Lung cancer

Neal, Richard D; Sun, Fei; Emery, Jon; Callister, Matthew

doi:10.1136/bmj.l1725

Cited by 60 publications

(45 citation statements)

References 30 publications

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“…Lung cancer is the leading cause of cancer morbidity and mortality globally. 1 It was estimated that 2.09 million new cases were diagnosed with lung cancer and 1.76 million people died from lung cancer in the world in 2018. 2 Non-small-cell lung cancer (NSCLC) accounts 80% to 85% of all lung cancers, and lung adenocarcinoma (LAD), the predominantly histological subtype of NSCLC, accounts for approximately 40% of all lung cancers.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

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Background: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). Materials and Methods: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. Results: MTT assay measured the IC 50 values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82fold increase in Vimentin expression in A549 cells. Conclusion: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin.

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Section: Introductionmentioning

confidence: 99%

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Wang¹,

Gao²,

Chen³

et al. 2020

OTT

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“…Non-small cell lung cancer (NSCLC) comprises 85% to 90% of lung cancers while small cell lung cancer (SCLC) represents 10–15% [ 1 , 2 , 3 ]. Survival varies according to the clinical stage ranging from 92% for earliest stage to 0% for advanced stage, respectively [ 4 ]. While surgery is the treatment of choice for early stages NSCLC, chemo-radiotherapy has been the therapy of choice for the advanced stages for many years [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases

Galetta

Cortes-Dericks

2020

Cancers

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Despite tremendous efforts to improve the treatment of lung cancer, prognosis still remains poor; hence, the search for efficacious therapeutic option remains a prime concern in lung cancer research. Cell cycle regulation including mitosis has emerged as an important target for cancer management. Novel pharmacological agents blocking the activities of regulatory molecules that control the functional aspects of mitosis such as Aurora kinases are now being investigated. The Aurora kinases, Aurora-A (AURKA), and Aurora B (AURKB) are overexpressed in many tumor entities such as lung cancer that correlate with poor survival, whereby their inhibition, in most cases, enhances the efficacy of chemo-and radiotherapies, indicating their implication in cancer therapy. The current knowledge on Aurora kinase inhibitors has increasingly shown high potential in ensuing targeted therapies in lung malignancies. In this review, we will briefly describe the biology of Aurora kinases, highlight their oncogenic roles in the pre-clinical and clinical studies in lung cancer and, finally, address the challenges and potentials of Aurora kinases to improve the therapy of this malignancy.

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“…Lung adenocarcinoma (LUAD) is the most common histological type and accounts for nearly 60% of non-small cell lung cancer (NSCLC), which comprises approximately 85% of lung cancer [ 2 – 4 ]. Surgical lobectomy remains the preferred treatment strategy for patients with operable early-stage LUAD [ 5 ]. Although patients with early-stage LUAD have a relatively superior prognosis, nearly 10–44% of these patients still die within 5 years after surgical intervention [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Development and validation of a robust immune-related prognostic signature in early-stage lung adenocarcinoma

Zheng

Wang

et al. 2020

J Transl Med

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Background The incidence of stage I and stage II lung adenocarcinoma (LUAD) is likely to increase with the introduction of annual screening programs for high-risk individuals. We aimed to identify a reliable prognostic signature with immune-related genes that can predict prognosis and help making individualized management for patients with early-stage LUAD. Methods The public LUAD cohorts were obtained from the large-scale databases including 4 microarray data sets from the Gene Expression Omnibus (GEO) and 1 RNA-seq data set from The Cancer Genome Atlas (TCGA) LUAD cohort. Only early-stage patients with clinical information were included. Cox proportional hazards regression model was performed to identify the candidate prognostic genes in GSE30219, GSE31210 and GSE50081 (training set). The prognostic signature was developed using the overlapped prognostic genes based on a risk score method. Kaplan–Meier curve with log-rank test and time-dependent receiver operating characteristic (ROC) curve were used to evaluate the prognostic value and performance of this signature, respectively. Furthermore, the robustness of this prognostic signature was further validated in TCGA-LUAD and GSE72094 cohorts. Results A prognostic immune signature consisting of 21 immune-related genes was constructed using the training set. The prognostic signature significantly stratified patients into high- and low-risk groups in terms of overall survival (OS) in training data set, including GSE30219 (HR = 4.31, 95% CI 2.29–8.11; P = 6.16E−06), GSE31210 (HR = 11.91, 95% CI 4.15–34.19; P = 4.10E−06), GSE50081 (HR = 3.63, 95% CI 1.90–6.95; P = 9.95E−05), the combined data set (HR = 3.15, 95% CI 1.98–5.02; P = 1.26E−06) and the validation data set, including TCGA-LUAD (HR = 2.16, 95% CI 1.49–3.13; P = 4.54E−05) and GSE72094 (HR = 2.95, 95% CI 1.86–4.70; P = 4.79E−06). Multivariate cox regression analysis demonstrated that the 21-gene signature could serve as an independent prognostic factor for OS after adjusting for other clinical factors. ROC curves revealed that the immune signature achieved good performance in predicting OS for early-stage LUAD. Several biological processes, including regulation of immune effector process, were enriched in the immune signature. Moreover, the combination of the signature with tumor stage showed more precise classification for prognosis prediction and treatment design. Conclusions Our study proposed a robust immune-related prognostic signature for estimating overall survival in early-stage LUAD, which may be contributed to make more accurate survival risk stratification and individualized clinical management for patients with early-stage LUAD.

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Lung cancer

Cited by 60 publications

References 30 publications

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

Promising Therapy in Lung Cancer: Spotlight on Aurora Kinases

Development and validation of a robust immune-related prognostic signature in early-stage lung adenocarcinoma

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