Evidence map›Paper›PMID 28943928›Full record

ArticleOncology letters2017

RecQ helicase BLM regulates prostate cancer cell proliferation and apoptosis.

Xiaosong Qian, Sujuan Feng, Dawei Xie, Dalin Feng, Yihang Jiang, Xiaodong Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. 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
1.3field-weighted citation impact, top 19% 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, 29 citations in OpenAlex.

  1. UpregulatedImmunoTargets and therapy · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells.Oxidative medicine and cellular longevity · 2019
    Article
  19. Article
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

6 authors at 2 institutions in 1 country.

Xiaosong QianInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Sujuan FengInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Dawei XieInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Dalin FengInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Yihang JiangInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Xiaodong ZhangInstitute of Uro-Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is a common malignant tumor and the second leading cause of morbidity and mortality in men worldwide. Considering the prevalence and effects of PCa in males, an understanding of the molecular mechanisms underlying PCa tumorigenesis are essential and may provide novel therapeutic strategies for treating PCa. Bloom syndrome protein (BLM) is a member of the RecQ helicase family. The major function of BLM is to uncoil the double-stranded DNA structure. It has previously been demonstrated that BLM acts as a 'genome caretaker', and dysregulation of BLM function has been implicated in the development of multiple tumor types; however, its potential for inducing PCa tumorigenesis remains undetermined. The present study aimed to explore the function of BLM in PCa progression. Reverse transcription-polymerase chain reaction, immunohistochemistry and western blot analyses were performed to detect the BLM expression pattern in PCa patients and cell lines. The proliferation, and migration and invasion capacities of prostate cells were determined by EdU and Transwell assays following transfection with BLM-targeting short hairpin RNA (shRNA). The expression of BLM was significantly increased in PCa tissues and PC3 cells compared with non-PCa tissues and benign prostatic hyperplasia cells. Knockdown of BLM via shRNA inhibited PCa cell proliferation, and promoted PCa cell apoptosis. Notably, reducing the expression of BLM had no effect on the migration or invasive abilities of PCa cells. These results suggest that downregulation of BLM may alleviate PCa development, providing a novel perspective for PCa tumorigenesis and a potential therapeutic target for PCa.

Indexed as

apoptosisbloom syndrome proteinproliferationprostate cancerRecQ

Identifiers

PMID28943928
PMCPMC5604177
OpenAlexW2740636419

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.