Non-SMC condensin I complex subunit H (NCAPH), a regulator of cell cycle, predicts poor prognosis in lung adenocarcinoma patients: a study mainly based on TCGA and GEO database

BackgroundLung adenocarcinoma (LUAD) is a leading malignancy and has a poor prognosis over the decades. LUAD is characterized by dysregulation of cell cycle. Immunotherapy has emerged as an ideal option for treating LUAD. Nevertheless, optimal biomarkers to predict outcomes of immunotherapy is still ill-defined and little is known about the interaction of cell cycle-related genes (CCRGs) and immunity-related genes (IRGs).MethodsWe downloaded gene expression and clinical data from TCGA and GEO database. LASSO regression and Cox regression were used to construct a differentially expressed CCRGs and IRGs signature. We used Kaplan-Meier analysis to compare survival of LUAD patients. We constructed a nomogram to predict the survival and calibration curves were used to evaluate the accuracy.ResultsA total of 61 differentially expressed CCRGs and IRGs were screened out. We constructed a new risk model based on 8 genes, including ACVR1B, BIRC5, NR2E1, INSR, TGFA, BMP7, CD28, NUDT6. Subgroup analysis revealed the risk model accurately predicted the overall survival in LUAD patients with different clinical features and was correlated with immune cells infiltration. A nomogram based on the risk model exhibited excellent performance in survival prediction of LUAD.ConclusionsThe 8 gene survival signature and nomogram in our study are effective and have potential clinical application to predict prognosis of LUAD.

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Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

BMC Cancer ◽

10.1186/s12885-021-08378-3 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Cheng Chen ◽

Yang Tang ◽

Wen-Dong Qu ◽

Xu Han ◽

Jie-Bin Zuo ◽

...

Keyword(s):

Cell Cycle ◽

Dna Replication ◽

Homologous Recombination ◽

Lung Adenocarcinoma ◽

Signaling Pathway ◽

Poor Prognosis ◽

Neoplasm Staging ◽

Smoking History ◽

P53 Signaling ◽

P53 Signaling Pathway

Abstract Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

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Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

10.21203/rs.3.rs-118595/v1 ◽

2020 ◽

Author(s):

Cheng Chen ◽

Yang Tang ◽

Wendong Qu ◽

Xu Han ◽

Jiebin Zuo ◽

...

Keyword(s):

Cell Cycle ◽

Dna Replication ◽

Homologous Recombination ◽

Lung Adenocarcinoma ◽

Signaling Pathway ◽

Poor Prognosis ◽

Neoplasm Staging ◽

Smoking History ◽

P53 Signaling ◽

P53 Signaling Pathway

Abstract Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatic tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

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Evaluation of Clinical Value and Potential Mechanism of MTFR2 in Lung Adenocarcinoma via Bioinformatics

10.21203/rs.3.rs-132516/v1 ◽

2021 ◽

Author(s):

Cheng Chen ◽

Yang Tang ◽

Wendong Qu ◽

Xu Han ◽

Jiebin Zuo ◽

...

Keyword(s):

Cell Cycle ◽

Dna Replication ◽

Homologous Recombination ◽

Lung Adenocarcinoma ◽

Signaling Pathway ◽

Poor Prognosis ◽

Neoplasm Staging ◽

Smoking History ◽

P53 Signaling ◽

P53 Signaling Pathway

Abstract Background: Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools.Results: We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions: Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

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Increased KIF15 Expression Predicts a Poor Prognosis in Patients with Lung Adenocarcinoma

Cellular Physiology and Biochemistry ◽

10.1159/000495155 ◽

2018 ◽

Vol 51 (1) ◽

pp. 1-10 ◽

Cited By ~ 9

Author(s):

Yuan Qiao ◽

Jingtao Chen ◽

Chao Ma ◽

Yingmin Liu ◽

Peitong Li ◽

...

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Lung Adenocarcinoma ◽

Small Cell Lung Cancer ◽

Messenger Rna ◽

Poor Prognosis ◽

Human Lung ◽

Small Cell ◽

Small Cell Lung ◽

Protein Levels

Background/Aims: Lung cancer is the leading cause of cancer-related deaths worldwide. The outcome of patients with non-small cell lung cancer remains poor; the 5-year survival rate for stage IV non-small cell lung cancer is only 1.0%. KIF15 is a tetrameric kinesin spindle motor that has been investigated for its regulation of mitosis. While the roles of kinesin motor proteins in the regulation of mitosis and their potentials as therapeutic targets in pancreatic cancer have been described previously, the role of KIF15 in lung cancer development remains unknown. Methods: Paired lung carcinoma specimens and matched adjacent normal tissues were used for protein analysis. Clinical data were obtained from medical records. We first examined KIF15 messenger RNA expression in The Cancer Genome Atlas database, and then determined KIF15 protein levels using immunohistochemistry and western blotting. Differences between the groups were analyzed using repeated measures analysis of variance. Overall survival was analyzed using the Kaplan–Meier method. Cell-cycle and proliferation assays were conducted using A549, NCI-H1299, and NCI-H226 cells. Results: KIF15 was significantly upregulated at both the messenger RNA and protein levels in human lung tumor tissues. In patients with lung adenocarcinoma, KIF15 expression was positively associated with disease stages; high KIF15 expression predicted a poor prognosis. KIF15 knockdown using short hairpin RNA in two human lung adenocarcinoma cell lines induced G1/S phase cell cycle arrest and inhibited cell growth, but there was no effect in human lung squamous cell carcinoma. Conclusion: Our findings show that KIF15 is involved in lung cancer carcinogenesis. KIF15 could therefore serve as a specific prognostic marker for patients with lung adenocarcinoma.

