Evidence map›Paper›PMID 36813922›Full record

ArticleCell death and differentiation2023

PDLIM3 supports hedgehog signaling in medulloblastoma by facilitating cilia formation.

Jie Zhang, Yijun Yang, Xinhua Li, Gen Li, Takuya Mizukami, Yanli Liu, Yuan Wang, Guoqiang Xu, Heinrich Roder, Li Zhang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
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  12. KIAA0753 enhances osteoblast differentiation suppressed by diabetes.Journal of cellular and molecular medicine · 2024
    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

11 authors at 2 institutions in 2 countries.

Jie ZhangPediatric Cancer Center, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Yijun YangCell Signaling and Epigenetics Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA, USA.
Xinhua LiPediatric Cancer Center, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Gen LiPediatric Cancer Center, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Takuya MizukamiMolecular Therapeutic Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA, USA.
Yanli LiuCollege of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Yuan WangPediatric Cancer Center, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Guoqiang XuCollege of Pharmaceutical Sciences, Soochow University, Suzhou, China.ORCID 0000-0002-4753-4769
Heinrich RoderMolecular Therapeutic Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA, USA.
Li ZhangPediatric Cancer Center, College of Pharmaceutical Sciences, Soochow University, Suzhou, China. lizhang@suda.edu.cn.
Zeng-Jie YangCell Signaling and Epigenetics Program, Fox Chase Cancer Center, Temple University Health System, Philadelphia, PA, USA. Zengjie.Yang@fccc.edu.ORCID 0000-0003-1205-0964
Soochow University · CNFox Chase Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated levels of PDLIM3 expression are frequently detected in sonic hedgehog (SHH) group of medulloblastoma (MB). However, the possible role of PDLIM3 in MB tumorigenesis is still unknown. Here, we found that PDLIM3 expression is necessary for hedgehog (Hh) pathway activation in MB cells. PDLIM3 is present in primary cilia of MB cells and fibroblasts, and such cilia localization is mediated by the PDZ domain of PDLIM3 protein. Deletion of PDLIM3 significantly compromised cilia formation and interfered the Hh signaling transduction in MB cells, suggesting that PDLIM3 promotes the Hh signaling through supporting the ciliogenesis. PDLIM3 protein physically interacts with cholesterol, a critical molecule for cilia formation and hedgehog signaling. The disruption of cilia formation and Hh signaling in PDLIM3 null MB cells or fibroblasts, was significantly rescued by treatment with exogenous cholesterol, demonstrating that PDLIM3 facilitates the ciliogenesis through cholesterol provision. Finally, deletion of PDLIM3 in MB cells significantly inhibited their proliferation and repressed tumor growth, suggesting that PDLIM3 is necessary for MB tumorigenesis. Our studies elucidate the critical functions of PDLIM3 in the ciliogenesis and Hh signaling transduction in SHH-MB cells, supporting to utilize PDLIM3 as a molecular marker for defining SHH group of MB in clinics.

Indexed as

Cerebellar NeoplasmsMedulloblastomaCarcinogenesisCholesterolCiliaHedgehog ProteinsHumansLIM Domain ProteinsMicrofilament ProteinsCholesterolHedgehog ProteinsLIM Domain ProteinsMicrofilament ProteinsPDLIM3 protein, human

Identifiers

PMID36813922
PMCPMC10154305
OpenAlexW4321489645

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.