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Abstract

Citation: Clin Oncol. 2020;5(1):1701.DOI: 10.25107/2474-1663-v5-id1701

Loss of EAF2 Facilitates Pancreatic Cancer Progression via Inhibiting the Apoptosis of the Neoplastic Cells

Cheng Yu-E, Cheng Mei-Lian, Bai Ling, Ji Xiao-Yuan and Hu Hai

Department of Medical Oncology, Shizuishan First People’s Hospital, China Department of Medical Oncology, Affiliated Hospital of Jiangsu University, China Department of Obstetrics and Gynecology, Shizuishan First People’s Hospital, China Department of Endocrine, Shizuishan First People’s Hospital, China Department of Respiratory Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China

*Correspondance to: Hu Hai 

 PDF  Full Text Research Article | Open Access

Abstract:

Line of studies indicated that EAF2 was a tumour suppressor gene in various human malignancies. However, little was known about its role in PDAC. In the present study, we examined the expression and the biological significance of EAF2 in PDAC. We found that EAF2 was decreased in both the cell lines and clinical samples of PDAC. Functionally, EAF2 was revealed to be positively associated with apoptosis, but not proliferation and migration of PDAC cells. Meanwhile, EAF2 expression was examined in a larger sample of PDAC, and the data showed that EAF2 expression was decreased associating with nodal stage of the patient. Statistically, the Kaplan-Meier in combined with the COX regression assay showed that both EAF2 and Bax low expression confers the worst prognosis and function as an independent prognostic factor for the patients. Taken together, our data suggested that EAF2 was anti-tumoral and might be a novel therapeutic target for PDAC.

Keywords:

EAF2; COX regression; PDAC; Apoptosis

Cite the Article:

Yu-E C, Mei-Lian C, Ling B, Xiao-Yuan J, Hai H. Loss of EAF2 Facilitates Pancreatic Cancer Progression via Inhibiting the Apoptosis of the Neoplastic Cells. Clin Oncol. 2020; 5: 1701.

Journal Basic Info

  • Impact Factor: 3.231**
  • H-Index: 11 
  • ISSN: 2474-1663
  • DOI: 10.25107/2474-1663
  • PubMed NLM ID: 101705590

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