Evidence map›Paper›PMID 23468530›Full record

ArticleMolecular cancer therapeutics2013

Targeting CXCR2 enhances chemotherapeutic response, inhibits mammary tumor growth, angiogenesis, and lung metastasis.

Bhawna Sharma, Dhananjay M Nawandar, Kalyan C Nannuru, Michelle L Varney, Rakesh K Singh

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
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  11. TGFβ1 induces CXCL1 to promote stemness features in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Exploration of Pyrido[3,4-Molecules (Basel, Switzerland) · 2023
    Article
  17. Article
  18. Article
  19. Bladder cancer, inflammageing and microbiomes.Nature reviews. Urology · 2022
    Review
  20. Tumor-Mediated Neutrophil Polarization and Therapeutic Implications.International journal of molecular sciences · 2022
    Review

16 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Bhawna SharmaDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Dhananjay M Nawandar
Kalyan C Nannuru
Michelle L Varney
Rakesh K Singh
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
TARGETED NANOCARRIER FOR SIRNA DELIVERY TO TUMOR VASCULATUREP20RR021937 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KABANOV, ALEXANDER V · 2008 to 2011
$8.6M
NCI NIH HHS P30 CA036727NCI NIH HHS P30CA036727NCRR NIH HHS P20 RR021937NCRR NIH HHS RR021937
6 · The paper itself

Abstract

Breast cancer is one of the leading causes of cancer deaths among females. Many challenges exist in the current management of advanced stage breast cancer as there are fewer recognized therapeutic strategies, often because of therapy resistance. How breast cancer cells evade chemotherapy and the underlying mechanism remains unclear. We and others have observed that malignant cells that survive initial chemo- and radiation therapy express higher levels of CXCR2 ligands, which may provide a survival benefit leading to therapy resistance. In this report, we test the hypothesis that CXCR2-dependent signaling in malignant cells may be critical for chemotherapy resistance and targeting this signaling axis may enhance the antitumor and antimetastatic activity of chemotherapeutic drugs and limit their toxicity. We used Cl66-wt, 4T1-wt, Cl66sh-CXCR2, and 4T1sh-CXCR2 cells expressing differential levels of the CXCR2 receptor to evaluate the role of targeting CXCR2 on chemotherapeutic responses. Knockdown of CXCR2 enhances paclitaxel and doxorubicin-mediated toxicity at suboptimal doses. Moreover, we observed an increase in the expression of CXCL1, a CXCR2 ligand in paclitaxel and doxorubicin-treated mammary tumor cells, which were inhibited following CXCR2 knockdown. Knockdown of CXCR2 enhanced antitumor activity of paclitaxel in an in vivo mammary tumor model. We observed significant inhibition of spontaneous lung metastases in animals bearing CXCR2 knockdown tumors and treated with paclitaxel as compared with the control group. Our data suggest the novel role of CXCR2 and its ligands in maintaining chemotherapy resistance and provide evidence that targeting CXCR2 signaling in an adjuvant setting will help circumvent chemotherapy resistance.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesLigandsLung NeoplasmsMammary Neoplasms, ExperimentalMiceNeovascularization, PathologicPaclitaxelReceptors, Interleukin-8BTumor BurdenAntineoplastic AgentsLigandsPaclitaxelReceptors, Interleukin-8B

Identifiers

PMID23468530
PMCPMC3653628
OpenAlexW2161286605

What OpenQuestion holds

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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.