A prognosis-related molecular subtype for early-stage non-small lung cell carcinoma by multi-omics integration analysis

Yang, Kai; Wu, Ying

doi:10.1186/s12885-021-07846-0

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…Even though prior research studies [35] were able to identify molecular subtypes for NSCLC in its early stages, immune gene-based molecular typing is still relatively uncommon. In this study, immune-related genes were utilized to classify early-stage NSCLC samples from the RNAseq and GSE datasets into two subgroups (C1 and C2).…”

Section: Discussionmentioning

confidence: 99%

Early Stage Finding of an Immune-Enhanced Genetic Subtype of Nonsmall Cell Lung Cancer Related with T-Cell Depletion

Yang

Shen

Dong

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Molecular categorization of lung cancer in medical care is becoming increasingly important on a regular basis. One of the molecular classifications of NSCLC (early-stage NSCLC) supports that tumors of different biological varieties differ in terms of their genomes and clinical characteristics. Methods. Based on published immune cell signatures and early-stage NSCLC gene expression data including cancer genome maps, we used consensus cluster analysis to identify immune molecular subtypes associated with early-stage NSCLC expression subtypes. These subtypes were correlated with early-stage NSCLC expression subtypes. Next, applying a wide range of statistical techniques, we evaluated the link between molecular subtypes and clinical features, immunological microenvironment, and immunotherapy reactivity. Molecular subtypes were defined as a classification of cancerous cells. Results. Multiple RNAseq cross-platform datasets of immune genes were used to identify two molecular subtypes (C1 and C2) of NSCLC, with C1 showing a more favorable prognosis than C2. The results were validated on the CSE datasets. In terms of clinical characteristics, C2 subtype samples with a worse prognosis showed a more advanced tumor stage and higher mortality. C2 showed immuno-infiltrative characteristics but had depletion of T-cells. Biological functions such as EMT were enriched on C2. A low TIDE score in C1 indicated that C1 samples could benefit from taking immunotherapy. C2 were more susceptible to standard chemotherapeutic treatments such paclitaxel, cisplatin, sorafenib, crizotinib, and erlotinib. Conclusion. According to our findings, early-stage NSCLC patients may benefit from receiving treatment with immune checkpoint blockade therapy.

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Section: Discussionmentioning

confidence: 99%

Early Stage Finding of an Immune-Enhanced Genetic Subtype of Nonsmall Cell Lung Cancer Related with T-Cell Depletion

Yang

Shen

Dong

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Previous studies have reported different LUAD subtypes based on methylation or gene expression (12,13). Moreover, methylation and gene expression have been combined to identify the pathologic subtypes of NSCLC, including small cell lung cancer and LUAD, instead of molecular typing (14).…”

Section: Introductionmentioning

confidence: 99%

Identification of molecular subtypes in lung adenocarcinoma based on DNA methylation and gene expression profiling—a bioinformatic analysis

Wang¹,

Liang²,

Guo³

et al. 2022

Ann Transl Med

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Background: Molecular typing based on deoxyribonucleic acid (DNA) methylation and gene expression can extend understandings of the molecular mechanisms involved in lung adenocarcinoma (LUAD) and enhance current diagnostic, treatment, and prognosis prediction approaches.Methods: Gene expression and DNA methylation data sets of LUAD were obtained from The Cancer Genome Atlas (TCGA), and the differential gene and methylation expression levels were analyzed.Results: We successfully divided the LUAD samples into 2 clinically relevant subtypes with significantly different survival times and tumor stages according to the transcriptome and methylation data. We found significant differences in the survival status, age, gender, tumor stage, node stage, and clinical stage between the 2 subtypes. The hub genes identified in the subnetworks, including NCAPG, CCNB1, DLGAP5, HLA-DQA1, HLA-DPA1, HLA-DPB1, SFTP, SCGBA1A, and SFTPD, were correlated with the cell cycle and immune system. The Gene Ontology annotation of the hub genes showed that the biological processes included organelle fission mitotic nuclear division, and sister chromatid segregation. The cellular components included chromosomal region, spindle, and kinetochore. The molecular functions included tubulin-binding, microtubule-binding, and DNA replication origin binding. The Kyoto Encyclopedia of Genes and Genomes signaling pathways related to the hub genes mainly included the cell cycle, human T-cell leukemia virus (type 1) infection, inflammatory bowel disease, and the intestinal immune network for immunoglobulin A production. The clinical stage difference was also confirmed in the validation group using the GSE32863 data set.Conclusions: Our findings extend understandings of the pathogenesis of LUAD and can be used to improve current diagnosis, treatment, and prognosis prediction strategies.

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“…Human crystallin alpha B ( CRYAB ), also known as human alpha B-crystallin (HspB5) or αB-crystallin, is a subtype of small heat shock protein (sHsp). It was first discovered in the lens of the eye and has been linked to a variety of diseases, including eye disease, heart disease and even breast, lung, prostate and ovarian cancers ( 1 ). CRYAB comprises of an N-terminal domain, a central domain, and a C-terminal domain ( 2 ).…”

Section: Introductionmentioning

confidence: 99%

Role of methylation-related genes CRYAB and SLC39A11 in the occurrence and development of lung adenocarcinoma

Wang¹,

Gui²,

Liu³

et al. 2022

Ann Transl Med

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Background: Previous studies have shown that human crystallin alpha B (CRYAB) is highly expressed in human cancers and associated with poor survival in cancer patients. Here we investigated whether SLC39A11 and CRYAB genes were related to the proliferation and development of lung adenocarcinoma (LUAD) to explore their potential as therapeutic targets and prognostic markers for LUAD. Methods: CRYAB and SLC39A11 genes were identified from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database. The human lung cancer cell lines A549 and H1975 were cultured, transfected, and subjected to RNA extraction. After genomic DNA removal, the RNA was reversetranscribed. Differences between 2 groups were compared using t-test.Results: Knockdown of SLC39A11 inhibited the proliferation of LUAD cells in A549 and H1975.Knockdown of CRYAB promoted the increase of LUAD cell clones, while knockdown of SLC39A11 suppressed LUAD cell clones. In both A549 and H1975 cell lines, knockout of CRYAB inhibited the apoptosis of LUAD cells, whereas knockout of SLC39A11 promoted the apoptosis of LUAD cells. In the H1975 cell line, knockout of CRYAB also lowered the proportion of cells in interphase and increased the proportion of mitotic cells, while knockout of SLC39A11 also slowed down the division cycle of tumor cells.Knockdown of CRYAB promoted the migration of LUAD cells in both the A549 cell line and H1975 cell line. In the H1975 cell line, knockout of SLC39A11 also reduced the invasive ability of LUAD cells.Conclusions: CRYAB and SLC39A11 could be used as prognostic indicators and therapeutic targets for LUAD.

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A prognosis-related molecular subtype for early-stage non-small lung cell carcinoma by multi-omics integration analysis

Cited by 7 publications

References 30 publications

Early Stage Finding of an Immune-Enhanced Genetic Subtype of Nonsmall Cell Lung Cancer Related with T-Cell Depletion

Early Stage Finding of an Immune-Enhanced Genetic Subtype of Nonsmall Cell Lung Cancer Related with T-Cell Depletion

Identification of molecular subtypes in lung adenocarcinoma based on DNA methylation and gene expression profiling—a bioinformatic analysis

Role of methylation-related genes CRYAB and SLC39A11 in the occurrence and development of lung adenocarcinoma

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