Review
Cell Biology
Ziping Han, Lingzhi Li, Yuyou Huang, Haiping Zhao, Yumin Luo
Summary: Accumulating evidence suggests PBK/TOPK plays a role in mitosis and cell-cycle progression, with potential therapeutic implications in cancer. However, further research is needed to understand the applicability of PBK/TOPK inhibitors in clinical practice, given their overexpression in normal and pathological proliferative cells.
Article
Endocrinology & Metabolism
Kejing Zhu, Xueting Cheng, Shuman Wang, Hong Zhang, Yu Zhang, Xiong Wang, Yonggang Chen, Jinhu Wu
Summary: Our study identified and validated the functional importance of TOPK as a potential molecular target for prolactinoma treatment. The TOPK inhibitor showed promising effects in suppressing tumor cell proliferation, migration, inducing apoptosis, reducing PRL secretion, and inhibiting tumor growth, potentially through mediating the p38 MAPK pathway.
FRONTIERS IN ENDOCRINOLOGY
(2022)
Article
Oncology
Kaijing Wang, Jie Wei, Jing Ma, Qingge Jia, Yixiong Liu, Jia Chai, Junpeng Xu, Tianqi Xu, Danhui Zhao, Yingmei Wang, Qingguo Yan, Shuangping Guo, Xinjian Guo, Feng Zhu, Linni Fan, Mingyang Li, Zhe Wang
Summary: TOPK and p-JAK2 are highly expressed in BL tissues. TOPK binds to and is phosphorylated by JAK2, playing a vital role in BL cell proliferation and tumorigenesis. The JAK2/TOPK/histone H3 axis is key in BL progression.
Article
Biochemistry & Molecular Biology
Dong-Hee Lee, Yu-Jeong Jeong, Ju-Young Won, Hye-In Sim, Yoon Park, Hyung-Seung Jin
Summary: PBK/TOPK, a serine/threonine kinase, is associated with tumor immunity and prognosis in colon cancer. Elevated PBK/TOPK expression predicts a favorable outcome and is positively correlated with immune infiltration levels and T-cell cytotoxicity gene expression in colon cancer.
Review
Oncology
Hai Huang, Mee-Hyun Lee, Kangdong Liu, Zigang Dong, Zeayoung Ryoo, Myoung Ok Kim
Summary: Cancer is a major global public health problem, and TOPK serves as a crucial factor in cell cycle regulation and mitotic progression. Abnormal overexpression or activation of TOPK in various cancers is associated with cancer development, dissemination, and poor prognosis. Targeting TOPK can be an important approach for cancer prevention and therapy.
Article
Oncology
Liang Qiao, Jinling Ba, Jiping Xie, Ruiping Zhu, Yi Wan, Min Zhang, Zeyu Jin, Zicheng Guo, Jiaxuan Yu, Sijing Chen, Yongqiang Yao
Summary: This study found that PBK/TOPK is overexpressed in breast cancer and is closely related to pathological features and patient prognosis. Breast cancer patients with high expression of PBK/TOPK have a poor prognosis, providing a potential indicator for breast cancer management.
WORLD JOURNAL OF SURGICAL ONCOLOGY
(2022)
Article
Endocrinology & Metabolism
Qi Zhu, Simin Yao, Yishan Dong, Dan Liu, Huiyan Wang, Peipei Jiang, Chenyan Dai, Haining Lv, Chenrui Cao, Zhenhua Zhou, Limin Wang, Wenjing Gou, Xiwen Zhang, Guangfeng Zhao, Yali Hu
Summary: The study found that genes related to cell division and cycle were inhibited, while inflammation and oxidative stress increased in thin endometrium patients. The decreased expression of PBK in HESCs affected cell proliferation and apoptosis.
REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY
(2022)
Article
Multidisciplinary Sciences
Jinxin Li, Huimin Sun, Meiling Fu, Zeyuan Zheng, Chunlan Xu, Kunao Yang, Yankuo Liu, Zuodong Xuan, Yang Bai, Jianzhong Zheng, Yue Zhao, Zhiyuan Shi, Chen Shao
Summary: This study demonstrates that high expression of TOPK in RCC promotes PD-L1 expression by activating ERK2 and TGF-beta/Smad pathways. TOPK is also shown to inhibit CD8(+) T cell infiltration and function, promoting immune escape in RCC. Inhibition of TOPK enhances CD8(+) T cell infiltration, activation, anti-PD-L1 therapeutic efficacy, and synergistically enhances anti-RCC immune response.
Article
Chemistry, Physical
He Wang, Xun Zhu, Yizhen Zhao, Yongjian Zang, Jianwen Zhang, Ying Kang, Zhiwei Yang, Peng Lin, Lei Zhang, Shengli Zhang
Summary: This study investigated the micromechanism of TOPK, a potential target for cancer therapy, through modeling and simulation. The results showed that the ENI motif of the NTPM is regulated by the N-C interaction zone, and mutations at specific residues promote conformational changes and phosphorylation. Furthermore, allosteric effects induce structural changes that are important for activation or binding. These findings provide insights for designing inhibitors and understanding the regulatory mechanisms of TOPK monomers.
JOURNAL OF PHYSICAL CHEMISTRY B
(2022)
Article
Oncology
Shubin W. Shahab, Christianna M. Roggeveen, Jiarong Sun, Haritha Kunhiraman, Leon F. McSwain, Kyle Juraschka, Sachin A. Kumar, Olivier Saulnier, Michael D. Taylor, Matthew Schniederjan, Robert W. Schnepp, Tobey J. MacDonald, Anna Marie Kenney
Summary: Children with G3 MB have a poor prognosis due to the lack of targeted therapy. The upregulation of LIN28B pathway is associated with worse survival in G3 MB. Inhibition of this pathway can reduce tumor growth in preclinical models.
MOLECULAR ONCOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Hongmin Cao, Mei Yang, Yufeng Yang, Jiayan Fang, Yejia Cui
Summary: This study revealed that high expression of PBK was correlated with oxaliplatin resistance in hepatocellular carcinoma cells, potentially providing a promising therapeutic target for treating HCC.
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
(2021)
Article
Oncology
Fangling Cheng, Xueyan Wan, Baofeng Wang, Youwei Li, Peng Peng, Sanpeng Xu, Chao Han, Feng Mao, Dongsheng Guo
Summary: This study successfully established a novel primary glioblastoma cell line, GWH04, and examined its genetic characteristics and tumor parameters. The results indicated that GWH04 had similar proliferation rate as U87 cell line, but faster than GL15 cell line, and possessed high capacity for clone formation and tumor formation. GWH04 showed resistance to temozolomide in drug sensitivity test. The genetic analysis revealed aneuploid karyotype and chromosomal structural abnormalities in GWH04, as well as mutations in several key genes. These findings suggest that GWH04 will be a valuable tool for human GBM studies in both in vitro and in vivo settings.
INTERNATIONAL JOURNAL OF ONCOLOGY
(2022)
Article
Pharmacology & Pharmacy
Yuqi Yang, Zhuo-Xun Wu, Jing-Quan Wang, Qiu-Xu Teng, Zi-Ning Lei, Sabrina Lusvarghi, Suresh V. Ambudkar, Zhe-Sheng Chen, Dong-Hua Yang
Summary: OTS964 is a potent inhibitor of TOPK that interacts with ABCG2 to affect multidrug resistance, and has an upregulating effect on ABCG2 transporter. It enhances resistance to ABCG2 substrate-drugs by inhibiting efflux function mediated by ABCG2.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Yuqi Yang, Qiu-Xu Teng, Zhuo-Xun Wu, Jing-Quan Wang, Zi-Ning Lei, Sabrina Lusvarghi, Suresh Ambudkar, Ning Ji, Zhe-Sheng Chen
Summary: Overexpression of ABCBC1 significantly reduces sensitivity to OTS964 in cells and tumors, which can be antagonized by verapamil. OTS964 also induces resistance to other ABCBC1 substrate-drugs by stimulating ATPase activity and upregulating ABCBC1 expression levels, with comparable affinity to the substrate-binding site of human ABCBC1 protein.
