ROS1-rearranged Non–small Cell Lung Cancer

Giustini, Nicholas P.; Bazhenova, Lyudmila

doi:10.1016/j.thorsurg.2020.01.007

Cited by 5 publications

(1 citation statement)

References 53 publications

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“…As a result, this route is a promising target for new antitumor treatments. 7,8 According to new data, in NSCLC, the PI3K/ AKT/mTOR signaling is often active and serves a critical involvement in carcinogenesis by increasing cell viability, development, multiplication, and motility. Treatment affecting this pathway is tested in clinical settings and has shown some effectiveness.…”

Section: Introductionmentioning

confidence: 99%

PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer

Alharbi

Samuel

Thangavelu

et al. 2022

J Environ Pathol Toxicol Oncol

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Lung cancer is the leading cause of cancer-related mortality across the globe. The most prevalent pathological form of lung cancer is non-small-cell lung cancer (NSCLC). Elevated stimulation of the PI3K/Akt/mTOR pathway causes a slew of cancer-related symptoms, making it a promising target for new anticancer drugs. The PI3K/Akt/mTOR path is involved extensively in carcinogenesis and disease advancement in NSCLC. Several new inhibitors targeting this pathway have been discovered in preclinical investigations and clinical trials. The etiology and epidemiology of NSCLC and biology of the PI3K/Akt/mTOR cascade and its role in NSCLC pathogenesis have all been discussed in this article. In this article, we've reviewed PI3K/Akt/mTOR cascade inhibitors that have been proven in vitro and in preclinical trials to be effective in NSCLC. Drugs targeting the PI3K/Akt/mTOR path in the treatment of NSCLC were also addressed. A better knowledge of the underlying molecular biology, including epigenetic changes, is also critical to detecting relevant biomarkers and guiding combination methods. Additionally, improved clinical trial designs will increase the capacity to test novel drugs and combinations for accounting for genomic variation and eventually improve patient outcomes.

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Section: Introductionmentioning

confidence: 99%

PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer

Alharbi

Samuel

Thangavelu

et al. 2022

J Environ Pathol Toxicol Oncol

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Prognostic Value of Immunotyping Combined with Targeted Therapy in Patients with Non-Small-Cell Lung Cancer and Establishment of Nomogram Model

Tian

Guo

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. Bioinformatics methods were used to analyze non-small-cell lung cancer gene chip data, screen differentially expressed genes (DEGs), explore biomarkers related to NSCLC prognosis, provide new targets for the treatment of NSCLC, and build immunotyping and line-map model. Methods. NSCLC-related gene chip data were downloaded from the GEO database, and the common DEGs of the two datasets were screened by using the GEO2R tool and FunRich 3.1.3 software. DAVID database was used for GO analysis and KEGG analysis of DEGs, and protein-protein interaction (PPI) network was constructed by STRING database and Cytoscape 3.8.0 software, and the top 20 hub genes were analyzed and screened out. The expression of pivot genes and their relationship with prognosis were verified by multiple external databases. Results. 159 common DEGs were screened from the two datasets. PPI network was constructed and analyzed, and the genes with the top 20 connectivity were selected as the pivotal genes of this study. The results of survival analysis and the patients’ survival curve was reflected in the line graph model of NSCLC. Conclusion. Through the screening and identification of the VIM-AS1 gene, as well as the analysis of immune infiltration and immune typing, the successful establishment of the rosette model has a certain guiding value for the molecular targeted therapy of patients with non-small-cell lung cancer.

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Homeobox D9 Promotes Malignant Progression of Non-Small Cell Lung Cancer Through Negatively Regulating Kallikrein Related Peptidase 9

Hao,

Shen,

2023

j biomed nanotechnol

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We investigated the association between HOXD9 expression and prognosis in non-small cell lung cancer (NSCLC) and explored its underlying mechanisms in tumor progression. HOXD9 expression was examined in 42 pairs of NSCLC tissue samples using qRT-PCR, and its effects were evaluated in NSCLC cell lines through lentiviral vector transfection, assessing cell growth and migration using CCK-8 and Transwell assays. Bioinformatics analysis identified KLK9 as a target gene of HOXD9, and their interaction was investigated in vitro and in vivo. HOXD9 mRNA expression was significantly higher in NSCLC tissues compared to adjacent tissues, positively correlating with metastasis incidence and poor prognosis. HOXD9 knockdown reduced NSCLC cell migration and proliferation, while overexpression had the opposite effect. Luciferase assays confirmed HOXD9′s binding to KLK9, leading to negative regulation of KLK9 expression. Knockdown of KLK9 reversed the inhibitory effect of HOXD9 on NSCLC cell migration and proliferation, while co-overexpression of KLK9 and HOXD9 had the opposite effect. Our findings demonstrate the close association of high HOXD9 expression in NSCLC tissues with metastasis incidence and poor prognosis. HOXD9 likely exerts its biological function in NSCLC by negatively regulating KLK9. These results provide valuable insights into the molecular mechanisms driving NSCLC progression, highlighting HOXD9 as a potential prognostic biomarker and therapeutic target.

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ROS1-rearranged Non–small Cell Lung Cancer

Cited by 5 publications

References 53 publications

PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer

PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer

Prognostic Value of Immunotyping Combined with Targeted Therapy in Patients with Non-Small-Cell Lung Cancer and Establishment of Nomogram Model

Homeobox D9 Promotes Malignant Progression of Non-Small Cell Lung Cancer Through Negatively Regulating Kallikrein Related Peptidase 9

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