Author of

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  P36 - Pathology - Prognosis (ID 106)

  • Event: WCLC 2020
  • Type: Posters
  • Track: Pathology, Molecular Pathology and Diagnostic Biomarkers
  • Presentations: 1
  • Moderators:
  • Coordinates: 1/28/2021, 00:00 - 00:00, ePoster Hall

  • 34763

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    P36.02 - CHEK1: Unfavourable Prognostic Hub Gene and Potential Therapeutic Target for Lung Adenocarcinoma (ID 2942)

    00:00 - 00:00  |  Presenting Author(s): 谭 Tan
    • Abstract
    • Slides

    Introduction
    

    Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer, while the molecular mechanism remains unclear. This study aimed to identify hub genes and explore the function for a deeper insight into LUAD.

    Methods
    

    Three GEO datasets were screened using GEO2R to find upregulated differentially expressed genes in LUAD. Gene ontology and KEGG pathway were analysed by WebGestalt. Then, STRING and Cytoscape were used to construct protein-protein interaction network and select hub genes followed by hub genes validation with GEPIA2, Oncomine, and HPA. CHEK1 expression in various cancers including in LUAD was investigated using Oncomine, GEPIA2, TIMER2.0, one GEO dataset, and UALCAN web. After that, CHEK1 promotor methylation was analysed with UALCAN and cBioPortal. Mutations and copy number alterations were examined by cBioPortal. miRNAs regulation was researched using TargetScanHuman, OncomiR, and ENCORI. Kaplan-Meier plotter was applied to probe into survival. Co-expressed genes with CHEK1 were explored by Oncomine, GEPIA2, UCSC Xena, cBioPortal, and WebGestalt. Additionally, EMBL-EBI SCEA and MSigDB were used to investigate CHEK1 expression in cell clusters.

    Results
    

    Using bioinformatics methods to integrate and process massive data, this study identified that CHEK1 is one of the key genes in LUAD. CHEK1 was overexpressed in various cancers including LUAD. Promotor methylation, amplification, as well as miR-195 and miR-497 regulation might lead to the unregulated expression of CHEK1. Moreover, CHEK1 overexpression was associated with poor prognosis in LUAD. CHEK1 with co-expressed genes enriched in cell cycle pathway. Additionally, CHEK1 expression might display intratumour heterogeneity, suggesting CHEK1 might be overexpressed in KRAS altered lung cancer cell clusters, which might provide a potential clue for future use of CHEK1 inhibitor targeted therapy for KRAS altered lung adenocarcinoma.

    

    Conclusion
    

    This study indicated CHEK1 is one of the key genes and could be used as a potential prognostic biomarker and therapeutic target for LUAD.

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