Article
Biotechnology & Applied Microbiology
Jieke Cui, Rong Guo, Yingjun Wang, Yue Song, Xuewen Song, Hongwen Li, Xiaoqin Song, Jiwei Li
Summary: This study identifies TOPK as a potential therapeutic target for DLBCL and demonstrates that acetylshikonin can suppress DLBCL cell growth through targeting TOPK signaling.
Article
Biochemistry & Molecular Biology
Awais A. Mughal, Zanina Grieg, Havard Skjellegrind, Artem Fayzullin, Mustapha Lamkhannat, Mrinal Joel, M. Shakil Ahmed, Wayne Murrell, Einar O. Vik-Mo, Iver A. Langmoen, Biljana Stangeland
Article
Oncology
Artem Fayzullin, Frode A. Tuvnes, Havard K. Skjellegrind, Jinan Behnan, Awais A. Mughal, Iver A. Langmoen, Einar O. Vik-Mo
EXPERIMENTAL CELL RESEARCH
(2016)
Article
Biochemistry & Molecular Biology
J. Behnan, B. Stangeland, S. A. M. Hosainey, M. Joel, T. K. Olsen, F. Micci, J. C. Glover, P. Isakson, J. E. Brinchmann
Article
Cell Biology
Jinan Behnan, Biljana Stangeland, Tiziana Langella, Gaetano Finocchiaro, Giovanni Tringali, Torstein R. Meling, Wayne Murrell
CELL DEATH & DISEASE
(2017)
Article
Multidisciplinary Sciences
Jinan Behnan, Biljana Stangeland, Tiziana Langella, Gaetano Finocchiaro, Wayne Murrell, Jan E. Brinchmann
SCIENTIFIC REPORTS
(2016)
Review
Clinical Neurology
Jinan Behnan, Gaetano Finocchiaro, Gabi Hanna
Correction
Biochemistry & Molecular Biology
Min Guo, Kaveh M. Goudarzi, Shiva Abedi, Melanie Pieber, Elin Sjoberg, Jinan Behnan, Xing-Mei Zhang, Robert A. Harris, Jiri Bartek, Mikael S. Lindstrom, Monica Nister, Daniel Hagerstrand
Article
Biochemistry & Molecular Biology
Min Guo, Kaveh M. Goudarzi, Shiva Abedi, Melanie Pieber, Elin Sjoberg, Jinan Behnan, Xing-Mei Zhang, Robert A. Harris, Jiri Bartek, Mikael S. Lindstrom, Monica Nister, Daniel Hagerstrand
Summary: In this study, SFRP2 was identified as an antagonist of SOX2, capable of inducing a mesenchymal subtype transition in glioma cells. The research confirmed that SFRP2 could decrease tumor sphere formation and stemness, while increasing cell motility; conversely, SOX2 had opposite effects.
Article
Multidisciplinary Sciences
Yizhou Hu, Yiwen Jiang, Jinan Behnan, Mariana Messias Ribeiro, Chrysoula Kalantzi, Ming-Dong Zhang, Daohua Lou, Martin Haring, Nilesh Sharma, Satoshi Okawa, Antonio Del Sol, Igor Adameyko, Mikael Svensson, Oscar Persson, Patrik Ernfors
Summary: The study suggests that Glioblastoma can originate from the brain's blood vessels, and patients with such Glioblastoma have a significantly poorer prognosis.
Article
Oncology
Isha Mondal, Oishika Das, Raymond Sun, Jian Gao, Bohyeon Yu, Aaron Diaz, Jinan Behnan, Abhishek Dubey, Zhipeng Meng, Emad Eskandar, Beisi Xu, Rongze Olivia Lu, Winson S. Ho
Summary: This study demonstrates the important role of the a-isoform of the catalytic subunit of protein phosphatase-2A (PP2Ac) in regulating the immunogenicity of glioma. The deficiency of PP2Ac in glioma cells promotes dendritic cell (DC) cross-presentation, sensitizes tumors to immune-checkpoint blockade and radiotherapy treatment. Loss of PP2Ac increases interferon signaling and reduces the expression of a tumor gene signature associated with worse patient survival.