RYR2mutation in non‐small cell lung cancer prolongs survival via down‐regulation ofDKK1and up‐regulation ofGS1‐115G20.1: A weighted gene Co‐expression network analysis and risk prognostic models

Ren, Wenjun; Li, Yongwu; Chen, Xi; Hu, Sheng; Cheng, Wanli; Cao, Yu; Gao, Jinliang; Chen, Xia; Xiong, Da; Li, Hongrong; Wang, Ping

doi:10.1049/syb2.12038

Cited by 8 publications

(7 citation statements)

References 56 publications

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“…TP53 status was a reliable and robust immune signature for identifying early-stage LUAD patients with a high risk of unfavorable survival [ 49 ]. TCGA data demonstrated that the RYR2 mutant group lived longer than the wild group [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular fingerprints of nuclear genome and mitochondrial genome for early diagnosis of lung adenocarcinoma

Yang

Wang

et al. 2023

J Transl Med

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Background Lung adenocarcinoma (LUAD) is the most prevalent subtype of lung cancer with high morbidity and mortality rates. Due to the heterogeneity of LUAD, its characteristics remain poorly understood. Exploring the clinical and molecular characteristics of LUAD is challenging but vital for early diagnosis. Methods This observational and validation study enrolled 80 patients and 13 healthy controls. Nuclear and mtDNA-captured sequencings were performed. Results This study identified a spectrum of nuclear and mitochondrial genome mutations in early-stage lung adenocarcinoma and explored their association with diagnosis. The correlation coefficient for somatic mutations in cfDNA and patient-matched tumor tissues was high in nuclear and mitochondrial genomes. The mutation number of highly mutated genes was evaluated, and the Least Absolute Shrinkage and Selection Operator (LASSO) established a diagnostic model. Receiver operating characteristic (ROC) curve analysis explored the diagnostic ability of the two panels. All models were verified in the testing cohort, and the mtDNA panel demonstrated excellent performance. This study identified somatic mutations in the nuclear and mitochondrial genomes, and detecting mutations in cfDNA displayed good diagnostic performance for early-stage LUAD. Moreover, detecting somatic mutations in the mitochondria may be a better tool for diagnosing early-stage LUAD. Conclusions This study identified specific and sensitive diagnostic biomarkers for early-stage LUAD by focusing on nuclear and mitochondrial genome mutations. This also further developed an early-stage LUAD-specific mutation gene panel for clinical utility. This study established a foundation for further investigation of LUAD molecular pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Molecular fingerprints of nuclear genome and mitochondrial genome for early diagnosis of lung adenocarcinoma

Yang

Wang

et al. 2023

J Transl Med

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“…Wang et al found that Rac3 acted on TFDP1, CCND1 , and MYC to regulate cell proliferation of LUAD during tumorigenesis [ 50 ]. Ren et al found that RYR2 mutation could lead to a better prognosis by downregulation of DKK1 , which was associated with TP53 , MTOR , and VEGF in NSCLC [ 51 ]. Therefore, the specific mechanism of genes cooccurred with TFDP1 alterations in LUAD may be worth further research.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis Reveals the Potential Roles of Transcription Factor Dp-1 in Lung Adenocarcinoma

Song

2023

World J Oncol

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Background Transcription factor Dp-1 (TFDP1) was overexpressed and interacted with other genes to impact multiple signaling pathways in various human cancers. However, there is less research about the TFDP1 specific roles in lung adenocarcinoma (LUAD). Methods We first explored TFDP1 expression levels and relative diseases from a pan-cancer perspective using the ONCOMINE, TIMER, and Open Targets Platform databases. Then, we used UALCAN, GEPIA 2, TCGA-LUAD data, and Kaplan-Meier plotter to examine TFDP1 clinicopathological features and prognosis in LUAD patients. Genomic alterations and DNA methylation analysis were performed by cBioPortal and MethSurv, respectively. Then, we used a cancer single-cell state atlas (CancerSEA) to find TFDP1 functions at a single-cell resolution. LinkedOmics was used to find TFDP1 coexpressed genes, biological processes, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Then, Gene Set Cancer Analysis (GSCA) was used to examine the drug resistence of TFDP1 in LUAD. Results We found that TFDP1 was overexpressed in most human cancers and related to various diseases, including LUAD. Moreover, LUAD patients with high TFDP1 expression levels might be significantly associated with individual cancer stages and have a poor prognosis. Multivariate analysis revealed that the American Joint Committee on Cancer (AJCC) pathologic stage, AJCC stage T, and AJCC stage N were the independent prognostic factors. LUAD patients with TFDP1 alterations suggested poor overall survival (OS), and disease-free survival (DFS), while hypermethylation might lead to a good prognosis. TFDP1 and its coexpressed genes were enriched in multiple signaling pathways and biological processes involved in the cell cycle, spliceosome, and DNA replication. Furthermore, TFDP1 was strongly positively related to the half-maximal inhibitory concentration (IC50) values of multiple drugs. Conclusions In summary, TFDP1 was a possible biomarker and potential therapeutic target for LUAD patients.

