Evidence map›Paper›PMID 41639489›Full record

ArticleFunctional & integrative genomics2026

Overexpression, clinical significance and potential mechanisms of protein kinase D1 in hepatocellular carcinoma: multi-omic analyses and pharmacological insights.

Zhen-Dong Chen, Hui-Ping Lu, Yan-Ting Zhan, Fei-Yan He, Liang-Qin Zhu, Yu-Long Deng, Xi-Ni Wei, Min-Ying Yang, Kai Qin, Yu-Xing Tang and 5 more

Abstract read
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In one paragraph

Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Zhen-Dong Chen *Department of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Hui-Ping Lu *Department of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Yan-Ting ZhanDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Fei-Yan HeDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Liang-Qin ZhuDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Yu-Long DengDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Xi-Ni WeiDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Min-Ying YangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Kai QinDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Yu-Xing TangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Ke-Jun WuDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Zhi-Guang HuangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Rong-Quan HeDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China.
Gang ChenDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China. chengang@gxmu.edu.cn.
Yi-Wu DangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, No. 6, Shuangyong Road, Nanning, PR, 530021, China. dangyiwu@gxmu.edu.cn.

Funding

Advanced Innovation Teams and Xinghu Scholars Program of Guangxi Medical University 2022future academic star of Guangxi Medical University WLXSZX23111Guangxi Medical University 2023 Undergraduate Innovation and Entrepreneurship Training Program 202310598173Guangxi Zhuang Autonomous Region Health Committee Scientific Research Project Z-A 20220469Innovation Project of Guangxi Graduate Education YCSW2023238Joint Project on Regional High-Incidence Diseases Research of Guangxi Natural Science Foundation under Grant 2024GXNSFAA010085Medical Excellence Award Funded by the Creative Research Development Grant from the First Affiliated Hospital of Guangxi Medical University 202407National Natural Science Foundation of China NSFC82160762
6 · The paper itself

Abstract

Protein kinase D1 (PRKD1), a serine/threonine kinase of the PKD family, has been implicated in tumor biology, but its role in hepatocellular carcinoma (HCC) remains unclear. We explored PRKD1 expression and function using immunohistochemistry, bulk and single-cell RNA sequencing, and in vitro functional assays. PRKD1 protein levels were significantly elevated in 339 HCC tissues compared to corresponding adjacent non-tumorous samples (11.390 ± 1.560 vs. 6.277 ± 2.357, P < 0.0001). Multicenter bulk transcriptomic data confirmed consistent PRKD1 mRNA overexpression (SMD = 0.26, 95% CI = 0.14-0.39), with single-cell transcriptomic profiling indicating specific enrichment in endothelial cells, smooth muscle cells, and hepatocytes. High PRKD1 expression was associated with advanced tumor stages and worse overall survival. Functionally, PRKD1-associated genes were enriched in extracellular matrix and focal adhesion pathways. Immune profiling revealed positive correlations with M2 macrophages, regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs), and negative correlations with CD8

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsProtein Kinase CCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansSorafenibProtein Kinase Cprotein kinase DSorafenibHepatocellular carcinomaImmune microenvironmentImmunohistochemistryNitidine chlorideProtein kinase D1Tyrosine kinase inhibitors

Identifiers

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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 Socratic graph.