Evidence map›Paper›PMID 27888634›Full record

ArticleOncotarget2016

Targeting protein kinase CK2 suppresses bladder cancer cell survival via the glucose metabolic pathway.

Xiaolei Zhang, Xiao Yang, Chengdi Yang, Peng Li, Wenbo Yuan, Xiaheng Deng, Yidong Cheng, Pengchao Li, Haiwei Yang, Jun Tao and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Protein Kinase CK2 in Cancer Energetics.Frontiers in oncology · 2020
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
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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

11 authors at 2 institutions in 1 country.

Xiaolei ZhangDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiao YangDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Chengdi YangDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Peng LiDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Wenbo YuanDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiaheng DengDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yidong ChengDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Pengchao LiDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Haiwei YangDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Jun TaoDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Qiang LuDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Casein kinase 2 (CK2) is a constitutively active serine/threonine kinase that promotes cell proliferation and resists apoptosis. Elevated CK2 expression has been demonstrated in several solid tumors. The expression of CK2α in bladder cancer was elevated in tumor tissues compared with that in adjacent normal tissues. Amplified expression of CK2α was highly correlated with histological grade in bladder cancer(P = 0.024). Knockdown of CK2α in bladder cancer cell lines resulted in a reduction in tumor aerobic glycolysis, accompanied with lower phosphorylated AKT. Moreover, low CK2α levels suppressed cell growth, and similar results could be reproduced after treatment with CX-4945 with a dose-dependent response. CX-4945 inhibited migration and induced apoptosis. Furthermore, knockdown of CK2α decreased the tumorigenicity of bladder cancer cells in vivo. This study is the first to report that CK2 increases glucose metabolism in human bladder cancer. Blocking CK2 function may provide novel diagnostic and potential therapeutic.

Indexed as

AdultAgedAnimalsCasein Kinase IICell Line, TumorCell SurvivalFemaleGlucoseHumansImmunohistochemistryMaleMetabolic Networks and PathwaysMiceMice, Inbred BALB CMiddle AgedNaphthyridinesCasein Kinase IICSNK2A1 protein, humanGlucoseNaphthyridinesPhenazinessilmitasertibbladder cancerCK2αglycolysisoncogeneprognosis

Identifiers

PMID27888634
PMCPMC5349994
OpenAlexW2556827888

What OpenQuestion holds

Textmetadata
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.