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E-Poster Display

1478P - FLVCR1 predicts poor prognosis and promotes malignant phenotype in esophageal squamous cell carcinoma via upregulating CSE1L

Date

17 Sep 2020

Session

E-Poster Display

Topics

Tumour Site

Oesophageal Cancer

Presenters

wenguang ye

Citation

Annals of Oncology (2020) 31 (suppl_4): S841-S873. 10.1016/annonc/annonc284

Authors

W. ye1, S. Zhou2

Author affiliations

  • 1 Gastroenterology, Taizhou Hospital Of Zhejiang Provincial, 317000 - Linhai/CN
  • 2 Radiation Oncology, Taizhou Hospital Of Zhejiang Provincial, 317000 - Linhai/CN

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Abstract 1478P

Background

Dysregulation of feline leukemia virus subgroup C receptor 1(FLVCR1) expression has been investigated in several tumors. However, the expression and role of FLVCR1 in esophageal squamous cell carcinoma (ESCC) remain largely unknown. In this study, we explored the clinical and biological significance of FLVCR1 in the progress of ESCC.

Methods

We performed immunohistochemical staining (IHC) to measure the expression of FLVCR1 in ESCC tissues and adjacent normal tissues. Celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, wound healing assay, transwell migration, and invasion assay were applied to assess the effects of FLVCR1 on the ability of proliferation, apoptosis, migration, and invasion in ESCC cell lines. Coimmunoprecipitation (CO-IP) and liquid chromatography-mass spectrometry (LC-MS) were used to identify protein interaction between FLVCR1 and CSE1L. Lentivirus was applied to establish ectopic expression patterns of FLVCR1 and CSE1L for ESCC cell lines. By in vivo imaging system (IVIS), the functions of FLVCR1 on the growth and metastatic capability of ESCC cells were investigated in a xenograft model and a tail vein metastasis model.

Results

Elevated expression of FLVCR1 was detected in ESCC tissues. FLVCR1 high expression predicted poor survival. Upregulated FLVCR1 was positively correlated with advanced tumor-node-metastasis (N) stage and tumor-node-metastasis (TNM) stage. FLVCR1 knockdown inhibited cell proliferation and colony formation ability, induced cell apoptosis, and repressed cell migration and invasion of ESCC in vitro. Inhibition of FLVCR1 markedly repressed tumorigenicity and metastasis of ESCC cells in vivo. Mechanistically, chromosome segregation 1–like (CSE1L) was identified to interact with FLVCR1 using CO-IP assay. Moreover, the inhibitory effect of FLVCR1 knockdown on proliferation and migration was counteracted by the exogenous expression of CSE1L.

Conclusions

FLVCR1 plays a pivotal role in ESCC cell survival, growth and migration, which may be partially dependent upon the protein interaction with CSE1L. Besides, FLVCR1 can be applied as a clinical prognostic marker for patients with ESCC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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