Cancer stem cell-like population is preferentially suppressed by EGFR-TKIs in EGFR-mutated PC-9 tumor models.

Aims: Although the epidermal growth factor receptor (EGFR) and Wnt/β-catenin signaling systems synergistically regulate many essential developmental and regenerative processes in lung cancer, the mechanisms of their crosstalk remain poorly defined. Our study aimed to investigate an interaction between EGFR and the β-catenin signal.

Results: In this study, we described a potent activation of β-catenin by EGFR, which is dependent of the PtdIns3K/AKT pathway.

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer.

Long non-coding RNAs (lncRNAs) are associated with the occurrence, development and prognoses of non-small cell lung cancer (NSCLC). In the present study, we investigated the functional mechanisms of the lncRNA XIST in two human NSCLC cell lines, A549 and NCI-H1299. In all the 5 NSCLC cell lines (NL9980, NCI-H1299, NCI-H460, SPC-A-1 and A549) tested, the expression levels of XIST were significantly elevated, as compared with those in normal human bronchial epithelial cell line BEAS-2B.

Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981.

Background: The tetraspanin KAI1/CD82 was identified as a tumor metastasis suppressor that down-regulated in malignant progression of lung cancer. However, the underlying mechanism of anti-metastasis role of KAI1 in lung cancer is hardly known. In this paper, we sought to study the function and regulatory mechanism of KAI1 in high metastasis lung cancer cell line.

[Nicotine Induced Lung Cancer Cells Epithelial-mesenchymal Transition and Promote Its Vitro Invasion Potential].

Background: Our previous study found that nicotine could induce lung cancer cell epithelial-mesenchymal transition (EMT). The aim of this study is to explore the relationship between nicotine-induced EMT and lung cancer invasion and metastasis.

Methods: Real-time PCR and Western blot were used to detect the expression changes of EMT-related markers, E-cadherin and Vimentin, in A549 lung cancer cells treated with nicotine; The transposition of β-catenin protein expression was determined by immunofluorescence; Scratch test and Transwell invasion assay were used to detect the effects of nicotine on lung cancer cell migration and invasion.

MiR-449a suppresses cell invasion by inhibiting MAP2K1 in non-small cell lung cancer.

Increasing evidence reveals that deregulation of miRNAs contributes to carcinogenesis of the human non-small cell lung cancer (NSCLC). Our study discovered that the expression of miR-449a was markedly decreased in NSCLC cells with high metastatic capacity and tissues of positive lymph node metastasis. Moreover, our results showed that miR-449a could act as a tumor suppressor by inhibiting the invasion of NSCLC cells in vitro and in vivo.

Pazopanib diminishes non-small cell lung cancer (NSCLC) growth and metastases in vivo.

Background: Anti-angiogenesis has been demonstrated to have a critical role in lung cancer pathogenesis. Here, we characterized the effect of the small-molecule angiogenesis inhibitor pazopanib on non-small cell lung cancer (NSCLC) cells.

Methods: NSCLC cells were tested for viability and migration after incubation with varying concentrations of pazopanib.

[Advances in the relationship between tumor cell metabolism and tumor metastasis].

Intracellular nutrients and the rate of energy flowing in tumor cells are often higher than that in normal cells due to the prolonged stress of tumor-specific microenvironment. In this context, the metabolism of tumor cells provides the fuel of bio-synthesis and energy required for tumor metastasis. Consistent with this, the abnormal metabolism such as extremely active glucose metabolism and excessive accumulating of fatty acid is also discovered in metastatic tumors.

[A meta-analysis of Association between MGMT gene promoter methylation and non-small cell lung cancer].

Background: DNA promoter methylation of the tumor suppressor genes was one of the key mechanism for gene silence. The aim of this study is to investigate the difference of MGMT gene promoter methylation rate in tumor tissue and autologous controls (serum, normal lung tissue and bronchial lavage fluid) in patients with non-small cell lung cancer (NSCLC).

Methods: The databases of Medline, EMBSE, CNKI and Wanfang were searched for selection of published articles of MGMT gene promoter methylation and non-small cell lung carcinoma risk.

[MiR-192 confers cisplatin resistance by targeting Bim in lung cancer].

Background And Objective: Cisplatin is the first-line drug for the chemotherapy of non-small cell lung cancer (NSCLC), but the acquired chemoresistance restricted the effect of its treatment. The aim of this study is to validate the miRNAs related to the Cisplatin resistance in lung cancer and elucidate the molecular mechanisms.

Methods: We performed miRNA microarray and RT-PCR to obtain the aberrant differential expressed miRNAs between A549 and its paired Cisplatin-resistant cell line A549/DDP cells, and then we investigated the biological functions of miR-192, which is the aberrant differential expressed miRNA.

MiR-517a-3p accelerates lung cancer cell proliferation and invasion through inhibiting FOXJ3 expression.

Aims: Aberrant expression of microRNAs (miRNAs) results in alterations of various biological processes (e.g., cell cycle, cell differentiation, and apoptosis) and cell transformation.

MiR-132 suppresses the migration and invasion of lung cancer cells via targeting the EMT regulator ZEB2.

MicroRNAs (miRNAs) are small, non-coding RNAs which can function as oncogenes or tumor suppressor genes in human cancers. Emerging evidence reveals that deregulation of miRNAs contributes to the human non-small cell lung cancer (NSCLC). In the present study, we demonstrated that the expression levels of miR-132 were dramatically decreased in examined NSCLC cell lines and clinical NSCLC tissue samples.

[Advances of hypoxia and lung cancer].

