Identification of molecular biomarkers associated with non-small-cell lung carcinoma (NSCLC) using whole-exome sequencing

Singh, Varsha; Katiyar, Amit; Malik, Prabhat; Kumar, Sunil; Mohan, Anant; Singh, Harpreet; Jain, Deepali

doi:10.3233/cbm-220211

Cited by 2 publications

(1 citation statement)

References 71 publications

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“…Its interaction with the copper chaperone for superoxide dismutase, a protein facilitating copper transport into mitochondria for cellular respiration and antioxidant defense, underscores its multifaceted role [ 8 ]. FDX1 modulates the activity of copper chaperone for SOD-1 (CCS), influencing copper availability for mitochondrial functions [ 9 ]. In scenarios of copper overload, FDX1 facilitates the sequestration of copper away from mitochondria, averting its accumulation and diminishing ROS production [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Liu,

Wu,

et al. 2024

J Transl Med

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Background Lung adenocarcinoma (LUAD) is a highly lethal form of lung cancer. Despite advancements in treatments, managing LUAD is still challenging due to its aggressive behavior. Recent studies indicate that various molecular pathways, including the dysregulation of ferredoxin 1 (FDX1), play roles in LUAD progression. FDX1, a crucial protein in cellular redox reactions and energy metabolism, has been linked to several cancers. However, its exact role in the development of LUAD is not yet fully understood. Methods We investigated the role of ferredoxin 1 (FDX1) in LUAD progression through analysis of its expression in LUAD tissues and its impact on patient survival. Functional assays were performed to assess the effects of FDX1 overexpression on LUAD cell proliferation, migration, and invasion. A xenograft model was employed to evaluate the tumorigenesis potential of LUAD cells with FDX1 overexpression. Mechanistic insights into FDX1 regulation were gained through depletion experiments targeting the G protein-regulated inducer of neurite outgrowth 2 (GPRIN2)/PI3K signaling pathway. Results FDX1 expression was down-regulated in LUAD tissues, correlating with shorter patient survival. Overexpression of FDX1 suppressed LUAD cell proliferation, migration, and invasion in vitro, and inhibited tumorigenesis in vivo. Mechanistically, the GPRIN2/PI3K signaling pathway was implicated in FDX1 regulation, as depletion of GPRIN2 reversed the effects of FDX1 overexpression on cellular functions. Conclusions Our findings highlight FDX1 as a potential tumor suppressor in LUAD, acting through modulation of the GPRIN2/PI3K signaling pathway. These results suggest FDX1 as a promising therapeutic target for LUAD treatment, warranting further investigation into its clinical relevance.

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Section: Introductionmentioning

confidence: 99%

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Liu,

Wu,

et al. 2024

J Transl Med

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Disulfidptosis-related long non-coding RNAs predict prognosis and indicate therapeutic response in non-small cell lung carcinoma

Liu,

He,

Tan

et al. 2024

Oncologie

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Objectives Disulfidptosis is a novel form of cell death, whose modulation in tumor cells may present a promising therapeutic strategy for cancer treatment. However, the role of disulfidptosis-related long non-coding RNAs (lncRNAs) in non-small cell lung carcinoma (NSCLC) remains poorly elucidated. This study aims to investigate the prognostic significance of disulfidptosis-related lncRNAs (DRLs) and reveal their relationship to the immune microenvironment of NSCLC. Methods DRLs were identified through co-expression analysis of NSCLC transcriptomic data obtained from the Genomic Data Commons (GDC) data portal. The DRLs prognostic signature (DRLPS) was established using the least absolute shrinkage and selection operator (LASSO) and Cox regression analyses. Samples were separated into high-DS and low-DS groups based on the median disulfidptosis score (DS) of DRLPS. Integrated analyses were then implemented to unveil the association between DRLs and NSCLC microenvironment. These involved the evaluation of functional enrichments, immune cell infiltrations, genetic alterations, and drug sensitivity. Results A prognostic signature was developed based on six prognostic DRLs, which are AL606489.1, LINC00857, AP003555.1, AP000695.1, AC113346.1, and LINC01615. The Kaplan–Meier survival curves demonstrated the significant association between DRLPS and NSCLC prognosis. The functional enrichment assessment revealed the pivotal involvement of DRLs in immune regulation and metabolism in NSCLC. The low-DS and high-DS subgroups of NSCLC patients exhibited distinct differences in terms of immune infiltration and tumor mutation burden. The potential to predict immunotherapy benefit and drug sensitivity in NSCLC treatments was observed in DRLPS. Conclusions In this study, disulfidptosis-related lncRNAs were identified and their roles in NSCLC were revealed. A novel prognostic signature with the potential to predict drug response in NSCLC treatment was developed.

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Identification of molecular biomarkers associated with non-small-cell lung carcinoma (NSCLC) using whole-exome sequencing

Cited by 2 publications

References 71 publications

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway

Disulfidptosis-related long non-coding RNAs predict prognosis and indicate therapeutic response in non-small cell lung carcinoma

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