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Krüppel-like factor 5 is upregulated and induces cell proliferation in endometrial cancer

Krüppel-like factor 5 (KLF5) is involved in various cellular processes, such as cell proliferation and survival. KLF5 has been implicated in cancer pathology. The aim of the present study was to investigate the expression levels and function of KLF5 in endometrial cancer. A total of 30 patients, inc...

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Detalles Bibliográficos
Autores principales: Moritake, Tetsuya, Kojima, Junya, Kubota, Kaiyu, Terauchi, Fumitoshi, Isaka, Keiichi, Nishi, Hirotaka
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8100953/
https://www.ncbi.nlm.nih.gov/pubmed/33968200
http://dx.doi.org/10.3892/ol.2021.12745
Descripción
Sumario:Krüppel-like factor 5 (KLF5) is involved in various cellular processes, such as cell proliferation and survival. KLF5 has been implicated in cancer pathology. The aim of the present study was to investigate the expression levels and function of KLF5 in endometrial cancer. A total of 30 patients, including 12 patients with endometrial cancer and 18 with benign gynecological diseases (controls), were enrolled at Tokyo Medical University (Tokyo, Japan) between March 2017 and May 2018. Endometrial cancer and control endometrium tissues were collected, and the expression levels of KLF5 were determined using reverse transcription-quantitative PCR, western blotting and immunohistochemistry. For the functional analyses of KLF5 in endometrial cancer, the present study employed a loss-of-function strategy in the human endometrial cancer cell lines in vitro. Ishikawa and HEC1 cells were transduced with lentiviral constructs expressing shRNAs targeting KLF5. MTT and TUNEL assays were performed in cells after knockdown to analyze the role of KLF5 in cell proliferation and survival. The results revealed that the mRNA and protein expression levels of KLF5 were increased in endometrial cancer tissues. In vitro analyses demonstrated that depletion of KLF5 inhibited cell proliferation and decreased the expression levels of cyclin E1. However, silencing KLF5 did not induce cell death. Overall, these results indicated that KLF5 may be crucial in the tumorigenesis of endometrial cancer and has potential as a therapeutic target.