title: Fentanyl inhibits the invasion and migration of colorectal cancer cells via inhibiting the negative regulation of Ets-1 on BANCR.
abstract: BACKGROUND
  Recent studies have shown the potential anti-tumor effect of fentanyl on colorectal cancer (CRC). However, its underling mechanism is still unclear. Since studies indicates the abnormal expression of transcription factor Ets-1 and BRAF-activated lncRNA (BANCR) in CRC progress, the relationship between Ets-1 and BANCR was investigated here to illustrate the fentanyl-induced mechanism on CRC in vitro.
  
  
  METHODS
  The expression levels of Ets-1 and BANCR were first detected in fentanyl-treated CRC cells. The interaction between Ets-1 and BANCR promoter was verified with chromatin immunoprecipitation assays, as well as corresponding acetylation of histones. The regulation of Ets-1 on BANCR expression was confirmed through luciferase assays and RT-PCR analysis. And, cell clone formation, cell migration and invasion were observed to evaluate the anti-tumor effects of fentanyl. Ets-1 overexpression or co-overexpression with BANCR was further performed by plasmids transfection to show the regulatory role of Ets-1 in fentanyl-induced mechanism.
  
  
  RESULTS
  Fentanyl induced BANCR upregulation and Ets-1 downregulation in CRC cells. Further studies showed that Ets-1 negatively regulated BANCR expression via the deacetylation of histones H3 within BANCR promoter. Moreover, fentanyl induced less cell clone formation, as well as inhibited cell migration and invasion in vitro, while Ets-1 overexpression inhibited fentanyl-induced effects that could be reversed by BANCR co-overexpression.
  
  
  CONCLUSIONS
  Fentanyl showed anti-tumor like effects on CRC cells, including less cell clone formation and inhibited cell migration and invasion. Furthermore, the regulatory role of Ets-1 on BANCR influenced fentanyl-induced mechanism, indicating their potential application in the therapeutic treatment of CRC.
authors: Department of Anesthesiology, Huaihe Hospital, Henan University, Kaifeng 475000, China. Electronic address: axianglx@163.com.
authors: Ai-xiang
authors: AX
authors: Li
authors: Department of Anesthesiology, Huaihe Hospital, Henan University, Kaifeng 475000, China.
authors: Wen-qi
authors: WQ
authors: Xin
authors: Department of Anesthesiology, Huaihe Hospital, Henan University, Kaifeng 475000, China.
authors: Chuan-gen
authors: CG
authors: Ma
mesh_terms: D000970:Antineoplastic Agents / Q000008:administration & dosage; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D015179:Colorectal Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D005283:Fentanyl / Q000008:administration & dosage*; D006801:Humans; D009361:Neoplasm Invasiveness; D011401:Promoter Regions, Genetic / Q000235:genetics; D050784:Proto-Oncogene Protein c-ets-1 / Q000378:metabolism*; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics*; D062085:RNA, Long Noncoding / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; C494041:ETS1 protein, human; D050784:Proto-Oncogene Protein c-ets-1; D062085:RNA, Long Noncoding; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D005283:Fentanyl
keywords: BRAF-activated lncRNA; Colorectal cancer; Ets-1; Fentanyl