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“…Liu et al found the RYR2 mutation was linked to a greater TMB and a better clinical outcome by enhancing the antitumor immune response in breast cancer and esophageal adenocarcinoma [ 26 ]. In nonsmall cell lung cancer, RYR2 mutation may prolong survival via downregulation of DKK1 and upregulation [ 27 ]. In this study, we found that RYR2 expression was negatively related to the PFS in CRC.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of Genomic and Expression Data Identified Potential Markers for Predicting Prognosis and Immune Response in CRC

Dai

Chen

et al. 2022

Genetics Research

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Colorectal cancer (CRC) is the most prevalent type of malignant tumor of the gastrointestinal tract. In the current study, we characterized the landscape of genomic alterations in CRC patients. Based on the results of whole-exome sequencing (WES), we identified 31 significantly mutated genes. Among them, several genes including TP53, KRAS, APC, PI3KCA, and BRAF were reported as significantly mutated genes in previous studies. In the current study, the most frequently mutated gene was TP53, which encodes tumor suppressor p53, affecting approximately 60% of CRC patients. In addition, we performed the expression profiles of significantly mutated genes between the normal group and tumor groups and identified 20 differentially expressed genes (DEGs); among them, CSMD3, DCHS2, LRP2, RYR2, and ZFHX4 were significantly negatively correlated with PFS. Moreover, consensus clustering analysis for CRC based on the expression of significantly somatic mutated genes was performed. In total, three subtypes of CRC were identified in CRC, including cluster1 (n = 453), cluster2 (n = 158), and cluster 3 (n = 9), based on expression level of significantly somatic mutated genes. Clinicopathological features analysis showed subtype C1 had the longest progression-free survival (PFS) with median time of 8.2 years, while subtypes C2 and C3 had 4.1 and 2.7 years of PFS, respectively. Moreover, we found three subtypes related to tumor infiltration depth, lymph node metastasis, and distant metastasis. Immune infiltration analysis showed the tumor infiltration levels of B cell native, T cell CD8+, T cell CD4+ memory activated, T cell gamma delta, NK cell resting, macrophage M0, macrophage M2, myeloid dendritic cell activated, mast cell activated, and mast cell resting significantly changed among the three groups, demonstrating the three subgroups classified by 22 somatically significantly mutated genes had a high capacity to differentiate patients with different immune statuses, which is helpful for the prediction of immunotherapy response of CRC patients. Our findings could provide novel potential predictive indicators for CRC prognosis and therapy targets for CRC immunotherapy.

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RYR2mutation in non‐small cell lung cancer prolongs survival via down‐regulation ofDKK1and up‐regulation ofGS1‐115G20.1: A weighted gene Co‐expression network analysis and risk prognostic models

Cited by 8 publications

References 56 publications

Molecular fingerprints of nuclear genome and mitochondrial genome for early diagnosis of lung adenocarcinoma

Molecular fingerprints of nuclear genome and mitochondrial genome for early diagnosis of lung adenocarcinoma

Comprehensive Analysis Reveals the Potential Roles of Transcription Factor Dp-1 in Lung Adenocarcinoma

Comprehensive Analysis of Genomic and Expression Data Identified Potential Markers for Predicting Prognosis and Immune Response in CRC

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