Genes and Pathology of Non-Small Cell Lung Carcinoma

Sakashita, Shingo; Sakashita, Masanori; Tsao, Ming‐Sound

doi:10.1053/j.seminoncol.2013.12.008

Cited by 53 publications

(46 citation statements)

References 110 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although advancement of scientific and clinical research has been made recently, the therapeutic outcome of NSCLC remains poor. This situation is primarily due to the fact that a large proportion of patients diagnosed with NSCLC are found to be in advanced stages, and therefore often suffered from metastasis and recurrence [3]. Chemotherapy with platinum-based drugs, such as cisplatin, is one of the most effective treatment regimens for NSCLC [3].…”

Section: Introductionmentioning

confidence: 99%

“…This situation is primarily due to the fact that a large proportion of patients diagnosed with NSCLC are found to be in advanced stages, and therefore often suffered from metastasis and recurrence [3]. Chemotherapy with platinum-based drugs, such as cisplatin, is one of the most effective treatment regimens for NSCLC [3]. Unfortunately, many NSCLC patients develop resistance to cisplatin during the course of treatment, leading to failure of chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

Lang

Kong

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Lung cancer is one of the leading causes for cancer mortality. The poor therapeutic outcome of non-small cell lung carcinoma (NSCLC) is mainly due to late diagnosis and chemoresistance. In this study, we investigated the role of Musashi1 (MSI1) in NSCLC malignancy and chemoresistance. Methods: Colony formation, MTT, glucose uptake and lactate production assays were employed to study lung cancer cell malignancy and chemoresistance. RT-PCR and Western blotting were performed to detect mRNA and protein expressions of genes. We used immunohistochemistry and Pearson correlation analysis to study the relationship of gene expression. Results: We demonstrated that MSI1 was able to promote the proliferation and glucose metabolism of NSCLC cells, and to mediate the sensitivity to chemotherapy drugs in NSCLC cells. Importantly, we found that MSI1 could regulate the activity of Akt signaling. The regulation of NSCLC proliferation, glucose metabolism and chemoresistance by MSI1 was dependent on the modulation of the activity of the Akt signaling pathway. We also found that MSI1 was a target of miR-181a-5p, a microRNA involved in the regulation of cancer development. The expression levels of MSI1 and miR-181a-5p were negatively correlated in NSCLC. Conclusion: MSI1 promotes non-small cell lung carcinoma malignancy and chemoresistance via activating the Akt signaling pathway, which provides a new strategy for the therapy of NSCLC.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

Lang

Kong

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Almost as many patients die of lung cancer every year than die of prostate, breast and colon cancer combined in the USA (2). According to the differences in clinical behavior and the aims of treatment, lung cancers can be divided into two broad categories; small cell lung cancer (SCLC) which accounts for 15% of all lung cancer cases and non-small cell lung cancer (NSCLC) which accounts for 85% of cases (3).…”

Section: Introductionmentioning

confidence: 99%

β2-adrenergic receptor activation promotes the proliferation of A549 lung cancer cells via the ERK1/2/CREB pathway

Liu

et al. 2016

Oncology Reports

View full text Add to dashboard Cite

Abstract. Lung cancer is one of the most common cancers worldwide and accounts for 28% of all cancer-related deaths. The expression of the β 2 -adrenergic receptor (β 2 -AR), one of the stress-inducible receptors, has been reported to be closely correlated with malignant tumors. However, the role of β 2 -AR activation in human lung epithelial-derived cancer A549 cells and the underlying mechanisms are not fully understood. In the present study, we found that activation of β 2 -AR but not β 1 -AR promoted the proliferation of A549 cells. Isoproterenol (ISO) stimulation of β 2 -AR induced extracellular signal-regulated kinase 1/2 (ERK 1/2 ) and cyclic adenosine monophosphate response element-binding protein (CREB) phosphorylation. Blocking the ERK 1/2 pathway by U0126 inhibited CREB phosphorylation and also suppressed A549 cell proliferation. Moreover, ISO treatment enhanced the expression of matrix metalloproteinase (MMP) family proteins such as MMP-2, MMP-9, and also vascular endothelial growth factor (VEGF), which were able to be blocked by knockdown of CREB. In conclusion, our data revealed that β 2 -AR induced ERK 1/2 phosphorylation which in turn activated CREB to promote A549 cell proliferation. These findings elucidate potential therapeutic targets for lung cancer treatment.

show abstract

“…ADCs commonly contain a heterogeneous mixture of histological growth patterns, classified as "mixed type"; therefore, new improved guidelines and classification for lung ADC which describe ADCs with different invasive potential as well as its main genetic aberrations, such as epidermal growth factor (EGFR) mutations (see below), have been proposed by international consortia (Travis et al, 2011). In addition to histopathological classification, the use of appropriate biomarkers for specific subtypes of lung ADC would be beneficial for the best choice of anti-cancer therapy (Sakashita et al, 2014).…”

Section: Lung Adenocarcinoma and Associated Genetic Abnormalitiesmentioning

confidence: 99%

“…Genomic abnormalities in lung ADCs were recently reviewed in (Sakashita et al, 2014, Viktorsson et al, 2014; therefore, here we will just list the most common mutations in ADC identified so far. Driving mutations seem to contribute to early carcinogenesis in over 80% of lung ADC cases (Dearden et al, 2013).…”

Section: Lung Adenocarcinoma and Associated Genetic Abnormalitiesmentioning

confidence: 99%

Cell death in cancer therapy of lung adenocarcinoma

Zagryazhskaya

Gyurászová²,

Zhivotovsky

2015

Int. J. Dev. Biol.

View full text Add to dashboard Cite

Lung cancer is the main cause of all cancer-related deaths in the world, with lung adenocarcinoma (ADC) being the most common subtype of this fatal disease. Lung ADC is often diagnosed at advanced stages involving disseminated metastatic tumors. This is particularly important for the successful development of new cancer therapy approaches. The high resistance of lung ADC to conventional radio-and chemotherapies represents a major challenge to treatment effectiveness. Here we discuss recent progress in understanding the mechanisms of ADC's broad resistance to treatment and its possible therapeutic implications. A number of driving oncogenic alterations were identified in a subset of lung ADCs, making them suitable for targeted therapies directed towards specific cancer-associated molecular changes. In addition, we discuss the molecular aberrations common in lung ADC that are currently being exploited or are potentially important for targeted cancer therapy, as well as limitations of this type of therapy. Furthermore, we highlight possible treatment modalities that hold promise for overcoming resistance to targeted therapies as well as alternative treatment options such as immunotherapies that are potentially promising for improving the clinical outcome of lung ADC patients.

show abstract

Genes and Pathology of Non-Small Cell Lung Carcinoma

Cited by 53 publications

References 110 publications

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

β2-adrenergic receptor activation promotes the proliferation of A549 lung cancer cells via the ERK1/2/CREB pathway

Cell death in cancer therapy of lung adenocarcinoma

Contact Info

Product

Resources

About