Evidence map›Paper›PMID 27486308›Full record

ArticleDrug design, development and therapy2016

SPOCK1 promotes tumor growth and metastasis in human prostate cancer.

Qi Chen, Yuan-Ting Yao, Huan Xu, Yan-Bo Chen, Meng Gu, Zhi-Kang Cai, Zhong Wang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. LINC00562 drives gastric cancer development by regulating miR-4636-AP1S3 axis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cancers · 2021
    Article
  18. Multiomic analysis of the function ofThe Journal of international medical research · 2021
    Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Qi ChenDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Yuan-Ting YaoInstitute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Huan XuDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Yan-Bo ChenDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Meng GuDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Zhi-Kang CaiDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Zhong WangDepartment of Urology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the most diagnosed noncutaneous cancer and ranks as the second leading cause of cancer-related deaths in American males. Metastasis is the primary cause of prostate cancer mortality. Survival rate is only 28% for metastatic patients, but is nearly 100% for patients with localized prostate cancers. Molecular mechanisms that underlie this malignancy remain obscure, and this study investigated the role of SPARC/osteonectin, cwcv, and kazal-like domain proteoglycan 1 (SPOCK1) in prostate cancer progression. Initially, we found that SPOCK1 expression was significantly higher in prostate cancer tissues relative to noncancerous tissues. In particular, SPOCK1 expression was also markedly high in metastatic tissues compared with nonmetastatic cancerous tissues. SPOCK1 expression knockdown by specific short hairpin RNA in PC3 cells was significantly inhibited, whereas SPOCK1 overexpression in RWPE-1 cells promoted cell viability, colony formation in vitro, and tumor growth in vivo. Moreover, the SPOCK1 knockdown in PC3 cells was associated with cell cycle arrest in G0/G1 phase, while the SPOCK1 overexpression in RWPE-1 cells induced cell cycle arrest in S phase. The SPOCK1 knockdown in PC3 cells even increased cell apoptosis. SPOCK1 modulation was also observed to affect cancerous cell proliferation and apoptotic processes in the mouse model of prostate cancer. Additionally, the SPOCK1 knockdown decreased, whereas the SPOCK1 overexpression increased cell migration and invasion abilities in vitro. Injection of SPOCK1-depleted PC3 cells significantly decreased metastatic nodules in mouse lungs. These findings suggest that SPOCK1 is a critical mediator of tumor growth and metastasis in prostate cancer.

Indexed as

AnimalsApoptosisCell CycleCell ProliferationGene Expression ProfilingHumansMaleMiceMice, NudeProstatic NeoplasmsProteoglycansRNA, Small InterferingTumor Cells, CulturedProteoglycansRNA, Small InterferingSPOCK1 protein, humangrowthmetastasisprostate cancerSPOCK1

Identifiers

PMID27486308
PMCPMC4958368
OpenAlexW2483785809

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.