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Author(s):  
Lu Zhang ◽  
Fei Wang ◽  
Huijun Yi ◽  
Svetlana P. Ermakova ◽  
Olesya S. Malyarenko ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Tingting Feng ◽  
Yan Zhang ◽  
Sunbin Ling ◽  
Chenyang Xu ◽  
Yingqi Lyu ◽  
...  

Background. PDZ binding kinase (PBK)/T-LAK cell-derived protein kinase (TOPK) is an important mitotic kinase that promotes tumor progression in some cancers. However, the pan-cancer analysis of PBK/TOPK and its role in tumor immunity are limited. Methods. The oncogenic and immune roles of PBK in various cancers were explored using multiple databases, including Oncomine, Human Protein Atlas, ULCAN, Tumor Immune Estimation Resource 2.0, STRING, and Gene Expression Profiling Interactive Analysis 2, and data collected from The Cancer Genome Atlas and Genotype-Tissue Expression Project. Several bioinformatics tools and methods were used for quantitative analyses and panoramic descriptions, such as the DESeq2 and Tumor Immune Dysfunction and Exclusion (TIDE) algorithm. Results. PBK was expressed at higher levels in most solid tumors than in normal tissues in multiple databases. PBK was associated with an advanced tumor stage and grade and a poor prognosis in most cases. PBK was associated with tumor immune cell infiltration in most cases and was especially positively correlated with TAMs, Tregs, MDSCs, and T cell exhaustion in KIRC, LGG, and LIHC. PBK was closely related to TMB, MSI, and immune checkpoint genes in various cancers, and patients with higher expression of PBK in KIRC, LGG, and LIHC had higher TIDE scores and lower immune responses in the predicted results. PBK was closely related to cell cycle regulation and immune-related processes in LIHC and LGG according to GO and KEGG enrichment analyses. Conclusions. PBK may play an oncogenic role in most solid tumors and promotes immune escape, especially in KIRC, LGG, and LIHC. This study suggests the potential value of PBK inhibitors combined with immunotherapy.


2021 ◽  
Author(s):  
Pichaya Thanindratarn ◽  
Ran Wei ◽  
Dylan C. Dean ◽  
Arun Singh ◽  
Noah Federman ◽  
...  

2020 ◽  
Author(s):  
Lama Alhawas ◽  
Karishma S Amin ◽  
Bharath Salla ◽  
Partha P Banerjee

Abstract Despite impressive advances in the treatment of prostate cancer with various efficacious inhibitors along the androgen/androgen receptor axis, eventual development of incurable metastatic Castration-Resistant Prostate Cancer (mCRPC) is inevitable and remains a major clinical challenge. Constitutively active androgen receptor (AR) spliced variants have emerged as primary means of resistance to anti-androgens and androgen synthesis inhibitors. The alternatively spliced AR variant, ARv7, has attracted significant interest due to its constitutively active status in CRPC that drives androgen-independence. Factors that are involved in regulating ARv7 levels in CRPC are not clearly known. We recently demonstrated that a protein kinase, T-LAK cell-originated protein kinase (TOPK) level correlates with the aggressiveness of prostate cancer and its invasive behavior. In this study we investigated whether TOPK plays a role in driving androgen-independence in prostate cancer cells. Our data demonstrate that TOPK overexpression in androgen-dependent LNCaP and VCaP induces ARv7 and drives androgen-independent growth. On the other hand, pharmacological inhibition of TOPK in androgen-independent LNCaP95 and 22Rv1 represses AR transactivation, and AR stability. In summary, this study illustrates a direct role of TOPK in regulating ARv7 and driving androgen-independence in prostate cancer cells.


2020 ◽  
Vol 53 (10) ◽  
Author(s):  
Pichaya Thanindratarn ◽  
Dylan C. Dean ◽  
Scott D. Nelson ◽  
Francis J. Hornicek ◽  
Zhenfeng Duan

2019 ◽  
Vol 10 ◽  
Author(s):  
Xiaoming Fan ◽  
Junyan Tao ◽  
Xin Cai ◽  
Mangaladoss Fredimoses ◽  
Junzi Wu ◽  
...  

2019 ◽  
Vol 147 ◽  
pp. 104366 ◽  
Author(s):  
Shangyun Lu ◽  
Linhu Ye ◽  
Shutao Yin ◽  
Chong Zhao ◽  
Mingzhu Yan ◽  
...  

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Xin Diao ◽  
Danfen Yang ◽  
Yu Chen ◽  
Wentian Liu

AbstractBaicalin is the main bioactive component extracted from the traditional Chinese medicine Baical Skullcap Root, and its anti-tumor activity has been studied in previous studies. PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK), a serine/threonine protein kinase, is highly expressed in many cancer cells and stimulates the tumorigenic properties, and so, it is a pivotal target for agent to cure cancers. We reported for the first time that baicalin suppressed PBK/TOPK activities by directly binding with PBK/TOPK in vitro and in vivo. Ex vivo studies showed that baicalin suppressed PBK/TOPK activity in JB6 Cl41 cells and H441 lung cancer cells. Moreover, knockdown of PBK/TOPK in H441 cells decreased their sensitivity to baicalin. In vivo study indicated that injection of baicalin in H441 tumor-bearing mice effectively suppressed cancer growth. The PBK/TOPK downstream signaling molecules Histone H3 and ERK2 in tumor tissues were also decreased after baicalin treatment. Taken together, baicalin can inhibit proliferation of lung cancer cells as a PBK/TOPK inhibitor both in vitro and in vivo.


2019 ◽  
Vol 10 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Yi Zhang ◽  
Xianjin Yang ◽  
Rong Wang ◽  
Xu Zhang

2018 ◽  
Vol 9 (11) ◽  
Author(s):  
Katharine J. Herbert ◽  
Thomas M. Ashton ◽  
Remko Prevo ◽  
Giacomo Pirovano ◽  
Geoff S. Higgins
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