TRAF6 Promoted Tumor Glycolysis in Non‐Small‐Cell Lung Cancer by Activating the Akt‐HIF<i>α</i> Pathway

Ling, Feng; Feng, Shuitu; Nie, Zhihua; Deng, Yan; Xuan, Yingmei; Chen, Xiaoping; Lu, Yaqun; Liang, Liuqin; Yide, Chen

doi:10.1155/2021/3431245

Cited by 11 publications

(6 citation statements)

References 45 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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“…TRAF6 exhibits high expression levels in breast cancer, particularly in cases with bone and brain metastases, and its expression is inversely correlated with breast cancer prognosis. Strategies aimed at reducing TRAF6 expression have been shown to inhibit the proliferation and metastasis of breast cancer cells [ 33 ]. These findings collectively underscore the intimate link between TRAF family genes and tumor development.…”

Section: Discussionmentioning

confidence: 99%

Pan-cancer analysis of the TRAF family genes and their correlation with prognosis, TME, immune and drug sensitivity

Yao,

Hu,

Chen

et al. 2024

Eur J Med Res

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Background Tumor necrosis factor receptor-associated factors family genes play a pivotal role in tumorigenesis and metastasis, functioning as adapters or E3 ubiquitin ligases across various signaling pathways. To date, limited research has explored the association between tumor necrosis factor receptor-associated factors family genes and the clinicopathological characteristics of tumors, immunity, and the tumor microenvironment (TME). This comprehensive study investigates the relationship between tumor necrosis factor receptor-associated factors family and prognosis, TME, immune response, and drug sensitivity in a pan-cancer context. Methods Utilizing current public databases, this study examines the expression levels and prognostic significance of tumor necrosis factor receptor-associated factors family genes in a pan-cancer context through bioinformatic analysis. In addition, it investigates the correlation between tumor necrosis factor receptor-associated factors expression and various factors, including the TME, immune subtypes, stemness scores, and drug sensitivity in pan-cancer. Results Elevated expression levels of tumor necrosis factor receptor-associated factor 2, 3, 4, and 7 were observed across various cancer types. Patients exhibiting high expression of these genes generally faced a worse prognosis. Furthermore, a significant correlation was noted between the expression of tumor necrosis factor receptor-associated factors family genes and multiple dimensions of the TME, immune subtypes, and drug sensitivity.

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“…Pathway enrichment analysis shows that these genes may be involved in various signaling pathways, such as PI3K-Akt signaling pathway, IL-17 signaling pathway, and endocrine resistance. AKT1 is an important signal pathway factor, which participates in all stages of lung cancer occurrence and development [ 29 ]; IL-17 can promote angiogenesis through the VEGF pathway, which may indirectly increase the production of NO in the lungs of NSCLC patients and promote the invasion and metastasis of lung cancer [ 30 ]. Therefore, these signaling pathways execute different functions in the occurrence and development of lung cancer, while Fisetin may play an intervention role by regulating these signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Exploration of Potential Targets and Mechanisms of Fisetin in the Treatment of Non-Small-Cell Lung Carcinoma via Network Pharmacology and In Vitro Validation

Ling

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Purpose. The morbidity and fatality rates of non-small-cell lung cancer (NSCLC) were high, although a combination of multiple treatments was used. Fisetin, a small flavonoid compound, had shown anticancer activities. Thus, we aimed at exploring the mechanisms of Fisetin in the treatment of NSCLC. Methods. TCMSP and Swiss target tools were used to screen the targets of Fisetin, and GeneCards was used to collect the genes related to NSCLC. The genes common to Fisetin and NSCLC were obtained by Venn analysis, whose possible functions were further annotated. A “Compound-Target-Disease” network was then constructed and hub genes were filtered. Also, molecular docking was performed to predict the binding abilities between Fisetin and the hub genes. Then, the effects of Fisetin on the expression of hub genes in lung adenocarcinoma cells were preliminarily evaluated in vitro. Results. A total of 131 genes common to Fisetin and NSCLC were filtered out, which might be enriched in several biological processes including antioxidation, cell proliferation, and various signaling pathways, such as PI3K-Akt and IL-17 signaling pathways. Among them, PIK3R1, CTNNB1, JUN, EGFR, and APP might be the hub genes. Molecular docking indicated the close bond between Fisetin and them. Experiments implied a possible effect of Fisetin on the expression of hub genes in A549 cells. Conclusion. The present study found a series of novel targets and pathways for Fisetin treating NSCLC. Multiple angles, targets, and pathways were involved in the biological processes, which need to be verified in further experiments.

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TRAF6 Promoted Tumor Glycolysis in Non‐Small‐Cell Lung Cancer by Activating the Akt‐HIFα Pathway

Cited by 11 publications

References 45 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

Pan-cancer analysis of the TRAF family genes and their correlation with prognosis, TME, immune and drug sensitivity

Exploration of Potential Targets and Mechanisms of Fisetin in the Treatment of Non-Small-Cell Lung Carcinoma via Network Pharmacology and In Vitro Validation

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