ArticlePeerJ2020
CKS2 and RMI2 are two prognostic biomarkers of lung adenocarcinoma.
Article in PeerJ, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Biological functions and therapeutic potential of CKS2 in human cancer.Frontiers in oncology · 2024Review
- A combined bioinformatics and experimental approach identifies RMI2 as a Wnt/β-catenin signaling target gene related to hepatocellular carcinoma.BMC cancer · 2023Article
- RMI2 is a novel prognostic and predictive biomarker for breast cancer.Cancer medicine · 2023Article
- Knockdown of DLK4 inhibits non-small cell lung cancer tumor growth by downregulating CKS2.Open life sciences · 2023Article
- Article
- RMI2 is a prognostic biomarker and promotes tumor growth in hepatocellular carcinoma.Clinical and experimental medicine · 2022Article
- Comprehensive Expression Profiling and Molecular Basis of CDC28 Protein Kinase Regulatory Subunit 2 in Cervical Cancer.International journal of genomics · 2022Article
- Expression Profile and Molecular Basis of Cyclin-Dependent Kinases Regulatory Subunit 2 in Endometrial Carcinoma Detected by Diversified Methods.Pathology oncology research : POR · 2022Article
- The Clinical Significance of RMI2 in Hepatocellular Carcinoma.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung adenocarcinoma (ACA) is the most common subtype of non-small-cell lung cancer. About 70%-80% patients are diagnosed at an advanced stage; therefore, the survival rate is poor. It is urgent to discover accurate markers that can differentiate the late stages of lung ACA from the early stages. With the development of biochips, researchers are able to efficiently screen large amounts of biological analytes for multiple purposes.
methodsOur team downloaded GSE75037 and GSE32863 from the Gene Expression Omnibus (GEO) database. Next, we utilized GEO's online tool, GEO2R, to analyze the differentially expressed genes (DEGs) between stage I and stage II-IV lung ACA. The using the Cytoscape software was used to analyze the DEGs and the protein-protein interaction (PPI) network was further constructed. The function of the DEGs were further analyzed by cBioPortal and Gene Expression Profiling Interactive Analysis (GEPIA) online tools. We validated these results in 72 pairs human samples.
resultsWe identified 109 co-DEGs, most of which were involved in either proliferation, S phase of mitotic cell cycle, regulation of exit from mitosis, DNA replication initiation, DNA replication, and chromosome segregation. Utilizing cBioPortal and University of California Santa Cruz databases, we further confirmed 35 hub genes. Two of these genes, encoding CDC28 protein kinase regulatory subunit 2 (CKS2) and RecQ-mediated genome instability 2 (RMI2), were upregulated in lung ACA compared with adjacent normal tissues. The Kaplan-Meier curves revealed upregulation of CKS2 and RMI2 are associated with worse survival. Using CMap analysis, we discovered 10 small molecular compounds that reversed the altered DEGs, the top five are phenoxybenzamine, adiphenine, resveratrol, and trifluoperazine. We also evaluated 72 pairs resected samples, results revealed that upregulation of CKS2 and RMI2 in lung ACA were associated with larger tumor size. Our results allow the deeper recognizing of the mechanisms of the progression of lung ACA, and may indicate potential therapeutic strategies for the therapy of lung ACA.
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