Our previous work showed that a proliferation-inducing ligand (APRIL) was involved in the development of acute lymphoblastic leukemia (ALL) in children. However, the precise role of APRIL in ALL remains unknown. To investigate this issue, we silenced and overexpressed APRIL in Nalm-6 ALL cells using short hairpin RNA targeting the APRIL gene and recombinant human APRIL, respectively, and evaluated the effects on cell proliferation, apoptosis, and migration. APRIL mRNA and APRIL and matrix metalloproteinase-2 protein levels were evaluated by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and western blott, respectively. We found that APRIL expression was reduced by shRNA-mediated knockdown in Nalm-6 cells; this was associated with a decrease in cell proliferation (P<0.05). APRIL knockdown increased apoptosis (P<0.01) but suppressed cell migration along with matrix metalloproteinase-2 protein level. Overexpressing recombinant human APRIL had the opposite effects in each case (P<0.05). These results demonstrate a link between APRIL expression and ALL development and suggest that APRIL is a potential therapeutic target for ALL treatment.
*Department of Pediatrics, Affiliated Hospital of Nantong University
‡Medical College of Nantong University, Nantong, Jiangsu Province
†Department of Pediatrics, People’s Hospital of Yangzhong City, Yangzhong, The People’s Republic of China
B.S. and Z.X. contributed equally.
Supported by the Women and Children Health Science Foundation of Jiangsu Province (no. F201405 and F201649); China Postdoctoral Science Foundation (no. 2016M591899); Postdoctoral Science Foundation of Jiangsu Province (no. 1601094C); and Youth Key Talent of Medical Foundation of Jiangsu Province (no. QNRC2016684).
The authors declare no conflict of interest.
Reprints: Youjia Wu, PhD, Department of Pediatrics, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, Jiangsu, 226001, The People’s Republic of China (e-mail: email@example.com).
Received November 20, 2017
Accepted March 20, 2018