IL-32α has differential effects on proliferation and apoptosis of human melanoma cell lines.
BACKGROUND
Interleukin-32 (IL-32) is a recently recognized intracellular, proinflammatory cytokine which may play a role in cancer metastasis and patient survival. The role of IL-32 in cancer, especially its direct effect on cancer cells, is not well understood.


METHODS
Clonogenic assay, PCNA staining, Quick Cell Proliferation assay, TUNEL staining, and caspase-3 activity assay were used to investigate the in vitro role for IL-32α in human melanoma growth. We further investigated the possible molecular mechanisms using RT-PCR and immunohistochemical staining.


RESULTS
Exogenous administration of IL-32α inhibited proliferation of the HTB-72 human melanoma cell line, but had little effect on other melanoma cell lines. Inhibition of proliferation in HTB-72 correlated with increased expression of p21 and p53. IL-32α administration also increased apoptosis in HTB-72. This finding correlated with increased expression of TRAILR1.


CONCLUSIONS
The data presented suggest a direct effect of IL-32α on the growth of human melanoma and give some insight into the mechanisms which may in part govern this effect. J. Surg. Oncol. 2016;113:364-369. © 2016 Wiley Periodicals, Inc.
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.|South Texas Veterans Health Care System, San Antonio, Texas.
Michael B
MB
Nicholl
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.|Luohu Hospital, Shenzhen, China.
Xuhui
X
Chen
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.|Luohu Hospital, Shenzhen, China.
Chenglu
C
Qin
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.
Qian
Q
Bai
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.
Ziwen
Z
Zhu
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.
Matthew R
MR
Davis
Ellis Fischel Cancer Center, University of Missouri School of Medicine, Columbia, Missouri.|Des Moines University, Des Moines, Iowa.
Yujiang
Y
Fang
D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry; D007378:Interleukins / Q000494:pharmacology*; D008545:Melanoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand / Q000096:biosynthesis; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; C496971:IL32 protein, human; D007378:Interleukins; D053220:Receptors, TNF-Related Apoptosis-Inducing Ligand; C105190:TNFRSF10A protein, human; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53
IL-32; apoptosis; proliferation