Coxsackievirus and adenovirus receptor promotes antitumor activity of oncolytic adenovirus H101 in esophageal cancer

Ma,Junfen; Zhao,Jimin; Lu,Jing; Jiang,Yanan; Yang,Hongyan; Li,Pei; Zhao,Mingyao; Liu,Kangdong; Dong,Ziming

doi:10.3892/ijmm.2012.1133

Coxsackievirus and adenovirus receptor promotes antitumor activity of oncolytic adenovirus H101 in esophageal cancer

Authors:
- Junfen Ma
- Jimin Zhao
- Jing Lu
- Yanan Jiang
- Hongyan Yang
- Pei Li
- Mingyao Zhao
- Kangdong Liu
- Ziming Dong
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Affiliations: Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, P.R. China
Published online on: September 19, 2012 https://doi.org/10.3892/ijmm.2012.1133
Pages: 1403-1409

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Abstract

Esophageal cancer is an intractable disease due to late diagnosis, high incidence of post-surgical locoregional recurrence and frequent distant metastasis. Oncolytic adenovirus (Ad) vectors are a promising method for cancer treatment. The H101 virus is a recombinant Ad which has replication-selective properties and replicates only in tumor cells. The coxsackievirus and adenovirus receptor (CAR) is considered a surrogate marker that monitors the outcome of Ad-mediated gene therapy. Accumulating evidence indicates that CAR expression levels are lower in various types of tumors such as ovarian, lung, breast and bladder when compared to their normal counterparts. In this study, we reported that trichostatin A (TSA) induced the expression of CAR in esophageal squamous cell carcinoma (ESCC) cell lines through the MAPK/ERK1/2 signaling pathway. The expression levels of CAR were positively related with the antitumor activity of H101. Our results suggest that TSA increases the antitumor activity of the oncolytic adenovirus H101 through the MAPK/ERK pathway.

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