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The downregulation of miR-200c promotes lactate dehydrogenase A expression and non-small cell lung cancer progression.
This study was aimed to investigate the function and mechanism of microRNA-200c (miR-200c) in the progression of non-small cell lung cancer (NSCLC). A total of 76 patients diagnosed as NSCLC were enrolled in this study. Then, the expression level of miR-200c in NSCLC tissues and cell lines was investigated using the quantitative realtime polymerase chain reaction (RT-qPCR) method. We found the expression of miR200c was significantly reduced in NSCLC tissues and cell lines compared with in normal lung tissues and human bronchial epithelial cell line. Force the expression of miR-200c using miR-200c mimic significantly suppre...
Source: Oncology Research - January 14, 2018 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Long Intergenic Noncoding RNA 319 (linc00319) Promotes Cell Proliferation and Invasion in Lung Cancer Cells by Directly Downregulating the Tumor Suppressor MiR-32.
In conclusion, linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32. PMID: 28800794 [PubMed - as supplied by publisher]
Source: Oncology Research - August 14, 2017 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

MiR-449a Suppresses LDHA-Mediated Glycolysis to Enhance the Sensitivity of Non-Small Cell Lung Cancer Cells to Ionizing Radiation.
Authors: Li L, Liu H, Du L, Xi P, Wang Q, Li Y, Liu D Abstract MicroRNA dysregulation contributes to malignant progression, dissemination and profound treatment resistance in multiple cancers. MiR-449a is recognized as a tumor suppresser. However, roles of miR-449a in lung cancers initiation and progression are largely unrevealed. Our study aims to investigate roles and the underlying mechanism of miR-449a in modulating sensitivity to ionizing radiation (IR) in non-small cell lung cancers (NSCLC). Lung cancer cells were transfected with miR-449a mimics or negative control and exposed to IR, levels of target protein...
Source: Oncology Research - August 14, 2017 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

MicroRNA-138 Inhibits Cell Growth, Invasion, and EMT of Non-Small Cell Lung Cancer Via SOX4/p53 Feedback Loop.
In this study, we investigated the biological functions and molecular mechanisms of miR-138 in NSCLC cell lines, discussing whether it could be a therapeutic biomarker of NSCLC in the future. In our study, we found that miR-138 is down-regulated in NSCLC tissues and cell lines. Moreover, the low level of miR-138 was associated with increased expression of SOX4 in NSCLC tissues and cell lines. Up-regulation of miR-138 significantly inhibited proliferation of NSCLC cells. In addition, invasion and EMT of NSCLC cells was suppressed by overexpression of miR-138. However, down-regulation of miR-138 promoted cell growth and meta...
Source: Oncology Research - June 28, 2017 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Gamma Irradiation Upregulates B-cell Translocation Gene 2 to Attenuate Cell Proliferation of Lung Cancer Cells Through JNK and NF κB Pathways.
In this study, we aimed to explore the role of γ-ray treatment and correlation with BTG2 in cell proliferation, apoptosis and cell cycle arrest regulation in lung cancer cell line. A549 cell viability, apoptosis rate, and cell cycle were investigated after γ-ray treatment. Then we used siRNA for BTG2 to detect the effect of BTG2 knockdown on the progress of γ-ray treated lung cancer cell. Finally, we investigated the singling pathway that γ-ray might regulate BTG2. We found that γ-ray inhibited A549 cell viability, promoted apoptosis and cell cycle arrest. While the BTG2 knockdown could relieve the effect caused by γ...
Source: Oncology Research - March 3, 2017 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells.
In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of PFTK1 endowed NSCLC cells with decreased migration and invasion abilities, as well as epithelial-mesenchymal transition (EMT) progress in A549 cells. A mechanistic study showed that knockdown of PFTK1 inhibited the expression of β-catenin, cyclin D1, and c-Myc in A549 cells. In summary, we report that small interfering RNA (siRNA)-PF...
Source: Oncology Research - July 29, 2016 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Inhibition of Lung Carcinoma A549 Cell Growth by Knockdown of Hexokinase 2 In Situ and In Vivo.
In this study, we explored the functional role of HK2 in lung cancer cell proliferation and tumorigenesis and determine its expression profile in lung cancer. HK2 expression was increased in primary lung cancer tissues of patients. Knocking down HK2 expression by small interfering RNA (siRNA) inhibited cell proliferation in lung cancer cells and nude mice. Thus, HK2 is required for sustained proliferation and survival of tumor cells in vitro and in vivo, and its aberrant expression may contribute to the pathogenesis of lung cancer. Thus, our study provided evidence that HK2 functions as a novel oncogene in lung cancer and ...
Source: Oncology Research - January 24, 2016 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Cullin7 is required for lung cancer cell proliferation and is overexpressed in lung cancer.
In this study, we explored the functional role of Cullin7 in lung cancer cell proliferation and tumorigenesis and determined its expression profile in lung cancer. Knocking down Cullin7 expression by small interfering RNA (siRNA) in lung cancer cells inhibited cell proliferation and elevated the expression of p53, p27, and p21 proteins. The enhanced p53 expression resulted from activation of the DNA damage response pathway. Cullin7 knockdown markedly suppressed xenograft tumor growth in vivo in mice. Moreover, Cullin7 expression was increased in primary lung cancer tissues of humans. Thus, Cullin7 is required for sustained...
Source: Oncology Research - February 26, 2015 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

FOXM1 Regulated by ERK Pathway MediatesTGF-β1-Induced EMT in NSCLC.
Authors: Kong FF, Zhu YL, Yuan HH, Wang JY, Zhao M, Gong XD, Liu F, Zhang WY, Wang CR, Jiang B Abstract FOXM1, a member of the Forkhead transcriptional family, plays an important role in the EMT process, and transforming growth factor-β1 (TGF-β1) has been identified as the most potent factor that can independently induce EMT in various types of cancer cells. Here we examine the important role of FOXM1 in TGF-β1-induced EMT and investigate the mechanism underlying the relationship between TGF-β1 and FOXM1. Lentivirus-mediated transfection was used to stably upregulate the expression of FOXM1, and a small interfe...
Source: Oncology Research - February 26, 2015 Category: Cancer & Oncology Tags: Oncol Res Source Type: research

Leptin promotes metastasis by inducing an epithelial-mesenchymal transition in a549 lung cancer cells.
Abstract Leptin, an adipocyte-derived cytokine associated with obesity, has been reported to participate in carcinogenesis. Epithelial-mesenchymal transition (EMT) is also considered as a key event in tumor metastasis. The aim of this study is to investigate the mechanism of leptin in the promotion of EMT leading to metastasis in A549 lung cancer cells. We investigated the effect of leptin on migration of A549 cells using wound healing and transwell assays. The incidence of EMT in A549 cells was examined by real-time PCR and immunofluorescence staining. The expression of TGF-β in A549 cells was detected by real-t...
Source: Oncology Research - February 17, 2014 Category: Cancer & Oncology Authors: Feng H, Liu Q, Zhang N, Zheng L, Sang M, Feng J, Zhang J, Wu X, Shan B Tags: Oncol Res Source Type: research