KLF16 overexpression deleteriously affects the proliferation and migration of retinoblastoma by transcriptionally repressing BCL2L15

Krüppel-like factors (KLFs) are transcription factors that control the expression of downstream genes. The role of KLFs has been reported in cancers. KLF16 promotes the proliferation of gastric cancer cells by upregulating p21, while suppresses the tumorigenesis of glioma through targeting TFAM. The...

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Published in:Biochemical and biophysical research communications 2020-09, Vol.529 (4), p.977-983
Main Authors: Zhang, Jing-xue, Yan, Xue-jing, Wu, Shen, Liu, Qian, Ma, Jian-min
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - genetics
BCL2L15
Cell Cycle - genetics
Cell Line, Tumor
Cell Movement
Cell Proliferation
Epithelial Cells - metabolism
Epithelial Cells - pathology
Gene Expression Regulation, Neoplastic
Genes, Reporter
Humans
KLF16
Kruppel-Like Transcription Factors - antagonists & inhibitors
Kruppel-Like Transcription Factors - genetics
Kruppel-Like Transcription Factors - metabolism
Luciferases - genetics
Luciferases - metabolism
Proliferation
Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors
Proto-Oncogene Proteins c-bcl-2 - genetics
Proto-Oncogene Proteins c-bcl-2 - metabolism
Retinal Neoplasms - genetics
Retinal Neoplasms - metabolism
Retinal Neoplasms - pathology
Retinal Pigment Epithelium - metabolism
Retinal Pigment Epithelium - pathology
Retinoblastoma
Retinoblastoma - genetics
Retinoblastoma - metabolism
Retinoblastoma - pathology
RNA, Small Interfering - genetics
RNA, Small Interfering - metabolism
Signal Transduction
Transcription, Genetic
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Summary:Krüppel-like factors (KLFs) are transcription factors that control the expression of downstream genes. The role of KLFs has been reported in cancers. KLF16 promotes the proliferation of gastric cancer cells by upregulating p21, while suppresses the tumorigenesis of glioma through targeting TFAM. The function of KLF16 is controversial in cancer development. In this study, we aimed to investigate the role of KLF16 in retinoblastoma (RB). KLF16 was highly expressed in RB tissues and cells. Overexpression of KLF16 promoted the proliferation, growth and migration of RB cells. By contrast, KLF16 interference showed opposite effects. Cell cycle arrest and apoptosis were induced or repressed by KLF16 knockdown or overexpression, respectively. Mechanistically, BCL2 like 15 (BCL2L15), an apoptosis gene, was negatively regulated by KLF16. Luciferase reporter and ChIP assay showed that KLF16 transcriptionally repressed the expression of BCL2L15 by binding to its promoter. BCL2L15 was lowly expressed in RB tissues. Additionally, overexpression of BCL2L15 inhibited the proliferation and increased the apoptosis in RB cells. Our study identifies that KLF16 contributes to RB cell proliferation and migration by negatively regulating BCL2L15. •KLF16 is highly expressed in retinoblastoma tissues and cells.•KLF16 promotes the proliferation, growth and migration of retinoblastoma cells.•KLF16 contributes to retinoblastoma cell proliferation by negatively regulating BCL2L15.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2020.06.027