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Poster display session

1054 - Characterization of a Novel Tumor-Suppressor Gene CHL1 at 3p26.3 in Esophageal Squamous Cell Carcinoma

Date

11 Sep 2017

Session

Poster display session

Topics

Translational Research;  Oesophageal Cancer

Presenters

Hongyan Wang

Citation

Annals of Oncology (2017) 28 (suppl_5): v22-v42. 10.1093/annonc/mdx363

Authors

H. Wang

Author affiliations

  • Internal Medicine, Henan Cancer Hospital, 450008 - Zhengzhou/CN
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Resources

Abstract 1054

Background

The major histologic subtype of esophageal cancer, esophageal squamous cell carcinoma (ESCC), is one of the most common cancers and has been ranked as the sixth leading cause of cancer-related deaths in the world. Using human genome U133 Plus 2.0 GeneChip, we identified gene down-regulation of Cell adhesion molecule L1 like (CHL1) located at 3p26.3 in ESCC. We analysed its down-regulated expression, biological effects and prognostic significance in ESCC.

Methods

To determine whether the down-regulation of CHL1 was associated with aberrant methylation. Methylation-specific PCR (MSP) was performed in ESCCs and their corresponding non-tumor tissues, as well as ESCC cell lines. Loss of heterozygosity status of CHL1 was evaluated by fluorescence in situ hybridization (FISH). The effects of CHL1 re-expression or knockdown were determined in proliferation, invasion and metastasis assay. CHL1 target genes and related pathways were identified by protein mass spectrometry, co-immunoprecipitation (Co-IP), immunofluorescence (IF) and western-blot. Clinical impact of CHL1 down-regulated expression was assessed in 287 patients with ESCC.

Results

The results showed that down-regulation of CHL1 was significantly associated with allele loss (14/21) and promoter methylation (19/21; P

Conclusions

CHL1 plays a pivotal tumor suppressive role in ESCC; its down-regulated expression is an independent prognostic factor of patient with ESCC.

Clinical trial identification

Legal entity responsible for the study

Henan Cancer Hospital

Funding

None

Disclosure

All authors have declared no conflicts of interest.

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