ALDH2 as a potential stem cell-related biomarker in lung adenocarcinoma: Comprehensive multi-omics analysis

Tran, Thi-Oanh; Vo, Thanh Hoa; Lam, Luu Ho Thanh; Le, Nguyen Quoc Khanh

doi:10.1016/j.csbj.2023.02.045

Cited by 45 publications

(29 citation statements)

References 26 publications

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“…Based on the database, bioinformatics methods are used to preliminarily investigate the expression of genes and analyze whether genes can be used for prognosis and diagnosis. This is a common way, 34,35 which is essential for subsequent experiments. The expression of genes in this study is determined based on bioinformatics methods and subjected to follow-up experiment.…”

Section: Discussionmentioning

confidence: 99%

Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR‐486‐5p/NEK2 axis

Fu,

Zhang,

Liu

et al. 2024

Clinical Respiratory J

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LINC00857 is frequently dysregulated in varying cancers, which in turn exerts carcinogenic effects; however, its DNA methylation status in promoter region and molecular mechanisms underlying the progression of lung adenocarcinoma (LUAD) remain rarely understood. Through bioinformatics analysis, we examined the expression state and methylation site of LINC00857 in LUAD and further investigated the properties of LINC00857 as a competitive endogenous RNA in the cancer progression. The current study revealed that the overexpression of LINC00857 in LUAD tissue and cells was mainly caused by the hypomethylation of the promoter region. LINC00857 knockdown prominently reduced cell proliferation, impeded cell migration and invasion, and restrained lymph node metastasis, with enhancing radiosensitivity. The effects of LINC00857 on tumor growth were also investigated in nude mice models. Subsequently, the downstream factors, miR‐486‐5p and NEK2, were screened, and the putative regulatory axis was examined. Overall, the regulatory effect of methylation‐mediated LINC00857 overexpression on miR‐486‐5p/NEK2 axis may be a new mechanism for LUAD progression.

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Section: Discussionmentioning

confidence: 99%

Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR‐486‐5p/NEK2 axis

Fu,

Zhang,

Liu

et al. 2024

Clinical Respiratory J

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“…Multi‐group bioinformatics analysis was used to confirm the association of biomarkers with patient outcomes after immunotherapy 22,23 . Statistical analyses were carried out using R 4.0.4.…”

Section: Methodsmentioning

confidence: 99%

The association of genomic alterations with PD‐L1 expression in Chinese patients with EGFR/ALK wild‐type lung adenocarcinoma and potential predictive value of Hippo pathway mutations to immunotherapy

Liu,

Zhang,

et al. 2024

Cancer Medicine

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BackgroundThe study focuses on PD‐L1 expression as an essential biomarker for gauging the response of EGFR/ALK wild‐type NSCLC patients to FDA‐approved immune checkpoint inhibitors (ICIs). It aims to explore clinical, molecular, and immune microenvironment characteristics associated with PD‐L1 expression in EGFR/ALK wild‐type lung adenocarcinoma patients eligible for ICI therapy.MethodsIn this retrospective study, tumor samples from 359 Chinese EGFR/ALK wild‐type lung adenocarcinoma patients underwent comprehensive evaluations for PD‐L1 expression and NGS‐targeted sequencing. The investigation encompassed the analysis and comparison of clinical traits, gene mutations, pathways, and immune signatures between two groups categorized by PD‐L1 status: negative (TPS < 1%) and positive (TPS ≥ 1%). Additionally, the study explored the link between genomic changes and outcomes following immunotherapy.ResultsHigh tumor mutational burden correlated significantly with PD‐L1 positivity in patients with EGFR/ALK wild‐type lung adenocarcinoma. Gene alterations, including TP53, KRAS, and others, were more pronounced in the PD‐L1 positive group. Pathway analysis highlighted higher frequencies of alterations in pathways like RTK/RAS, p53, and Hippo in PD‐L1‐positive patients. The Hippo pathway's relevance was confirmed in separate immunotherapy cohorts, associated with better outcomes. In terms of immune cell infiltration, Hippo mutants exhibited higher levels of CD68+PD‐L1+ macrophages, CD8+ T cells, and CD8+PD‐1− T cells.ConclusionsThis study offers insights into genomic features of Chinese EGFR/ALK wild‐type lung adenocarcinoma patients based on PD‐L1 expression. Notably, Hippo pathway alterations were linked to improved immunotherapy outcomes. These findings suggest connections between the Hippo pathway and PD‐L1 expression, warranting further clinical and functional investigations. The research advances our understanding of PD‐L1 expression's genomic context and immunotherapy response in EGFR/ALK wild‐type lung adenocarcinoma.

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“…Statistical analysis and bioinformatics analysis were conducted as previously described 26,27 . Specifically, Spearman correlation was used to evaluate the correlations between genes.…”

Section: Methodsmentioning

confidence: 99%

Depletion of CPNE7 sensitizes colorectal cancer to 5‐fluorouracil by downregulating ATG9B expression

Xu,

Tang,

Yang

et al. 2024

J Cellular Molecular Medi

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We aimed to explore the biological function of CPNE7 and determine the impact of CPNE7 on chemotherapy resistance in colorectal cancer (CRC) patients. According to the Gene Expression Profiling Interactive Analysis database and previously published data, CPNE7 was identified as a potential oncogene in CRC. RT‐qPCR and Western blotting were performed to verify the expression of CPNE7. Chi‐square test was used to evaluate the associations between CPNE7 and clinical features. Cell proliferation, colony formation, cell migration and invasion, cell cycle and apoptosis were assessed to determine the effects of CPNE7. Transcriptome sequencing was used to identify potential downstream regulatory genes, and gene set enrichment analysis was performed to investigate downstream pathways. The effect of CPNE7 on 5‐fluorouracil chemosensitivity was verified by half maximal inhibitory concentration (IC50). Subcutaneous tumorigenesis assay was used to examine the role of CPNE7 in sensitivity of CRC to chemotherapy in vivo. Transmission electron microscopy was used to detect autophagosomes. CPNE7 was highly expressed in CRC tissues, and its expression was correlated with T stage and tumour site. Knockdown of CPNE7 inhibited the proliferation and colony formation of CRC cells and promoted apoptosis. Knockdown of CPNE7 suppressed the expression of ATG9B and enhanced the sensitivity of CRC cells to 5‐fluorouracil in vitro and in vivo. Knockdown of CPNE7 reversed the induction of the autophagy pathway by rapamycin and reduced the number of autophagosomes. Depletion of CPNE7 attenuated the malignant proliferation of CRC cells and enhanced the chemosensitivity of CRC cells to 5‐fluorouracil.

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ALDH2 as a potential stem cell-related biomarker in lung adenocarcinoma: Comprehensive multi-omics analysis

Cited by 45 publications

References 26 publications

Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR‐486‐5p/NEK2 axis

Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR‐486‐5p/NEK2 axis

The association of genomic alterations with PD‐L1 expression in Chinese patients with EGFR/ALK wild‐type lung adenocarcinoma and potential predictive value of Hippo pathway mutations to immunotherapy

Depletion of CPNE7 sensitizes colorectal cancer to 5‐fluorouracil by downregulating ATG9B expression

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