Molecular Pathology of Non–Small Cell Lung Cancer

Serracino, Hilary S.; Franklin, Wilbur A.; Aisner, Dara L.

doi:10.1016/j.path.2012.08.006

Cited by 3 publications

(2 citation statements)

References 117 publications

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“…Non-small cell lung cancer (NSCLC) comprises approximately 85% of all types of lung cancer cases, among which lung adenocarcinoma (AC) and lung squamous cell carcinoma (SCC) are the two most common histologic subtypes [2]. In detail, SCC accounts for approximately 35% of NSCLC cases and causes an estimated 0.4 million deaths every year worldwide [3]. Increasing evidence has identified that low expression of tumour suppressor genes and/or hyper-activation of oncogenes obviously accelerates the occurrence and development of lung SCC [4–7].…”

Section: Introductionmentioning

confidence: 99%

Glypican-3 promotes cell proliferation and tumorigenesis through up-regulation of β-catenin expression in lung squamous cell carcinoma

et al. 2019

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As a cell surface proteoglycan anchored by glycosyl-phosphatidylinositol, Glypican-3 (GPC3) is reported to be highly expressed in hepatocellular carcinoma (HCC) and to promote cell proliferation and tumorigenesis through activating Wnt/β-catenin signalling. GPC3 is also overexpressed in lung squamous cell carcinoma (SCC), but its effects and mechanisms in the progression of lung SCC remain unknown. The present study aims to explore the role and molecular mechanism of GPC3 in the occurrence and development of lung SCC. Immunohistochemistry, Western blot (WB) and real-time PCR (RT-PCR) assays were used to determine the expression patterns of GPC3 in lung SCC tissues and cells. MTT, flow cytometry and in vivo xenotransplantation assays were used to evaluate the influence of GPC3 on the growth, apoptosis and tumorigenesis of lung SCC cells. The results showed that GPC3 expression levels in lung SCC tissues and cells were significantly elevated, and the high expression of GPC3 significantly promoted cell growth and tumorigenesis and repressed cell apoptosis, as well as increased β-catenin expression. Moreover, knockdown of β-catenin obviously weakened GPC3 role in the promotion of cell proliferation and tumorigenesis, as well as the inhibition of cell apoptosis. In conclusion, the present study demonstrates that up-regulation of GPC3 accelerates the progression of lung SCC in a β-catenin-dependent manner. Our study provides a theoretical basis for GPC3/β-catenin as a novel diagnostic marker and therapeutic target for lung SCC.

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Section: Introductionmentioning

confidence: 99%

Glypican-3 promotes cell proliferation and tumorigenesis through up-regulation of β-catenin expression in lung squamous cell carcinoma

et al. 2019

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“…Most NSCLC patients are generally diagnosed at a moderate or advanced stage which have lost the chance of surgery 3. Patients who drive gene mutations can choose molecular-targeted therapy, which has achieved significant effects on mutations of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) and ROS1 translocation/rearrangement, while these mutations are accounting for only 5–15% of NSCLC 3,4. For wild-type patients, platinum-based chemotherapy is the main treatment, while the disease remission rate is only 15–30%, the average survival time is 12.9 months and the 5-year survival rate is less than 15%; thus, the overall efficacy is still unsatisfactory 5–8.…”

Section: Introductionmentioning

confidence: 99%

<p>Decreased IFIT2 Expression In Human Non-Small-Cell Lung Cancer Tissues Is Associated With Cancer Progression And Poor Survival Of The Patients</p>

Su¹,

Xiao²,

Chen³

et al. 2019

OTT

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BackgroundIFIT2 (interferon-induced proteins with tetratricopeptide repeats 2), also known as ISG54, is an important interferon-stimulated gene family protein, which has been confirmed to play a crucial role in anti-cancer as well as anti-virus process. In the present study, we aimed to investigate the IFIT2 expression in human non-small-cell cancer (NSCLC) tissues and its clinical implications.MethodsThe immunohistochemistry assay was used to identify the clinical significance and prognostic value of IFIT2 expression in NSCLC tissues. The depletion of IFIT2 was achieved using RNAi approach to assess the role of IFIT2 in the regulation of biological behaviors in human lung cancer cell lines.ResultsDecreased IFIT2 expression was found in human NSCLC tissues (both in lung adenocarcinoma and lung squamous cell carcinoma) in contrast to the adjacent normal tissues (both P<0.0001, respectively). We did not find any significant correlations between the IFIT2 expression and patient’s clinicopathological features. The survival analysis showed that the overall survival (OS) of patients in IFIT2 low expression group was significantly poorer than that in IFIT2 high expression group (in lung adenocarcinoma: P=0.027; and in lung squamous cell carcinoma: P=0.029). The Cox model analysis also indicated that the distant metastasis (P=0.043) could be used as an independent prognostic factor for lung adenocarcinoma patients, and the lymph node metastasis (P=0.045) and IFIT2 low expression (P=0.020) could be used as independent prognostic factors for lung squamous cell carcinoma patients. Moreover, the depletion of IFIT2 in human lung cancer cell lines A549, H1975 and SK-MES-1 significantly increased the cellular abilities, such as viability, migration and invasion.ConclusionDecreased IFIT2 was involved in the initiation and the progression of human NSCLC, and its underlying mechanisms still needs further investigation.

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Forkhead Box S1 Inhibits the Progression of Lung Squamous Cell Carcinoma Cells by Mediating Wnt/β-Catenin Pathway

Wang

2022

Chinese Journal of Physiology

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Lung squamous cell carcinoma (SCC) is considered the frequent subtype of non-small cell lung cancer (NSCLC) and results in high mortality worldwide every year. Forkhead box S1 (FOXS1) is correlated to multiple cancers, but the role and the mechanism of FOXS1 in lung SCC are unclear. This study revealed that FOXS1 was low expressed in the lung SCC tissues by utilizing UALCAN and TIMER databases. Western blotting analysis was introduced to estimate the FOXS1 expression in the lung SCC cells. Functionally, overexpression of FOXS1 dramatically inhibited cell proliferation, migration, invasion, and epithelial–mesenchymal transition in the lung SCC cells. However, knockdown of FOXS1 exerted diverse effects on lung SCC cell progression. Moreover, FOXS1 overexpression suppressed tumor growth in nude mice remarkably. Furthermore, FOXS1 overexpression reduced the activity of Wnt/β-catenin signal, while FOXS1 silence reversed the roles notably. In conclusion, our present study proved that FOXS1 inhibited lung SCC development in vitro and in vivo might by modulating Wnt/β-catenin signaling pathway.

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Molecular Pathology of Non–Small Cell Lung Cancer

Cited by 3 publications

References 117 publications

Glypican-3 promotes cell proliferation and tumorigenesis through up-regulation of β-catenin expression in lung squamous cell carcinoma

Glypican-3 promotes cell proliferation and tumorigenesis through up-regulation of β-catenin expression in lung squamous cell carcinoma

<p>Decreased IFIT2 Expression In Human Non-Small-Cell Lung Cancer Tissues Is Associated With Cancer Progression And Poor Survival Of The Patients</p>

Forkhead Box S1 Inhibits the Progression of Lung Squamous Cell Carcinoma Cells by Mediating Wnt/β-Catenin Pathway

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