Evidence map›Paper›PMID 26823919›Full record

ArticleInternational journal of clinical and experimental pathology2015

Knockdown of WISP1 inhibit proliferation and induce apoptosis in ALL Jurkat cells.

Xiaomin Zhang, Xi Chen, Juan Liu, Xiushuai Dong, Yinglan Jin, Yaoyao Tian, Yanming Xue, Liyan Chen, Yuying Chang, Yao Liu and 1 more

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. The role of CCN4/WISP-1 in the cancerous phenotype.Cancer management and research · 2018
    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

11 authors at 1 institution in 1 country.

Xiaomin ZhangDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Xi ChenDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Juan LiuDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Xiushuai DongDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Yinglan JinDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Yaoyao TianDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Yanming XueDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Liyan ChenDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Yuying ChangDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Yao LiuDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Jinghua WangDepartment of Hematology, The Second Affiliated Hospital, Harbin Medical University Harbin 150086, Heilongjiang, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

WISP1, a Wnt-induced secreted protein, has been found to have anticancer activity. ALL is a leading cause of death. Here we investigate the WISP1 effects on ALL Jurkat cells. Cell viability was assessed by CCK-8. Cell cycle and apoptosis were detected by flow cytometry. Mitochondrial membrane potential (MMP) was monitored using TMRM. Generation of reactive oxygen species (ROS) was quantified using DCFH-DA. Western blot was used to detect the expression of cell proliferation and apoptosis related genes. The results showed that knockdown of WISP1 significantly inhibited proliferation of Jurkat cells. Parallelly, cell cycle distribution was increased at G1 phase and apoptotic rate was induced after WISP1 knockdown. Furthermore, knockdown of WISP1 induced apoptosis of Jurkat cells was also associated with loss of MMP and generation of ROS. Western blot results showed that the protein expression p-AKT, PCNA, CDK1, P-ERK, CDK2, VEGF, VEGFR2 and Bcl2 were decreased, while the expression of Bax was up-regulated. In conclusion, WISP1 plays an important role in proliferation and apoptosis of Jurkat cells in mitochondria dependent pathway, the specific mechanisms need further study.

Indexed as

ApoptosisCell ProliferationGene Knockdown TechniquesApoptosis Regulatory ProteinsCCN Intercellular Signaling ProteinsCell Cycle ProteinsDown-RegulationG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansJurkat CellsK562 CellsMembrane Potential, MitochondrialPrecursor Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene ProteinsReactive Oxygen SpeciesApoptosis Regulatory ProteinsCCN4 protein, humanCCN Intercellular Signaling ProteinsCell Cycle ProteinsProto-Oncogene ProteinsReactive Oxygen SpeciesALLapoptosisMMPproliferationROSWISP1

Identifiers

PMID26823919
PMCPMC4713705
OpenAlexW2411379858

What OpenQuestion holds

Textmetadata
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.