Transcription factor KLF13 inhibits AKT activation and suppresses the growth of prostate carcinoma cells.

Abstract

BACKGROUND:

Krüppel-like factor 13 (KLF13), a member of the KLF family, is involved in the development of immunological diseases and tumor progression. However, the expression patterns and potential functions of KLF13 in prostate carcinoma are still unknown. Here, we aimed to study the roles and mechanisms of KLF13 in prostate cancer.

METHODS:

The expression levels of KLF13 was detected by Immunohistochemistry in prostate tumor tissues and the paired non-tumor tissues. The effects of KLF13 up-regulation was tested by performing CCK8, cell colon formation, flow cytometric analysis and measurement of tumor proliferation in nude mice. Signaling pathway was analyzed by Western blot.

RESULTS:

The current study, for the first time, found that KLF13 was downregulated in prostate tumor tissues as compared to the paired non-tumor tissues. The overexpression of KLF13 dramatically inhibited cell proliferation and induced apoptosis by suppressing the AKT pathway in human prostate cancer cells. Moreover, the ectopic expression of KLF13 efficiently delayed the onset of PC3 xenografts and inhibited the tumor growth in vivo.

CONCLUSIONS:

KLF13 functions as a tumor suppressor protein in PCa, and the pharmacological activation of KLF13 might represent a potential approach for the treatment of prostate cancer.

• Authors: Qiang Wang, Ruixian Peng, Boshi Wang, Jifeng Wang, Wandong Yu, Yongzhong Liu, Guowei Shi
• Journal: Cancer biomarkers : section A of Disease markers (Cancer Biomark) Vol. 22 Issue 3 Pg. 533-541 ( 2018) ISSN: 1875-8592 [Electronic] Netherlands
• PMID: 29843216 (Publication Type: Journal Article)

Chemical References

• Biomarkers, Tumor
• Cell Cycle Proteins
• KLF13 protein, human
• Kruppel-Like Transcription Factors
• Repressor Proteins
• Proto-Oncogene Proteins c-akt

Topics

• Animals
• Apoptosis (genetics)
• Biomarkers, Tumor
• Cell Cycle Proteins (metabolism)
• Cell Line, Tumor
• Cell Proliferation
• Cell Survival (genetics)
• Disease Models, Animal
• Enzyme Activation
• Gene Expression
• Gene Expression Regulation, Neoplastic
• Heterografts
• Humans
• Immunohistochemistry
• Kruppel-Like Transcription Factors (metabolism)
• Male
• Mice
• Prostatic Neoplasms (genetics, metabolism, pathology)
• Proto-Oncogene Proteins c-akt (metabolism)
• Repressor Proteins (metabolism)