Overexpression of LCMR1 is significantly associated with clinical stage in human NSCLC

Chen, Liangan; Liang, Zhixin; Tian, Qing; Li, Chunsun; Ma, Xin; Yang, Zhen; Wang, Ping; Li, Yanqin

doi:10.1186/1756-9966-30-18

Cited by 16 publications

(19 citation statements)

References 15 publications

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“…Therefore, understanding of the carcinogenic mechanisms and genes involved in lung cancer cell's fast growth is of much importance in developing more precise treatments compared to conventional treatment methods. Recent discoveries in terms of the molecular basis of cancer brought fundamental changes in cancer treatment (Chen et al, 2011;Skrzypski et al, 2011). One of them is usage of small interfering RNA (siRNA) to manipulate the targeting genes for the prevention of certain cancer…”

Section: Introductionmentioning

confidence: 99%

Silencing of the COPS3 Gene by siRNA Reduces Proliferation of Lung Cancer Cells Most Likely via induction of Cell Cycle Arrest and Apoptosis

Wang

Cui²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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The COPS3 gene has stimulating effect on cell proliferation and progression of osteosarcomas and related cells. However, the features of COPS3 and its potential application as a therapeutic target in other cancers has not yet been studied. In this study, therefore, the effect of COPS3 silencing via COPS3 siRNA on lung cancer cell proliferation was examined. Expression levels of COPS3 gene in COPS3 siRNA infected cells and control siRNA infected cells were compared with real time PCR and Western blot analysis. Cell proliferation levels were comprehensively analyzed by MTT, BrdU incorporationy, and colony formation assays. For mechanistic assessment the effects of COPS3 silencing on cell cycle and apoptosis were analyzed using flow cytometry. Results showed that successful silencing of the COPS3 gene at both translational and transcriptional levels significantly reduced the proliferation and colony formation by lung cancer cells (p<0.01). Flow cytometry showed cell cycle arrest in the G0/G1 phase after COPS3 silencing, and more importantly, apoptosis was induced as a result of COPS3 knockdown, which negatively affected cell survival. Therefore, these results provide another piece of important evidence that the COPS3 gene expressed in lung cancer cells may play a critical role in stimulating proliferation. Down-regulation of COPS3 could significantly inhibit lung cancer cell growth, which was most likely mediated via induction of cell cycle arrest in G0/G1 phase and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Silencing of the COPS3 Gene by siRNA Reduces Proliferation of Lung Cancer Cells Most Likely via induction of Cell Cycle Arrest and Apoptosis

Wang

Cui²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Subsequently, genetic studies implicated the ROX3 gene in proper expression of genes controlled by diverse regulatory pathways, consistent with the idea that it has a general role in transcriptional regulation [36, 37]. In human cells, MED19 is also known as LCMR1 (Lung Cancer Metastasis Related Protein 1) because of its overexpression in some lung cancers [38]. …”

Section: The S Cerevisiae Mediator Complexmentioning

confidence: 74%

Origins and activity of the Mediator complex

Conaway

2011

Seminars in Cell & Developmental Biology

101

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The Mediator is a large, multisubunit RNA polymerase II transcriptional regulator that was first identified in Saccharomyces cerevisiae as a factor required for responsiveness of Pol II and the general initiation factors to DNA binding transactivators. Since its discovery in yeast, Mediator has been shown to be an integral and highly evolutionarily conserved component of the Pol II transcriptional machinery with critical roles in multiple stages of transcription, from regulation of assembly of the Pol II initiation complex to regulation of Pol II elongation. Here we provide a brief overview of the evolutionary origins of Mediator, its subunit composition, and its remarkably diverse collection of activities in Pol II transcription.

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“…LCMR1 was overexpressed in NSCLC and its expression was significantly associated with the clinical stage of the disease. These results suggest that LCMR1 plays a critical role in the oncogenesis of lung cancer (4).…”

Section: Introductionmentioning

confidence: 67%

“…Lung cancer metastasis-related protein 1 (LCMR1) is a novel gene cloned from PLA-801, a poorly differentiated human large-cell lung carcinoma cell line, using a differential display polymerase chain reaction technique in our laboratory in 2002 (4). Information regarding this gene has been submitted to the National Center for Biotechnology Information (NCBI), and a Genbank accession number (AY148462) has been assigned.…”

Section: Introductionmentioning

confidence: 99%

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Suppression of lung cancer metastasis-related protein 1 promotes apoptosis in lung cancer cells

Tian

et al. 2012

International Journal of Molecular Medicine

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Lung cancer is one of the most common human cancers and the leading cause of cancer-related death worldwide. The identification of lung cancer associated genes is essential for the diagnosis and treatment of this disease. Lung cancer metastasis-related protein 1 (LCMR1) is a novel gene cloned by differential display polymerase chain reaction in our laboratory. This study was designed to investigate the role of LCMR1 in the generation of apoptosis in lung cancer cells. RNA interference (RNAi) approach was used to knock down LCMR1 in lung cancer cells. The impacts of LCMR1 knockdown on the apoptosis of lung cancer cells were assessed using flow cytometry, quantitative real-time RT-PCR and western blotting. The results demonstrated that the inhibition of LCMR1 by RNAi enhanced apoptotic activity in lung cancer cells and this process required the involvement of p53. In addition, LCMR1 knockdown resulted in the upregulation of Bax and downregulation of Mcl-1. In conclusion, LCMR1 suppresses apoptosis in lung cancer cells and this effect is associated with multiple apoptosis-related proteins, including p53, Bax and Mcl-1. These results provide new insights into the potential role of LCMR1 in the regulation of lung cancer carcinogenesis.

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Overexpression of LCMR1 is significantly associated with clinical stage in human NSCLC

Cited by 16 publications

References 15 publications

Silencing of the COPS3 Gene by siRNA Reduces Proliferation of Lung Cancer Cells Most Likely via induction of Cell Cycle Arrest and Apoptosis

Silencing of the COPS3 Gene by siRNA Reduces Proliferation of Lung Cancer Cells Most Likely via induction of Cell Cycle Arrest and Apoptosis

Origins and activity of the Mediator complex

Suppression of lung cancer metastasis-related protein 1 promotes apoptosis in lung cancer cells

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