Evidence map›Paper›PMID 25544759›Full record

ArticleOncotarget2015

Silencing of CXCR4 sensitizes triple-negative breast cancer cells to cisplatin.

Sixian Liang, Xun Peng, Xiaoli Li, Ping Yang, Linhao Xie, Yaochen Li, Caiwen Du, Guojun Zhang

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy.Medical oncology (Northwood, London, England) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Three-dimensional models of breast cancer-fibroblasts interactions.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Sixian LiangDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Xun PengDepartment of Radiotherapy, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Xiaoli LiDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Ping YangDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Linhao XieDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Yaochen LiThe Breast Center, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Caiwen DuDepartment of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Guojun ZhangThe Breast Center, Cancer Hospital of Shantou University Medical College, Shantou 515031, PR China.
Shantou University · CNCancer Hospital of Shantou University Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer for which there is no effective treatment. Previously, we and others demonstrated that CXCR4 surface expression is an independent prognostic factor for disease relapse and survival in breast cancer. In this study, we investigated the effects of CXCR4 gene silencing on cisplatin chemosensitivity in human triple-negative breast cancer cell lines. We found that CXCR4 silencing significantly inhibited cell growth, decreased colony formation, and enhanced cisplatin sensitivity while overexpression of CXCR4 rendered cells more resistant to cisplatin. Moreover, the percentage of apoptosis and cell cycle arrest at the G2/M phase of cisplatin-treated CXCR4 knockdown cells was significantly higher than control cells. Furthermore, we demonstrated CXCR4 knockdown cells showed lower levels of mutant p53 and Bcl-2 protein than the control group, while also having higher levels of caspase-3 and Bax. However overexpression of CXCR4 had the reverse effect. In vivo experiments confirmed that downregulation of CXCR4 enhanced cisplatin anticancer activity in tumor-bearing mice, and that this enhanced anticancer activity is attributable to tumor cell apoptosis. Thus, this study indicates that CXCR4 can modulate cisplatin sensitivity in TNBC cells and suggests that CXCR4 may be a therapeutic target for TNBC.

Indexed as

RNA InterferenceXenograft Model Antitumor AssaysAnimalsAntineoplastic AgentsApoptosisbcl-2-Associated X ProteinBlotting, WesternCaspase 3Cell Line, TumorCell ProliferationCisplatinFemaleG2 Phase Cell Cycle CheckpointsHumansImmunohistochemistryMice, Inbred BALB CAntineoplastic Agentsbcl-2-Associated X ProteinCaspase 3CisplatinCXCR4 protein, humanProto-Oncogene Proteins c-bcl-2Receptors, CXCR4

Identifiers

PMID25544759
PMCPMC4359214
OpenAlexW1604362135

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.