title: Elevated TrkA receptor expression is associated with all-trans retinoic acid-induced neuroblastoma differentiation.
abstract: Neuroblastoma is the most common and one of the deadliest among pediatric tumors; however, a subset of infants with neuroblastoma display spontaneous regression. The mechanism of spontaneous regression remains to be elucidated. TrkA plays an essential role in the differentiation and functionality of neurons; abundant TrkA expression is associated with favorable prognosis of neuroblastoma. All-trans retinoic acid (ATRA), a first-line drug for acute promyelocytic leukemia (APL) treatment, has been shown to induce differentiation and inhibit cell growth. Neuroblastoma tissues in our hospital inpatient were collected, primary cell culture was performed, and the cells were separated and purified to be cell line. Trypan blue exclusion was used to count the numbers of cells alive, morphological changes were observed under the phase-contrast microscope. RT-PCR was used to determine the expression level of TrkA. In this study, a human neuroblastoma cell line was successfully established; in addition, we demonstrated that ATRA induces growth arrest and promotes the differentiation of neuroblastoma cells. In addition, ATRA was shown to significantly increase the levels of TrkA mRNA expression. Therefore, we concluded that the elevated expression of the TrkA receptor is associated with ATRA-induced growth arrest and differentiation o neuroblastoma cells. The results of this study provide a theoretical basis for the clinical application of differentiation-inducing ATRA for neuroblastoma therapy.
authors.affiliation: Department of Pediatric Surgery, Qingdao Women and Children Hospital, Qingdao, Shandong, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Gao
authors.affiliation: Department of Pediatric Surgery, Linyi People's Hospital, No. 27, Jiefang Road, Linyi, Shandong, China.
authors.forename: C F
authors.initials: CF
authors.lastname: Chen
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Dong
authors.affiliation: Department of Biochemistry, Medical College, Qingdao University, Qingdao, Shandong, China.
authors.forename: L
authors.initials: L
authors.lastname: Hou
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: X
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: Y L
authors.initials: YL
authors.lastname: Zhi
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: X
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: H T
authors.initials: HT
authors.lastname: Lu
authors.affiliation: Department of Pediatric Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
authors.forename: H Y
authors.initials: HY
authors.lastname: Zhang
mesh_terms: D059447:Cell Cycle Checkpoints / Q000187:drug effects / Q000235:genetics; D002454:Cell Differentiation / Q000187:drug effects* / Q000235:genetics*; D045744:Cell Line, Tumor; D015870:Gene Expression; D006801:Humans; D009447:Neuroblastoma / Q000235:genetics* / Q000473:pathology*; D012333:RNA, Messenger / Q000235:genetics; D020917:Receptor, trkA / Q000235:genetics*; D014212:Tretinoin / Q000494:pharmacology*
chemical_list: D012333:RNA, Messenger; D014212:Tretinoin; D020917:Receptor, trkA