Lung cancer is one of the malignant tumors with fastest growing rates in incidence and mortality in our country, also with largest threat to human health and life. However, the exact mechanisms underlying lung cancer development remain unclear. The microenvironment of tumor hypoxia was discovered in 1955, but hypoxia in lung cancer tissues had not been successfully detected till 2006.

[Research advance on mechanism and application of HATs and HDACs in epithelial-mesenchymal transition of lung cancer].

Lung cancer is one of the most common diseases that endanger health and life of people domestically. A number of recurrence and death of lung cancer originated from metastasis. As a key step in metastasis of lung cancer, epithelial to mesenchymal transition involved down-regulation of E-cadherin, as well as regulated by EMT transcription factors.

Association between P(16INK4a) promoter methylation and non-small cell lung cancer: a meta-analysis.

Background: Aberrant methylation of CpG islands acquired in tumor cells in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates P(16INK4a) gene promoter hypermethylation is involved in non-small cell lung carcinoma (NSCLC), indicating it may be a potential biomarker for this disease. The aim of this study is to evaluate the frequency of P(16INK4a) gene promoter methylation between cancer tissue and autologous controls by summarizing published studies.

[Advances of DNA methylation in early diagnosis of lung cancer].

Lung cancer is the leading cause of cancer-related death and thus a major health problem nowadays. No early diagnostic method is ideal up to now. Changes in DNA methylation occur on early stage of lung cancer.

[Screening of metastasis-related microRNAs in the large-cell lung cancer cell lines with different metastastic potentials].

Background And Objective: MicroRNAs (miRNAs) regulate a wide range of cancer-associated processes, including cell division, proliferation, cell cycle, apoptosis, angiogenesis, invasion, and metastasis. A microarray was performed to analyze metastasis-related miRNAs with different metastastic potentials and to further elucidate their mechanism in the large-cell lung cancer cell lines.

Methods: L9981 and NL9980 cells were harvested, and total RNA was extracted for CY3.

Dickkopf-1 is involved in invasive growth of esophageal cancer cells.

Dickkopf-1 (DKK1) is an inhibitor of Wnt/β-catenin signaling pathway. High levels of DKK1 protein were found in a series of cancers. However, the role of DKK1 in the progression of esophageal carcinoma is not fully understood.

[Enrichment and function research of large cell lung cancer stem cell-like cells].

Background And Objective: There are no universal method to recognize and screen for lung cancer stem cell markers and indicators. Commonly used methods are flow Cytometry and learning from other cancer stem cell sorting tags to sort lung cancer stem cells. But this method has low specificity screening, the workload is huge.

[Screening and identification of microRNAs related to acquired gefitinib-resistance in lung adenocarcinoma cell lines].

Background And Objective: Acquired gefitinib-resistance was closely related to inefficiency of EGFR-TKI treatment in lung adenocarcinoma. However, it was not clear that how microRNAs influenced the acquired gefitinib-resistance in lung adenocarcinoma. The aim of this study is to screen and identify the microRNAs correlated with the acquired gefitinib -resistance in lung adenocarcinoma.

A novel positive feedback loop involving FASN/p-ERK1/2/5-LOX/LTB4/FASN sustains high growth of breast cancer cells.

Aim: To investigate the endogenous signaling pathways associated with high proliferation potential of breast cancer cells.

Methods: Breast cancer cell lines LM-MCF-7 and MCF-7 with high and low proliferation capability were used. The promoter activity of fatty acid synthase (FASN) was examined using luciferase reporter gene assay.

miR-223 regulates migration and invasion by targeting Artemin in human esophageal carcinoma.

Background: Artemin (ARTN) is a neurotrophic factor belonging to the glial cell-derived neurotrophic factor family of ligands. To develop potential therapy targeting ARTN, we studied the roles of miR-223 in the migration and invasion of human esophageal carcinoma.

Methods: ARTN expression levels were detected in esophageal carcinoma cell lines KYSE-150, KYSE-510, EC-9706, TE13, esophageal cancer tissues and paired non-cancerous tissues by Western blot.

[Meta analysis of association between Ser326Cys polymorphism of hOGG1 gene and risk of lung cancer].

Background And Objective: Human 8-hydroxyguanine glycosylase (hOGG1) is one of the DNA repair genes, which can repair damaged DNA by specifically excising 8-dihydro-8-oxoguanine (8-OH-G). A considerable number of studies investigating hOGG1 Ser326Cys polymorphism were in relation to various cancers. However, the association of hOGG1 Ser326Cys polymorphism with risk of lung cancer is inconsistency.

[Mutational analysis of hOGG1 gene promoter in patients with non-small cell lung cancer].

Background And Objective: 8-hydroxygumine DNA glycosylase 1 (OGG1) is a DNA repair enzyme, which can repair damaged DNA by excising 8-dihydro-8-oxoguanine (8-OH-G). Polymorphisms in human OGG1 gene (hOGG1) may alter glycosylase activity, thereby affects its repair to the damaged DNA, resulting in contribution to carcinogenesis. However, an association of genetic variants of hOGG1 promoter with non-small cell lung cancer (NSCLC) remains unclear.

The N-terminal kinase suppressor of Ras complex has a weak nucleoside diphosphate kinase activity.

Introduction: An increasing number of studies have proven that the kinase suppressor of Ras (KSR1) functions as a scaffolding protein that coordinates the assembly of a multiprotein complex containing mitogen-activated protein kinase and its upstream regulators. However, a few studies have reported that KSR1 can activate c-Raf-1. Therefore, whether KSR1 possesses a kinase activity has been an unresolved issue until now.