Evidence map›Paper›PMID 34215720›Full record

ArticleCell death & disease2021

FAM64A is an androgen receptor-regulated feedback tumor promoter in prostate cancer.

Yingchen Zhou, Longhua Ou, Jinming Xu, Haichao Yuan, Junhua Luo, Bentao Shi, Xianxin Li, Shangqi Yang, Yan Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Frontiers in oncology · 2023
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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 4 institutions in 1 country.

Yingchen ZhouDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China.ORCID 0000-0001-7615-6157
Longhua OuDepartment of Urology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Jinming XuDepartment of Urology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Haichao YuanDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China.
Junhua LuoDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China.
Bentao ShiDepartment of Urology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Xianxin LiDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China. xianxinli@163.com.ORCID 0000-0002-5690-0150
Shangqi YangDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China. yangshangqi88@aliyun.com.
Yan WangDepartment of Urology, Peking University Shenzhen Hospital, Institute of Urology, Shenzhen PKU-HKUST Medical Center, Shenzhen, China. wangyan198614@163.com.ORCID 0000-0001-5906-7435
Peking University Shenzhen Hospital · CNShenzhen Second People's Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShenzhen International Travel Health Care Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocrine therapy for prostate cancer (PCa) mainly inhibits androgen receptor (AR) signaling, due to increased androgen synthesis and AR changes, PCa evolved into castration-resistant prostate cancer (CRPC). The function of Family With Sequence Similarity 64 Member A (FAM64A) and its association with prostate cancer has not been reported. In our research, we first reported that FAM64A is up-regulated and positively associated with poor prognosis of patients with prostate cancer (PCa) by TCGA database and immunohistochemistry staining. Moreover, knockdown of FAM64A significantly suppressed the proliferation, migration, invasion, and cell cycle of PCa cells in vitro. Mechanistically, FAM64A expression was increased by dihydrotestosterone (DHT) through direct binding of AR to FAM64A promoter, and notably promoted the proliferation, migration, invasion, and cell cycle of androgen-dependent cell line of PCa. In addition, abnormal expression of FAM64A affects the immune and interferon signaling pathway of PCa cells. In conclusion, FAM64A was up-regulated by AR through directly binding to its specific promoter region to promote the development of PCa, and was associated with the immune mechanism and interferon signaling pathway, which provided a better understanding and a new potential for treating PCa.

Indexed as

Binding SitesCell CycleCell MovementCell ProliferationDatabases, GeneticGene Expression Regulation, NeoplasticHumansInterferonsIntracellular Signaling Peptides and ProteinsMaleMiddle AgedNeoplasm InvasivenessNuclear ProteinsPC-3 CellsPromoter Regions, GeneticProstatic NeoplasmsAR protein, humanInterferonsIntracellular Signaling Peptides and ProteinsNuclear ProteinsPIMREG protein, humanReceptors, Androgen

Identifiers

PMID34215720
PMCPMC8253826
OpenAlexW3176695881

What OpenQuestion holds

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LicenceCC BY
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.