Non-small cell lung cancer

Skřičková, Jana; Kadlec, Bohdan; Venclíček, Ondřej

doi:10.36290/vnl.2017.159

Cited by 15 publications

(9 citation statements)

References 28 publications

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“…Non-small cell lung cancer (NSCLC) is a typical type of lung cancer. 1,2 NSCLC can be further subdivided into adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, depending on the histological differences among the NSCLC subtypes. [3][4][5] The main risk for NSCLC is smoking.…”

Section: Backg Rou N Dmentioning

confidence: 99%

Circular RNA hsa_circ_0018189 drives non‐small cell lung cancer growth by sequestering miR‐656‐3p and enhancing xCT expression

Cai

Zheng

Dong

et al. 2022

Clinical Laboratory Analysis

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Background Non‐small cell lung cancer (NSCLC) is one of the cancers with a high mortality rate. CircRNAs have emerged as an important regulatory factor in tumorigenesis in recent years. However, the detailed regulatory mechanism of a circular RNA cullin 2 (hsa_circ_0018189; hsa_circ_0018189) is still unclear in NSCLC. Methods RNA levels of hsa_circ_0018189, microRNA (miR)‐656–3p, and Solute carrier family seven member 11 (SLC7A11, xCT) were analyzed by real‐time quantitative reverse transcription‐polymerase chain reaction (RT‐qPCR), and protein level was assessed by Western blot and immunohistochemical assay. Enzyme‐linked immunosorbent assay was conducted to detect cell glutamine metabolism. Effects of hsa_circ_0018189 on cell proliferation, apoptosis, migration, and invasion were analyzed by corresponding assays. Luciferase reporter assay and RNA‐immunoprecipitation assay confirmed the target relationship between miR‐656‐3p and hsa_circ_0018189 or xCT. The in vivo function of hsa_circ_0018189 was verified by xenograft mouse models. Results Hsa_circ_0018189 abundance was overexpressed in NSCLC cells and samples. Deficiency of hsa_circ_0018189 lowered NSCLC cell proliferative, migrating, invading, and glutamine metabolism capacities, and hsa_circ_0018189 silencing inhibited the growth of tumors in vivo. Hsa_circ_0018189 could up‐regulate xCT by sponging miR‐656‐3p. And miR‐656‐3p downregulation or xCT overexpression partly overturned hsa_circ_0018189 knockdown or miR‐656‐3p mimic‐mediated repression of NSCLC cell malignancy. Conclusion Hsa_circ_0018189 drove NSCLC growth by interacting with miR‐656‐3p and upregulating xCT.

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Section: Backg Rou N Dmentioning

confidence: 99%

Circular RNA hsa_circ_0018189 drives non‐small cell lung cancer growth by sequestering miR‐656‐3p and enhancing xCT expression

Cai

Zheng

Dong

et al. 2022

Clinical Laboratory Analysis

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“…[ 1 ] Among them, non-small cell lung cancer accounts for approximately 80% to 85% of the cases, [ 2 ] and adenocarcinoma is the main subtype. [ 3 ] Chemotherapy, radiotherapy, targeted treatment, and immunotherapy are therapeutic options used to manage non-small cell lung cancer. Although they are clinically beneficial, they cause many serious adverse reactions, and are often not tolerated by patients, leading to treatment interruption, which can seriously affect the treatment and prognosis.…”

Section: Introductionmentioning

confidence: 99%

Determining the mechanism of action of the Qishan formula against lung adenocarcinoma by integration of network pharmacology, molecular docking, and proteomics

