Evidence map›Paper›PMID 39505875›Full record

ArticleCell death & disease2024

KIF1A promotes neuroendocrine differentiation in prostate cancer by regulating the OGT-mediated O-GlcNAcylation.

Qianqian Zhou, Muyi Yang, Jiawei Fu, Xinyu Sun, Jiajia Wang, Hanwen Zhang, Jing Hu, Bo Han

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

8 authors.

Qianqian ZhouThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250000, P R China.
Muyi YangDepartment of Oncology-Pathology, Karolinska Institute, Stockholm, Sweden.
Jiawei FuThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250000, P R China.
Xinyu SunJinan Central Hospital, Shandong University, Jinan, Shandong, 250000, P R China.
Jiajia WangThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250000, P R China.
Hanwen ZhangThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250000, P R China.
Jing HuDepartment of Pathology, Shandong University Qilu Hospital, Jinan, Shandong, 250000, P R China.
Bo HanThe Key Laboratory of Experimental Teratology, Ministry of Education and Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250000, P R China. boh@sdu.edu.cn.ORCID 0000-0003-4966-1398

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82172818National Natural Science Foundation of China (National Science Foundation of China) 82303905National Natural Science Foundation of China (National Science Foundation of China) 82473405Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) L248055
6 · The paper itself

Abstract

Neuroendocrine prostate cancer (NEPC) arises from prostate adenocarcinoma after endocrine treatment failure and implies lethality and limited therapeutic options. Deciphering the molecular mechanisms underlying transdifferentiation from adenocarcinoma to NEPC may provide valuable therapeutic strategies. We performed a pan-cancer differential mRNA abundance analysis and identified that Kinesin-like protein (KIF1A) was highly expressed in NEPC. KIF1A knockdown impaired neuroendocrine(NE) features, including NE marker gene expression, stemness, and epithelial-mesenchymal transition (EMT), whereas KIF1A overexpression promoted these processes. Targeting KIF1A inhibited the growth of NE differentiated prostate cancer (PCa) cells in vitro and in vivo. Mechanistically, KIF1A bound with O-linked N-acetylglucosamine transferase (OGT) and regulated its protein expression and activity. Nuclear accumulation of OGT induced by KIF1A overexpression promoted intranuclear O-GlcNAcylation of β-catenin and OCT4 in nucleus. More importantly, our data revealed that OGT was critical for KIF1A induced NE differentiation and aggressive tumor growth. An OGT inhibitor, OSMI-1, can significantly inhibited NE differentiated PCa cell proliferation in vitro and tumor growth in vivo. Our findings showed that KIF1A promotes NE differentiation to NEPC by regulating the OGT-mediated O-GlcNAcylation. Targeting O-GlcNAcylation may impede the development of NEPC for a group of PCa patients with elevated KIF1A expression.

Indexed as

KinesinsN-AcetylglucosaminyltransferasesProstatic NeoplasmsAnimalsbeta CateninCell DifferentiationCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeOctamer Transcription Factor-3beta CateninKIF1A protein, humanKinesinsN-AcetylglucosaminyltransferasesOctamer Transcription Factor-3OGT protein, human

Identifiers

PMID39505875
PMCPMC11542072

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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.