Evidence map›Paper›PMID 21448932›Full record

ArticleInternational journal of cancer2011

Acetyl-11-keto-β-boswellic acid suppresses invasion of pancreatic cancer cells through the downregulation of CXCR4 chemokine receptor expression.

Byoungduck Park, Bokyung Sung, Vivek R Yadav, Sung-Gook Cho, Mingyao Liu, Bharat B Aggarwal

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Targeting CXCL12/CXCR4 Axis in Tumor Immunotherapy.Current medicinal chemistry · 2019
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

6 authors at 3 institutions in 1 country.

Byoungduck ParkCytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Bokyung Sung
Vivek R Yadav
Sung-Gook Cho
Mingyao Liu
Bharat B Aggarwal
The University of Texas MD Anderson Cancer Center · USTexas A&M Health Science Center · USTexas A&M University · US

Funding

TARGETING NF-KB ACTIVATION IN REGULATION OF SYMPTOMS IN PATIENTS WITH MULTIPLEP01CA124787 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI REUBEN, JAMES MARTIN · 2008 to 2012
$10.6M
NCI NIH HHS CA-124787-01A2NCI NIH HHS P01 CA124787
6 · The paper itself

Abstract

Ninety percent of cancer-mediated deaths are due to metastasis of the tumor; however, the mechanisms controlling metastasis remain poorly understood. Thus, no therapy targeting this process has yet been approved. Chemokines and their receptors are mediators of chronic inflammation and have been linked to the metastasis of numerous cancers. More recently, the Cysteine X Cysteine (CXC) chemokine receptor 4 (CXCR4) has emerged as a key mediator of tumor metastasis; therefore, identification of inhibitors of this receptor has the potential to abrogate metastasis. In this report, we demonstrate that acetyl-11-keto-β-boswellic acid (AKBA), a component of the therapeutic plant Boswellia serrata, can downregulate CXCR4 expression in pancreatic cancer cells. The reduction in CXCR4 induced by this terpenoid was found to be cell-type specific, as its expression was also abrogated in leukemia, myeloma and breast cancer cell lines. Neither proteasome inhibitors nor lysosomal stabilization could prevent the AKBA-induced reduction in CXCR4 expression. This downregulation occurred at the transcriptional level. Suppression of CXCR4 by AKBA was accompanied by the inhibition of pancreatic cancer cell invasion, which is induced by CXCL12, the ligand for CXCR4. In addition, abrogation of the expression of chemokine receptor by AKBA was found in human pancreatic tissues from orthotopic animal model. AKBA also abolished breast tumor cell invasion, and this effect correlated with the disappearance of both the CXCR4 messenger RNA and CXCR4 protein. Overall, our results show that AKBA is a novel inhibitor of CXCR4 expression and, thus, has the potential to suppress the invasion and metastasis of cancer cells.

Indexed as

Blotting, WesternCell Line, TumorChromatin ImmunoprecipitationDown-RegulationElectrophoretic Mobility Shift AssayHumansImmunohistochemistryNeoplasm InvasivenessPromoter Regions, GeneticReceptors, CXCR4Reverse Transcriptase Polymerase Chain ReactionTriterpenesacetyl-11-ketoboswellic acidReceptors, CXCR4Triterpenes

Identifiers

PMID21448932
PMCPMC3082612
OpenAlexW2005850424

What OpenQuestion holds

Textmetadata
LicenceTDM
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.