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Your search keyword '"Ying Xu"' showing total 4 results
4 results on '"Ying Xu"'

1. Overexpression of MTA3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer

Author

Haiying Li, Liangliang Sun, Ying Xu, Zixuan Li, Wenting Luo, Zhongping Tang, Xueshan Qiu, and Enhua Wang

Subjects
Anatomy and Physiology, Lung Neoplasms, Gene Expression, Down-Regulation, lcsh:Medicine, Lung and Intrathoracic Tumors, Molecular Genetics, Diagnostic Medicine, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Cyclins, Molecular Cell Biology, Genetics, Pathology, Humans, lcsh:Science, Biology, Cell Proliferation, Multidisciplinary, lcsh:R, Computational Biology, Cancers and Neoplasms, Prognosis, Survival Analysis, Non-Small Cell Lung Cancer, Neoplasm Proteins, respiratory tract diseases, Oncology, Lymphatic Metastasis, Disease Progression, Medicine, Clinical Immunology, lcsh:Q, Biomarkers, Molecular Pathology, Research Article, General Pathology
Abstract

The objective of the current study was to investigate the expression pattern and clinicopathological significance of MTA3 in patients with non-small cell lung cancer (NSCLC). The expression profile of MTA3 in NSCLC tissues and adjacent noncancerous lung tissues was detected by immunohistochemistry. MTA3 was overexpressed in 62 of 108 (57.4%) human lung cancer samples and correlated with p-TNM stage (p

Published
2013

2. A Comparative Study of Gene-Expression Data of Basal Cell Carcinoma and Melanoma Reveals New Insights about the Two Cancers

Author

Chi Zhang, Xizeng Mao, Ying Xu, Minesh Mehta, Juan Cui, and Kun Xu

Subjects
Oncology, Skin Neoplasms, Angiogenesis, lcsh:Medicine, Apoptosis, Metastasis, 0302 clinical medicine, Neoplasm Metastasis, lcsh:Science, Skin Tumors, Melanoma, 0303 health sciences, Multidisciplinary, Neovascularization, Pathologic, Statistics, Genomics, 3. Good health, 030220 oncology & carcinogenesis, Disease Progression, Medicine, Research Article, Genetic Markers, medicine.medical_specialty, Malignant Skin Neoplasms, Dermatology, Biology, 03 medical and health sciences, Genome Analysis Tools, Internal medicine, Pancreatic cancer, medicine, Humans, Neoplasm Invasiveness, Basal cell carcinoma, Cell Proliferation, 030304 developmental biology, Cell growth, Gene Expression Profiling, lcsh:R, Computational Biology, Cancers and Neoplasms, Cancer, medicine.disease, Carcinoma, Basal Cell, Anaerobic glycolysis, lcsh:Q, Energy Metabolism, Mathematics
Abstract

A comparative analysis of genome-scale transcriptomic data of two types of skin cancers, melanoma and basal cell carcinoma in comparison with other cancer types, was conducted with the aim of identifying key regulatory factors that either cause or contribute to the aggressiveness of melanoma, while basal cell carcinoma generally remains a mild disease. Multiple cancer-related pathways such as cell proliferation, apoptosis, angiogenesis, cell invasion and metastasis, are considered, but our focus is on energy metabolism, cell invasion and metastasis pathways. Our findings include the following. (a) Both types of skin cancers use both glycolysis and increased oxidative phosphorylation (electron transfer chain) for their energy supply. (b) Advanced melanoma shows substantial up-regulation of key genes involved in fatty acid metabolism (β-oxidation) and oxidative phosphorylation, with aerobic metabolism being far more efficient than anaerobic glycolysis, providing a source of the energetics necessary to support the rapid growth of this cancer. (c) While advanced melanoma is similar to pancreatic cancer in terms of the activity level of genes involved in promoting cell invasion and metastasis, the main metastatic form of basal cell carcinoma is substantially reduced in this activity, partially explaining why this cancer type has been considered as far less aggressive. Our method of using comparative analyses of transcriptomic data of multiple cancer types focused on specific pathways provides a novel and highly effective approach to cancer studies in general.

Published
2012

3. Overexpression of CARMA3 in Non-Small-Cell Lung Cancer Is Linked for Tumor Progression.

Author

Zixuan Li, Lianyue Qu, Qianze Dong, Bo Huang, Haiying Li, Zhongping Tang, Ying Xu, Wenting Luo, Lifeng Liu, Xueshan Qiu, and Enhua Wang

Subjects
LUNG cancer, CANCER patients, CANCER invasiveness, CELL culture, CANCER cells, CELL proliferation
Abstract

We aimed to investigate the clinical significance of the expression of novel scaffold protein CARMA3 in non-small-cell lung cancer (NSCLC) and the biological function of CARMA3 in NSCLC cell lines. We observed moderate to high CARMA3 staining in 68.8% of 141 NSCLC specimens compared to corresponding normal tissues. The overexpression of CARMA3 was significantly correlated with TNM stage (P = 0.022) and tumor status (P = 0.013). CARMA3 upregulation also correlated with a shorter survival rate of patients of nodal status N0 (P = 0.042)as well as the expression of epidermal growth factor receptor (EGFR) (P = 0.009). In EGFR mutation positive cases, CARMA3 expression was much higher (87.5%) compared to nonmutation cases (66.1%). In addition, we observed that knockdown of CARMA3 inhibits tumor cell proliferation and invasion, and induces cell cycle arrest at the boundary between the G1 and S phase. We further demonstrated a direct link between CARMA3 and NF-kB activation. The change of biological behavior in CARMA3 knockdown cells may be NF-kB-related. Our findings demonstrated, for the first time, that CARMA3 was overexpressed in NSCLC and correlated with lung cancer progression, EGFR expression, and EGFR mutation. CARMA3 could serve as a potential companion drug target, along with NF-kB and EGFR in EGFR-mutant lung cancers. [ABSTRACT FROM AUTHOR]

Published
2012
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4. CCL21/CCR7 Prevents Apoptosis via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells.

Author

Ying Xu, Lifeng Liu, Xueshan Qiu, Zihui Liu, Haiying Li, Zixuan Li, Wenting Luo, and Enhua Wang1,2

Subjects
*CHEMOKINE receptors, *CELL proliferation, *APOPTOSIS, *LUNG cancer, *CANCER cells, *MESSENGER RNA, *WESTERN immunoblotting
Abstract

Previously, we confirmed that C-C chemokine receptor 7 (CCR7) promotes cell proliferation via the extracellular signalregulated kinase (ERK) pathway, but its role in apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. A549 and H460 cells of NSCLC were used to examine the effect of CCL21/CCR7 on apoptosis using flow cytometry. The results showed that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant decline in the percent of apoptosis. Western blot and real-time PCR assays indicated that activation of CCR7 significantly caused upregulation of anti-apoptotic bcl-2 and downregulation of pro-apoptotic bax and caspase-3, but not p53, at both protein and mRNA levels. CCR7 small interfering RNA significantly attenuated these effects of exogenous CCL21. Besides, PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished these effects of CCL21/CCR7. Coimmunoprecipitation further confirmed that there was an interaction between p-ERK and bcl-2, bax, or caspase-3, particularly in the presence of CCL21. These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC. [ABSTRACT FROM AUTHOR]

Published
2012
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