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01.12.2014 | Research | Ausgabe 1/2014 Open Access

World Journal of Surgical Oncology 1/2014

Overexpression of lactate dehydrogenase-A in human intrahepatic cholangiocarcinoma: its implication for treatment

World Journal of Surgical Oncology > Ausgabe 1/2014
Yaping Yu, Minqi Liao, Ruiwen Liu, Jian Chen, Hao Feng, Zan Fu
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1477-7819-12-78) contains supplementary material, which is available to authorized users.
Yaping Yu, Minqi Liao contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

YY and ML carried out the molecular genetic studies, participated in the clinical studies and drafted the manuscript. ZF participated in the design of the study and performed the manuscript review. RL carried out the literature research and data acquisition. JC participated in the data analysis and statistical analysis. HF carried out the manuscript editing. All authors read and approved the final manuscript.



Previous studies have shown that lactate dehydrogenase-A (LDH-A) is strongly expressed in several malignancies, that LDH-A expression is associated with poor prognosis, and that LDH-A inhibition severely diminishes tumorigenicity. However, little is known about the implications of LDH-A expression in intrahepatic cholangiocarcinoma. The purpose of this study was to investigate the expression of LDH-A and to clarify its effect on intrahepatic cholangiocarcinoma.


We studied the expression of LDH-A in tissue samples from patients with intrahepatic cholangiocarcinoma (n = 54) using the ultrasensitive surfactant protein (S-P) immunohistochemical method. We then inhibited LDH-A using small hairpin RNA (shRNA) in the cholangiocarcinoma cell line HuCCT-1 in vitro to study the role it plays in promoting growth and escaping apoptosis.


We report that LDH-A was overexpressed in 52 of 54 (96%) paraffin-embedded cancer tissue samples and 0 of 54 para-carcinoma tissue samples. Reduction of LDH-A by RNA interference (RNAi) inhibited cell growth and induced apoptosis in HuCCT-1 cells. This result correlated with the elevation of cytoplasmic reactive oxygen species (ROS) levels.


LDH-A expression is closely correlated with histopathological variables of intrahepatic cholangiocarcinoma, indicating that LDH-A may serve as a new treatment target.
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