks to support rapid survival and proliferation. This metabolic reorganization has been recognized as a hallmark of cancer. The increased uptake of glucose and the increased activity of the glycolytic pathway have been extensively described. However, over the past years, increasing evidence has shown that lung cancer cells also require glutamine to fulfill their metabolic needs. As a nitrogen source, glutamine contributes directly (or indirectly upon conversion to glutamate) to many anabolic processes in cancer, such as the biosynthesis of amino acids, nucleobases, and hexosamines. It plays also an important role in the redox homeostasis, and last but not least, upon conversion to α-ketoglutarate, glutamine is an energy and anaplerotic carbon source that replenishes tricarboxylic acid cycle intermediates. The latter is generally indicated as glutaminolysis. In this review, we explore the role of glutamine metabolism in lung cancer. Because lung cancer is the leading cause of cancer death with limited curative treatment options, we focus on the potential therapeutic approaches targeting the glutamine metabolism in cancer.

scholarly journals Nestin regulates cellular redox homeostasis in lung cancer through the Keap1–Nrf2 feedback loop

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Jiancheng Wang ◽  
Qiying Lu ◽  
Jianye Cai ◽  
Yi Wang ◽  
Xiaofan Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Feedback Loop ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Cellular Redox ◽  
Anti Cancer ◽  
Oxidative Stress Status ◽  
Kelch Domain ◽  
Antioxidant Response Elements

Abstract Abnormal cancer antioxidant capacity is considered as a potential mechanism of tumor malignancy. Modulation of oxidative stress status is emerging as an anti-cancer treatment. Our previous studies have found that Nestin-knockdown cells were more sensitive to oxidative stress in non-small cell lung cancer (NSCLC). However, the molecular mechanism by which Nestin protects cells from oxidative damage remains unclear. Here, we identify a feedback loop between Nestin and Nrf2 maintaining the redox homeostasis. Mechanistically, the ESGE motif of Nestin interacts with the Kelch domain of Keap1 and competes with Nrf2 for Keap1 binding, leading to Nrf2 escaping from Keap1-mediated degradation, subsequently promoting antioxidant enzyme generation. Interestingly, we also map that the antioxidant response elements (AREs) in the Nestin promoter are responsible for its induction via Nrf2. Taken together, our results indicate that the Nestin–Keap1–Nrf2 axis regulates cellular redox homeostasis and confers oxidative stress resistance in NSCLC.

scholarly journals TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

2020 ◽  
Vol 11 (4) ◽  
pp. 1015-1025
Author(s):  
Chun‐cheng Hao ◽  
Jia‐ning Luo ◽  
Cui‐yang Xu ◽  
Xin‐yu Zhao ◽  
Zhen‐bin Zhong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ionizing Radiation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Redox Homeostasis ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals SPINK1 is a prognosis predicting factor of non‑small cell lung cancer and regulates redox homeostasis

2019 ◽  
Author(s):  
Maoqing Guo ◽  
Xuan Zhou ◽  
Xiao Han ◽  
Youwen Zhang ◽  
Luning Jiang
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Redox Homeostasis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Predicting Factor

EGCG maintained Nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cells

2019 ◽  
Vol 62 ◽  
pp. 103553 ◽  
Author(s):  
Suchisnigdha Datta ◽  
Dona Sinha
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Redox Homeostasis ◽  
Lung Cancer Cells

Proteomic Analysis of the Non-genetic Response to Cisplatin in Lung Cancer Cells

2021 ◽  
Vol 1 (3) ◽  
pp. 235-243
Author(s):  
CRISTINE DE SOUZA DUTRA ◽  
CAROLINA LUMERTZ MARTELLO ◽  
NATHAN ARAUJO CADORE ◽  
HENRIQUE BUNSELMEYER FERREIRA ◽  
ARNALDO ZAHA ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Redox Homeostasis ◽  
Genetic Resistance ◽  
Telomere Maintenance ◽  
Advanced Lung Cancer ◽  
Genetic Response ◽  
Drug Induced ◽  
Cytoskeletal Remodeling ◽  
Canonical Amino Acid ◽  
Genetic Mechanisms

Background: Drug resistance is the main cause of therapy failure in advanced lung cancer. Although non-genetic mechanisms play important roles in tumor chemoresistance, drug-induced epigenetic reprogramming is still poorly understood. Materials and Methods: The A549 cell line was used to generate cells with non-genetic resistance to cisplatin (CDDP), namely A549/CDDP cells. Bioorthogonal non-canonical amino acid tagging (BONCAT) and mass spectrometry were used to identify proteins modulated by CDDP in A549 and A549/CDDP cells. Results: Proteins related to proteostasis, telomere maintenance, cell adhesion, cytoskeletal remodeling, and cell redox homeostasis were found enriched in both cell lines upon CDDP exposure. On the other hand, proteins involved in drug response, metabolic pathways and mRNA processing and splicing were up-regulated by CDDP only in A549/CDDP cells. Conclusion: Our study revealed proteome dynamics involved in the non-genetic response to CDDP, pointing out potential targets to monitor and overcome epigenetic resistance in lung cancer.

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