et al. 2023

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Background: Lung adenocarcinoma (LUAD) is the main pathological type of lung cancer. Qishan formula (QSF) is reportedly efficacious against LUAD. However, its mechanisms of action currently remain elusive. Therefore, network pharmacology, molecular docking techniques and proteomics were used to verify the potential pharmacological effects of QSF in the treatment of LUAD. Methods: The active ingredients and potential targets of QSF were obtained from the TCMSP, chemical source network and construct a drug-component-target networks using Cytoscape v3.7.2. Data for disease targets were obtained from 5 databases: TCGA, OMIM, DrugBank, DisGeNET, and GeneCards. Drug disease cross targets were used to construct protein-protein interaction networks for selecting the core targets using the STRING database and enrichment pathway networks using the DAVID database. Finally, TMT quantitative proteomics was used to identify the possible core targets and action pathways. Molecular docking to verify the affinity between components and targets. Results: Network pharmacology identified core components of QSF against LUAD included baicalein, methylophiopogonone B, quercetin, kaempferol, isorhamnetin, and luteolin, which can act on 10 key targets ( SRC, TP53, PIK3R1, MAPK3, STAT3, MAKP1, HSP90AA1, PIK3CA, HRAS , and AKT1 ). QSF might play a therapeutic role in LUAD by regulating biological processes such as signal transduction, protein phosphorylation, cell proliferation, and apoptosis, as well as the PI3K/AKT, MAPK, FoxO, and other signaling pathways. Proteomics identified 207 differentially expressed proteins, and by integrating with network pharmacology and molecular docking results we found that 6 core components of QSF may target TP53 against LUAD through the PI3K/AKT signaling pathway. Conclusion: QSF is a multitarget recipe potentially exerting pleiotropic effects in LUAD.

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“…Abundant genomic alterations in epidermal growth factor receptor (EGFR) have been revealed, including point mutations, deletions, and insertions within exon 18-21 of the EGFR gene [3][4][5]. The mutational constitutive activation of the kinase domain of EGFR is linked to non-small cell lung cancer (NSCLC), [6][7][8] accounting for 80% of lung cancer [9]. About 85% of observed EGFR mutations are common mutations occurring frequently in NSCLC patients, while the remaining 15% cover various rare mutations [3,10].…”

Section: Introductionmentioning

confidence: 99%

Uncovering the Molecular Basis for the Better Gefitinib Sensitivity of EGFR with Complex Mutations over Single Rare Mutation: Insights from Molecular Simulations

Xie

et al. 2022

Molecules

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Epidermal growth factor receptor (EGFR) is an intensively focused target for anti-tumor compounds used in non-small cell lung cancer (NSCLC) therapy. Compared to the classical activating mutations, there are still many uncommon EGFR mutations associated with poorer responses to EGFR inhibitors. A detailed understanding of the molecular basis for multiple EGFR mutants exhibiting diverse responses to inhibitors is of critical importance for related drug development. Herein, we explored the molecular determinants contributing to the distinct responses of EGFR with a single rare mutation (G719S) or combined mutations (G719S/L858R and G719S/l861Q) to Gefitinib (IRE). Our results indicated that interactions, formed within the tetrad of residues S768 (in the αC-helix), D770 (in the αC-β4 loop), Y827 (in the αE-helix), and R831 (in the catalytic loop), play an important role in the stability of αC-helix and the maintenance of K745–E762 salt bridge in the absence of IRE, which are weakened in the EGFRG719S system and enhanced in the EGFRG719S/L858R system upon IRE binding. Besides, the introduced hydrogen bonds by the co-occurring mutation partner also contribute to the stability of αC-helix. The work done for inhibitor dissociation suggests that IRE exhibits a stronger binding affinity to EGFRG719S/L858R mutant. Together, these findings provide a deeper understanding of minor mutations, which is essential for drug development targeting EGFR with less common mutations.

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Non-small cell lung cancer

Cited by 15 publications

References 28 publications

Circular RNA hsa_circ_0018189 drives non‐small cell lung cancer growth by sequestering miR‐656‐3p and enhancing xCT expression

Circular RNA hsa_circ_0018189 drives non‐small cell lung cancer growth by sequestering miR‐656‐3p and enhancing xCT expression

Determining the mechanism of action of the Qishan formula against lung adenocarcinoma by integration of network pharmacology, molecular docking, and proteomics

Uncovering the Molecular Basis for the Better Gefitinib Sensitivity of EGFR with Complex Mutations over Single Rare Mutation: Insights from Molecular Simulations

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