Evidence map›Paper›PMID 38235618›Full record

ArticleTranslational oncology2024

MALAT1 promotes FOXA1 degradation by competitively binding to miR-216a-5p and enhancing neuroendocrine differentiation in prostate cancer.

Fanchang Zeng, Daoyuan Li, Xinli Kang, Qinghui Wu, Mi Song, Zhewen Ou, Zuobing Yang, Jing Yang, Liumei Luo

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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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

9 authors at 2 institutions in 1 country.

Fanchang ZengDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Daoyuan LiDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Xinli KangDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Qinghui WuDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Mi SongDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Zhewen OuDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Zuobing YangDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Jing YangDepartment of Urology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China.
Liumei LuoDepartment of Scientific Research, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), No. 19, Xiuhua Road, Xiuying District, Haikou, Hainan 570311, China. Electronic address: luoliumei@163.com.
Hainan General Hospital · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesProstate cancer (PC) is a leading cause of cancer-related death in males worldwide. Neuroendocrine differentiation (NED) is a feature of PC that often goes undetected and is associated with poor patient outcomes. Long non-coding RNAs (lncRNAs), microRNAs (miRNAs/miRs), and messenger RNAs (mRNAs) play important roles in the development and progression of PC.

methodsIn this study, we used transcriptome sequencing and bioinformatics analysis to identify key regulators of NED in PC. Specifically, we examined the expression of PC-related lncRNAs, miRNAs, and mRNAs in PC cells and correlated these findings with NED phenotypes.

resultsOur data revealed that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and zinc finger protein 91 (ZFP91) were upregulated in PC, while miR-216a-5p was down-regulated. Ectopic expression of MALAT1 induced NED and promoted malignant phenotypes of PC cells. Furthermore, we found that MALAT1 competitively bound to miR-216a-5p, upregulated ZFP91, and promoted the degradation of forkhead box A1 (FOXA1), a key gene involved in NED of PC.

conclusionTaken together, these results suggest that MALAT1 plays an oncogenic role in NED and metastasis of PC via the miR-216a-5p/ZFP91/FOXA1 pathway. Our study highlights the potential of targeting this pathway as a novel therapeutic strategy for PC.

Indexed as

ceRNA mechanismFOXA1 degradationMALAT1miR-216a-5pNeuroendocrine differentiationProstate cancerZFP91

Identifiers

PMID38235618
PMCPMC10628887
OpenAlexW4388178256

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.