Evidence map›Paper›PMID 35402071›Full record

ArticleMolecular therapy. Nucleic acids2022

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Lei Xia, Qing Han, Xuehui Duan, Yinjie Zhu, Jiahua Pan, Baijun Dong, Weiliang Xia, Wei Xue, Jianjun Sha

Abstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. The mFrontiers in pharmacology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Research progress of mAsian journal of andrology
    Review
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.

Lei XiaDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Qing HanSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Xuehui DuanDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Yinjie ZhuDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Jiahua PanDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Baijun DongDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Weiliang XiaSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Wei XueDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.
Jianjun ShaDepartment of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor splice variant 7 (AR-v7), a constitutively active transcription factor, plays a crucial role in the progression of castration-resistant prostate cancer (CRPC). Here, we found that the cleavage and polyadenylation specificity factor 1 (CPSF1) (the largest subunit of the multi-protein cleavage and polyadenylation specificity complex), regulated by the E3 ubiquitin ligases SIAH1, promoted AR-v7 expression. The data from microarray-based analysis and clinical specimen-based analysis showed that SIAH1 expression was decreased in PCa and was negatively correlated with aggressive phenotypes of PCa. SIAH1 repressed PCa cell growth and invasion under castrate conditions. SIAH1 directly interacted with CPSF1 and promoted ubiquitination and degradation of CPSF1. CPSF1 expression was negatively correlated with SIAH1 expression, but positively with PCa progression. CPSF1 overexpression switched the AR splicing pattern and facilitated the generation of the oncogenic isoform (AR-v7) by binding to the AAUAAA polyadenylation signal contained in AR-cryptic exon CE3. Functionally, SIAH1 acted as a tumor suppressor in PCa pathogenesis by repressing CPSF1-mediated AR-v7 generation. Finally, we demonstrated that m

Indexed as

androgen receptorARAR-v7CPSF1MT: RNA/DNA Editingprostate cancerSIAH1

Identifiers

PMID35402071
PMCPMC8965770

What OpenQuestion holds

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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.