Lung cancer

Neal, Richard D; Hamilton, William; Rogers, Trevor

doi:10.1136/bmj.g6560

Cited by 27 publications

(22 citation statements)

References 7 publications

(9 reference statements)

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“…Nowadays, the ability to sequence the genomes of NSCLC patients has given a greater insight into the disease through the identification of aberrant genes, leading to new biomarkers and therapeutic targets [2,50]. Table 1 summaries known mutant genes in both adenocarcinoma and squamous-cell carcinoma.…”

Section: The Abnormality Of Genome In Non-small-cell Lung Cancer (mentioning

confidence: 99%

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Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer

Liu

Pei

Yang³

et al. 2017

IJMS

295

248

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Non-small-cell lung cancer (NSCLC) constitutes 85% of all lung cancers, and is the leading cause of cancer-related death worldwide. The poor prognosis and resistance to both radiation and chemotherapy warrant further investigation into the molecular mechanisms of NSCLC and the development of new, more efficacious therapeutics. The processes of autophagy and apoptosis, which induce degradation of proteins and organelles or cell death upon cellular stress, are crucial in the pathophysiology of NSCLC. The close interplay between autophagy and apoptosis through shared signaling pathways complicates our understanding of how NSCLC pathophysiology is regulated. The apoptotic effect of autophagy is controversial as both inhibitory and stimulatory effects have been reported in NSCLC. In addition, crosstalk of proteins regulating both autophagy and apoptosis exists. Here, we review the recent advances of the relationship between autophagy and apoptosis in NSCLC, aiming to provide few insights into the discovery of novel pathogenic factors and the development of new cancer therapeutics.

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Section: The Abnormality Of Genome In Non-small-cell Lung Cancer (mentioning

confidence: 99%

“…Adenocarcinoma accounts for 40%–70% and is found at the outer area of the lung. Large-cell carcinoma accounts for 10%–15% of cases and can be found throughout the lung [2]. …”

Section: Introductionmentioning

confidence: 99%

Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer

Liu

Pei

Yang³

et al. 2017

IJMS

295

248

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“…The majority of lung cancer cases worldwide, are diagnosed as non-small-cell lung cancer; accounting for 85% of lung cancer-related deaths (33). The identification of an effective therapeutic approach to lung cancer is therefore an urgent issue.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rh2 activates α‑catenin phosphorylation to inhibit lung cancer cell proliferation and invasion

Zhang

Chen

et al. 2020

Exp Ther Med

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The efficacy of ginsenoside Rh2 (Rh2) in cancer therapy has been reported; however, its function in lung cancer remains unknown. To analyze the role of Rh2 in the inhibition of lung cancer cell proliferation in the present study, protein expression levels of E-cadherin, vimentin, β-catenin, Smo, Gli1, and α-catenin were assessed by western blotting, whilst mRNA expression levels of TCF7 FZD8, Smo, Gli1, Gli2, and Gli3 were determined by reverse transcription-quantitative PCR in the A549 cell line. Phosphorylation sites were detected by proteomic methods and cell proliferation was analyzed by MTT assay. The present study revealed that Rh2 treatment significantly inhibited cell proliferation. Western blotting indicated that the expression levels of E-cadherin were increased and vimentin was downregulated in Rh2-treated cells compared with control cells. Treatment of A549 cells with Rh2 suppressed phosphorylation of five distinct proteins and increased phosphorylation of nine proteins. Among them, the phosphorylation of α-catenin at S641 was significantly induced. Rh2 treatment suppressed the expression levels of key genes involved in Wnt (Wnt3, transcription factor 7 and frizzled class receptor 8) and hedgehog [smoothened, frizzled class receptor (Smo), GLI family zinc finger (Gli)1, Gli2, and Gli3] signaling. Immunoblotting results indicated that β-catenin, Smo and Gli1 protein expression levels were also suppressed by treatment with Rh2 compared with control treatment. Expression of α-catenin S641D, a phosphomimetic form of α-catenin, inhibited the accumulation of β-catenin and Gli1 and inhibited cell proliferation and invasion. Furthermore, knockdown of β-catenin (CTNNB1) or Gli1 with specific small interfering RNAs inhibited cell proliferation, whereas overexpression of these genes had an opposite effect. Additionally, overexpression of β-catenin or Gli1 activated cell proliferation, even in the presence of Rh2, suggesting that Rh2 affects A549 cell proliferation through inhibition of Wnt and hedgehog signaling by phosphorylation of α-catenin at S641. Together, these data suggested that Rh2 treatment may inhibit the proliferation of A549 lung cancer cells. Further exploration of the underlying mechanism by which Rh2 inhibits cell proliferation is warranted.

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“…The fiveyear survival varies from 4-17%, leads to a need to explore new therapeutic targets and treatments (Gray et al 2019;Hirsch et al 2017). According to the histological classification, lung cancer is divided into small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC), the latter of which accounts for approximately 85% of all cases (Neal et al 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Squamous cell carcinoma and adenocarcinoma account for approximately 90% of the total NSCLC cases, which make them the most common types of lung cancer (Neal et al 2014). The poor therapeutic effect of NSCLC is mainly due to the lack of effective indicators for detecting the development of tumors at the early stage.…”

Section: Introductionmentioning

confidence: 99%

Peer Review #3 of "Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma (v0.1)"

2020

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There is plenty of evidence showing that autophagy plays an important role in the biological process of cancer. The purpose of this study was to establish a novel autophagy-related prognostic marker for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Methods: The mRNA microarray and clinical data in The Cancer Genome Atlas (TCGA) were analyzed by using a univariate Cox proportional regression model to select candidate autophagy-related prognostic genes. Bioinformatics analysis of gene function using the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) platforms was performed. A multivariate Cox proportional regression model helped to develop a prognostic signature from the pool of candidate genes. On the basis of this prognostic signature, we could divide LUAD and LUSC patients into high-risk group and lowrisk groups. Further survival analysis demonstrated that high-risk patients had significantly shorter disease-free survival (DFS) than the low-risk patients. The signature which contains 6 autophagy-related genes (EIF4EBP1, TP63, BNIP3, ATIC, ERO1A and FADD) showed good performance for predicting the survival of LUAD and LUSC patients by having a better Area Under Curves (AUC) than other clinical parameters. Its efficacy was also validated by data from the Gene Expression Omnibus (GEO) database. Conclusion: Collectively, the prognostic signature we proposed is a promising biomarker for monitoring the outcomes of LUAD and LUSC.

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Lung cancer

Cited by 27 publications

References 7 publications

Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer

Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer

Ginsenoside Rh2 activates α‑catenin phosphorylation to inhibit lung cancer cell proliferation and invasion

Peer Review #3 of "Development of an autophagy-related gene prognostic signature in lung adenocarcinoma and lung squamous cell carcinoma (v0.1)"

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