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Knockdown of DNA/RNA-binding protein KIN17 promotes apoptosis of triple-negative breast cancer cells

Effective therapy for breast cancer has been extensively studied worldwide, particularly for triple-negative breast cancer and drug-resistant subtypes. DNA/RNA-binding protein KIN17 (kin17) has been reported to be significantly upregulated in breast cancer cells, and is proposed to serve a role in t...

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Detalles Bibliográficos
Autores principales: Gao, Xiang, Liu, Zhenping, Zhong, Meifeng, Wu, Kunhe, Zhang, Yuzhao, Wang, Hongmei, Zeng, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6313201/
https://www.ncbi.nlm.nih.gov/pubmed/30655766
http://dx.doi.org/10.3892/ol.2018.9597
Descripción
Sumario:Effective therapy for breast cancer has been extensively studied worldwide, particularly for triple-negative breast cancer and drug-resistant subtypes. DNA/RNA-binding protein KIN17 (kin17) has been reported to be significantly upregulated in breast cancer cells, and is proposed to serve a role in the regulation of cell proliferation. The present study further investigated the association of kin17-knockdown with breast cancer cell apoptosis. Cell Counting kit-8, flow cytometry, TUNEL assay and caspase 3/7 analysis were performed on MDA-MB-231 cells to determine the association between kin17 and breast cancer cell apoptosis. In addition, western blot analysis was performed to investigate the mechanism of kin17 in the apoptosis of MDA-MB-231 cells. The results revealed that knockdown of kin17 inhibited proliferation and promoted apoptosis of MDA-MB-231 cells, and suggested a poly (adenosine diphosphate-ribose) polymerase-related mechanism behind the apoptosis of the cells. These findings suggested that kin17 could become a novel target for breast cancer therapy.