NDLI: LDHA is necessary for the tumorigenicity of esophageal squamous cell carcinoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yao, Feng Zhao, Tiejun Zhong, Chenxi Zhu, Ji Zhao, Heng
Description	Country affiliation: China Author Affiliation: Yao F ( Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huaihai Rd, Shanghai, 200030, China.)
Abstract	Esophageal squamous cell carcinoma (ESCC) is one of the most common lethal tumors in the world, and the development of new therapeutic targets is needed. Recent studies have shown that aerobic glycolysis, also known as the Warburg effect, mediated the anti-apoptotic effects in cancer cells. Lactate dehydrogenase A (LDHA) which executed the final step of aerobic lactate production has been reported to be involved in the tumor progression. However, the function of LDHA in ESCC has not been investigated. In this study, it was found that LDHA was up-regulated in ESCC clinical samples. Knockdown of the expression of LDHA inhibited cell growth and cell migration in vitro as well as tumorigenesis in vivo. With regard to the molecular mechanism, silencing the expression of LDHA was related to decreased AKT activation and cyclin D1 expression and increased cleavage of PARP and caspase 8. Taken together, our findings suggest that LDHA plays an important role in the progression of ESCC by modulating cell growth, and LDHA might be a potential therapeutic target in ESCC.
File Format	HTM / HTML
ISSN	10104283
Issue Number	1
Volume Number	34
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2013-02-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Carcinoma, Squamous Cell Enzymology Cell Transformation, Neoplastic Esophageal Neoplasms L-lactate Dehydrogenase Metabolism Adult Apoptosis Genetics Pathology Caspase 8 Cell Cycle Cell Line, Tumor Cell Movement Cell Proliferation Cyclin D1 Biosynthesis Enzyme Activation Female Glycolysis Humans Isoenzymes Male Middle Aged Poly(adp-ribose) Polymerases Proto-oncogene Proteins C-akt Rna Interference Rna, Small Interfering Signal Transduction Up-regulation Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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