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LONG NON-CODING RNA AHIF PREDICTS POOR PROGNOSIS IN EPITHELIAL OVARIAN CANCER AND AFFECTS CELL PROLIFERATION THROUGH THE REGULATION OF CELL CYCLE, APOPTOSIS AND SENESCENCE

10.26226/morressier.5770e29cd462b80290b4c0f3 ◽

2016 ◽

Author(s):

junjun qiu

Keyword(s):

Cell Cycle ◽

Ovarian Cancer ◽

Cell Proliferation ◽

Epithelial Ovarian Cancer ◽

Poor Prognosis ◽

Non Coding Rna ◽

Regulation Of Cell Cycle ◽

Long Non Coding Rna

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Stromal FAP is an independent poor prognosis marker in non-small cell lung adenocarcinoma and associated with p53 mutation

Lung Cancer ◽

10.1016/j.lungcan.2021.02.028 ◽

2021 ◽

Author(s):

Pablo Moreno-Ruiz ◽

Sara Corvigno ◽

Nienke C. te Grootenhuis ◽

Linnéa La Fleur ◽

Max Backman ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Poor Prognosis ◽

P53 Mutation ◽

Small Cell ◽

Small Cell Lung ◽

Prognosis Marker

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Long noncoding RNA LMO7DN inhibits cell proliferation by regulating the cell cycle in lung adenocarcinoma

Pathology - Research and Practice ◽

10.1016/j.prp.2021.153475 ◽

2021 ◽

pp. 153475

Author(s):

Lizhong Zeng ◽

Yang Chen ◽

Jingyan Yuan ◽

Xin Lyu ◽

LeiZhang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Lung Adenocarcinoma ◽

Long Noncoding Rna ◽

Noncoding Rna

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Bioinformatics study on genes related to a high-risk postoperative recurrence of lung adenocarcinoma

Science Progress ◽

10.1177/00368504211018053 ◽

2021 ◽

Vol 104 (3) ◽

pp. 003685042110180

Author(s):

Xiao Lin ◽

Meng Zhou ◽

Zehong Xu ◽

Yusheng Chen ◽

Fan Lin

Keyword(s):

Cell Cycle ◽

Gene Ontology ◽

High Risk ◽

Lung Adenocarcinoma ◽

Candidate Genes ◽

Postoperative Recurrence ◽

High Expression ◽

Ppi Network ◽

Hub Genes ◽

Expression Levels

In this study, we aimed to screen out genes associated with a high risk of postoperative recurrence of lung adenocarcinoma and investigate the possible mechanisms of the involvement of these genes in the recurrence of lung adenocarcinoma. We identify Hub genes and verify the expression levels and prognostic roles of these genes. Datasets of GSE40791, GSE31210, and GSE30219 were obtained from the Gene Expression Omnibus database. Enrichment analysis of gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were performed for the screened candidate genes using the DAVID database. Then, we performed protein–protein interaction (PPI) network analysis through the database STRING. Hub genes were screened out using Cytoscape software, and their expression levels were determined by the GEPIA database. Finally, we assessed the relationships of Hub genes expression levels and the time of survival. Forty-five candidate genes related to a high-risk of lung adenocarcinoma recurrence were screened out. Gene ontology analysis showed that these genes were enriched in the mitotic spindle assembly checkpoint, mitotic sister chromosome segregation, G2/M-phase transition of the mitotic cell cycle, and ATP binding, etc. KEGG analysis showed that these genes were involved predominantly in the cell cycle, p53 signaling pathway, and oocyte meiosis. We screened out the top ten Hub genes related to high expression of lung adenocarcinoma from the PPI network. The high expression levels of eight genes (TOP2A, HMMR, MELK, MAD2L1, BUB1B, BUB1, RRM2, and CCNA2) were related to short recurrence-free survival and they can be used as biomarkers for high risk of lung adenocarcinoma recurrence. This study screened out eight genes associated with a high risk of lung adenocarcinoma recurrence, which might provide novel insights into researching the recurrence mechanisms of lung adenocarcinoma as well as into the selection of targets in the treatment of the disease.

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