miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

Tian, Wenxian; Yuan, Xia; Song, Yong-ping; Jian-xia, Zhai; Wei, Haixia; Wang, Linna; Li, Dan; Chen, Qiusheng

doi:10.3892/etm.2020.9538

Cited by 6 publications

(3 citation statements)

References 40 publications

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“…The up-regulation of glycolysis levels has been observed in many cancers, including primary and metastatic cancers, and aerobic glycolysis is the most commonly used and preferred mechanism of glucose metabolism in cancer cells [ 54 ]. Previous studies [ 55 , 56 , 57 , 58 , 59 , 60 , 61 ] showed that signaling pathways such as Akt, Myc, ERK, and NF-κB play an important regulatory role during glycolysis. In NSCLC, high levels of glucose transporter 1 (GLUT1) and hexokinase 2 (HK2) promoted glucose uptake by lung cancer cells, which was the initial step of glucose metabolism [ 62 , 63 ].…”

Section: Resultsmentioning

confidence: 99%

miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer

Wei

Chai

et al. 2022

IJMS

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Lung cancer is the leading cause of cancer death worldwide. miR-199a, which has two mature molecules: miR-199a-3p and miR-199a-5p, plays an important biological role in the genesis and development of tumors. We collected recent research results on lung cancer and miR-199a from Google Scholar and PubMed databases. The biological functions of miR-199a in lung cancer are reviewed in detail, and its potential roles in lung cancer diagnosis and treatment are discussed. With miR-199a as the core point and a divergence outward, the interplay between miR-199a and other ncRNAs is reviewed, and a regulatory network covering various cancers is depicted, which can help us to better understand the mechanism of cancer occurrence and provide a means for developing novel therapeutic strategies. In addition, the current methods of diagnosis and treatment of lung cancer are reviewed. Finally, a conclusion was drawn: miR-199a inhibits the development of lung cancer, especially by inhibiting the proliferation, infiltration, and migration of lung cancer cells, inhibiting tumor angiogenesis, increasing the apoptosis of lung cancer cells, and affecting the drug resistance of lung cancer cells. This review aims to provide new insights into lung cancer therapy and prevention.

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Section: Resultsmentioning

confidence: 99%

miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer

Wei

Chai

et al. 2022

IJMS

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“…The authors also found that miR-218, which is elevated in DKD, negatively regulates DACH1 (15). Since miR-218 inhibits glucose uptake in cancer (16), it would be interesting to investigate the direct or indirect effects of DACH1 on glucose uptake in renal cells, for example, by regulating SGLT2. Doke et al identified DACH1 as a potential candidate gene in a genetic a positive correlation of DACH1 expression with kidney function and a negative correlation with kidney fibrosis, inflammation, and cell proliferation (13).…”

Section: Dach1 and Renal Tubular Injurymentioning

confidence: 98%

DACH1 as a multifaceted and potentially druggable susceptibility factor for kidney disease

Merscher

Faul

2021

Journal of Clinical Investigation

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Getting a grip on kidney diseaseDiabetes, high blood pressure, and a family history of kidney disease are major risk factors contributing to the high prevalence of kidney disease. While the genetic origins of kidney diseases have been extensively studied in the past, research in recent years has shifted toward a better understanding of the epigenetic components that make the kidney more vulnerable to consecutive insults.

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“…Moreover, autophagy inhibitors protect recombinant human arginase (rhArg)-treated NSCLC cells, and thus, rhArg-induced autophagy and apoptosis is anti NSCLC progression [ 172 ]. Through influencing arginine synthesis, Aconiti Radix Cocta (ARC) is suggested to be an anti-tumor by regulating the energy metabolism that influence arginine synthesis [ 173 ].…”

Section: Blocking Common Nsclc Metabolic Pathways As Anti-nsclcmentioning

confidence: 99%

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Bajinka,

Ouedraogo,

Golubnitschaja

et al. 2024

EPMA Journal

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Energy metabolism is a hub of governing all processes at cellular and organismal levels such as, on one hand, reparable vs. irreparable cell damage, cell fate (proliferation, survival, apoptosis, malignant transformation etc.), and, on the other hand, carcinogenesis, tumor development, progression and metastazing versus anti-cancer protection and cure. The orchestrator is the mitochondria who produce, store and invest energy, conduct intracellular and systemically relevant signals decisive for internal and environmental stress adaptation, and coordinate corresponding processes at cellular and organismal levels. Consequently, the quality of mitochondrial health and homeostasis is a reliable target for health risk assessment at the stage of reversible damage to the health followed by cost-effective personalized protection against health-to-disease transition as well as for targeted protection against the disease progression (secondary care of cancer patients against growing primary tumors and metastatic disease).The energy reprogramming of non-small cell lung cancer (NSCLC) attracts particular attention as clinically relevant and instrumental for the paradigm change from reactive medical services to predictive, preventive and personalized medicine (3PM). This article provides a detailed overview towards mechanisms and biological pathways involving metabolic reprogramming (MR) with respect to inhibiting the synthesis of biomolecules and blocking common NSCLC metabolic pathways as anti-NSCLC therapeutic strategies. For instance, mitophagy recycles macromolecules to yield mitochondrial substrates for energy homeostasis and nucleotide synthesis. Histone modification and DNA methylation can predict the onset of diseases, and plasma C7 analysis is an efficient medical service potentially resulting in an optimized healthcare economy in corresponding areas. The MEMP scoring provides the guidance for immunotherapy, prognostic assessment, and anti-cancer drug development. Metabolite sensing mechanisms of nutrients and their derivatives are potential MR-related therapy in NSCLC. Moreover, miR-495-3p reprogramming of sphingolipid rheostat by targeting Sphk1, 22/FOXM1 axis regulation, and A2 receptor antagonist are highly promising therapy strategies. TFEB as a biomarker in predicting immune checkpoint blockade and redox-related lncRNA prognostic signature (redox-LPS) are considered reliable predictive approaches.Finally, exemplified in this article metabolic phenotyping is instrumental for innovative population screening, health risk assessment, predictive multi-level diagnostics, targeted prevention, and treatment algorithms tailored to personalized patient profiles—all are essential pillars in the paradigm change from reactive medical services to 3PM approach in overall management of lung cancers. This article highlights the 3PM relevant innovation focused on energy metabolism as the hub to advance NSCLC management benefiting vulnerable subpopulations, affected patients, and healthcare at large.

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miR‑218 inhibits glucose metabolism in non‑small cell lung cancer via the NF‑κB signaling pathway

Cited by 6 publications

References 40 publications

miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer

miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer

DACH1 as a multifaceted and potentially druggable susceptibility factor for kidney disease

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

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