Acyl-CoA dehydrogenase long chain expression is associated with esophageal squamous cell carcinoma progression and poor prognosis
Authors Yu DL, Li HW, Wang Y, Li CQ, You D, Jiang L, Song YP, Li XH
Received 22 April 2018
Accepted for publication 11 September 2018
Published 31 October 2018 Volume 2018:11 Pages 7643—7653
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Dr Faris Farassati
Dong-Lin Yu,1,* Hong-Wei Li,2,* Yang Wang,2 Cun-Qi Li,2 Dong You,2 Lei Jiang,3 Yi-Peng Song,2 Xing-Hua Li2
1Department of Basic Theory of Traditional Chinese Medicine, Binzhou Medical University, Yantai, People’s Republic of China; 2Department of Radiotherapy, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, People’s Republic of China; 3Department of Pathology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, People’s Republic of China
*These authors contributed equally to this work
Background: Acyl-CoA dehydrogenase long chain (ACADL) was revealed to have a correlation with malignant progression of cancer. However, whether ACADL plays a role in clinical therapy remains unclear. The clinicopathological role of ACADL in esophageal squamous cell carcinoma (ESCC) will be discussed in this study.
Materials and methods: The expression of ACADL was analyzed via real-time PCR and Western blotting to assess mRNA and protein levels in ESCC cell lines and normal esophageal epithelial cells (NEECs), in six paired ESCC tumors and relative normal tissues. Furthermore, immunohistochemical staining was performed on 135 paraffin-embedded ESCC specimens to assess ACADL expression. The clinicopathological significance of ACADL expression was further investigated via survival analysis and Cox regression analysis.
Results: ACADL was found to be markedly upregulated in ESCC cell lines when compared with NEECs. Moreover, various experiments such as quantitative real-time PCR, Western blot, and immunohistochemical analyses all revealed that ACADL expression was increased in all six paired ESCC tumors and matched normal tissues. Furthermore, immunohistochemical analysis revealed an increased level of ACADL protein expression in all 135 paraffin-embedded samples from ESCC patients, which increased with disease progression.
Conclusion: We demonstrated that ACADL is overexpressed in ESCC, both in cell lines and clinical specimens. ACADL is found to be a vital regulator in ESCC progression and can predict a worse outcome for ESCC patients, suggesting that ACADL might be a valuable molecule to be targeted for clinical therapy of ESCC treatment.
Keywords: ESCC, ACADL, prognosis, IHC, target
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