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Published in: Cancer Cell International 1/2021

Open Access 01-12-2021 | Lymphoma | Primary research

KIF15 is involved in development and progression of Burkitt lymphoma

Authors: Zhao Wang, Meiting Chen, Xiaojie Fang, Huangming Hong, Yuyi Yao, He Huang

Published in: Cancer Cell International | Issue 1/2021

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Abstract

Background

Burkitt lymphoma (BL) is a highly aggressive, fast-growing B-cell non-Hodgkin's lymphoma, manifested in several subtypes, including sporadic, endemic, and immunodeficiency-related forms, the mechanism of which is still not clear. Abundant evidence reported that KIF15 was involved in the progression of human cancer. The emphasis of this study is to explore the functions of KIF15 in the development of BL.

Methods

Firstly, tumor and normal tissues were collected for detecting expression of KIF15 in BL. Lentivirus-mediated shRNA knockdown of KIF15 was used to construct BL cell model, which was verified by qRT-PCR and Western Blot. The cell proliferation was detected by CCK8 assay, cell apoptosis and cell cycle were measured through flow cytometry. Transwell assay was conducted to detect the migration.

Results

We first found that KIF15 is highly expressed in BL. Knockdown of KIF15 can inhibit proliferation and migration, promote apoptosis and arrest the cell cycle. Moreover, KIF15 is involved in BL cell activity through regulating expression of apoptosis-related proteins (Caspase3, Caspase8, HTRA, IGFBP-6, p53, SMAC, sTNF-R1, TNF-β and Bcl-2) and downstream pathways, such as p-Akt, CCND1, CDK6 and PIK3CA.

Conclusions

These findings justify the search for small molecule inhibitors targeting KIF15 as a novel therapeutic strategy in BL.
Appendix
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Metadata
Title
KIF15 is involved in development and progression of Burkitt lymphoma
Authors
Zhao Wang
Meiting Chen
Xiaojie Fang
Huangming Hong
Yuyi Yao
He Huang
Publication date
01-12-2021
Publisher
BioMed Central
Keyword
Lymphoma
Published in
Cancer Cell International / Issue 1/2021
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/s12935-021-01967-z

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