Evidence map›Paper›PMID 35546143›Full record

ArticleCell death & disease2022

TOPK/PBK is phosphorylated by ERK2 at serine 32, promotes tumorigenesis and is involved in sorafenib resistance in RCC.

Huimin Sun, Jianzhong Zheng, Juanjuan Xiao, Juntao Yue, Zhiyuan Shi, Zuodong Xuan, Chen Chen, Yue Zhao, Wenbin Tang, Shaopei Ye and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 32 citations in OpenAlex.

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  9. Exploring treatment options in cancer: Tumor treatment strategies.Signal transduction and targeted therapy · 2024
    Review
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  11. Review
  12. Article
  13. Article
  14. FYN/TOPK/HSPB1 axis facilitates the proliferation and metastasis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023
    Article
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 1 country.

Huimin Sun *Central Laboratory, Xiang'an Hospital of Xiamen University, Xiamen, 361102, Fujian, China.ORCID 0000-0002-2892-5596
Jianzhong Zheng *School of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Juanjuan Xiao *Cancer Research Institute, the Affiliated Hospital of Guilin Medical University, Guilin, 541001, Guangxi, China.
Juntao YueDepartment of Urology, 985th hospital of PLA, Taiyuan, 030002, Shanxi, China.
Zhiyuan ShiSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Zuodong XuanSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Chen ChenSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Yue ZhaoSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Wenbin TangSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Shaopei YeSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Jinxin LiSchool of Medicine, Xiamen University, Xiamen, 361102, Fujian, China.
Qiumin DengThe Key Laboratory for Endocrine-Related Cancer precision Medicine of Xiamen, Xiamen, 361102, Fujian, China.
Lei ZhangDepartment of Public healthy, Xiamen University, Xiamen, 361102, Fujian, China.
Feng ZhuCancer Research Institute, the Affiliated Hospital of Guilin Medical University, Guilin, 541001, Guangxi, China. fengzhu@hust.edu.cn.
Chen ShaoDepartment of Urology, Xiang'an Hospital of Xiamen University, Xiamen, 361102, Fujian, China. cshao@xah.xmu.edu.cn.ORCID 0000-0002-6818-6660
Xiamen University · CNGuilin Medical University · CN82th Hospital of Pla · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TOPK/PBK (T-LAK Cell-Originated Protein Kinase) is a serine/threonine kinase that is highly expressed in a variety of human tumors and is associated with poor prognosis in many types of human malignancies. Its activation mechanism is not yet fully understood. A bidirectional signal transduced between TOPK and ERK2 (extracellular signal-regulated kinase 2) has been reported, with ERK2 able to phosphorylate TOPK at the Thr9 residue. However, mutated TOPK at Thr9 cannot repress cellular transformation. In the present study, Ser32 was revealed to be a novel phosphorylated site on TOPK that could be activated by ERK2. Phospho-TOPK (S32) was found to be involved in the resistance of renal cell carcinoma (RCC) to sorafenib. Herein, combined a TOPK inhibitor with sorafenib could promoted the apoptosis of sorafenib-resistant RCC. High expression of HGF/c-met contributes to activation of p-TOPK (S32) during the development of sorafenib resistance in RCC. The current research presents a possible mechanism of sorafenib resistance in RCC and identifies a potential diagnostic marker for predicting sorafenib resistance in RCC, providing a valuable supplement for the clinically targeted treatment of advanced RCC.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsCell Transformation, NeoplasticHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesSerineSorafenibMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesPDZ-binding kinaseSerineSorafenib

Identifiers

PMID35546143
PMCPMC9095598
OpenAlexW4280553362

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.