Evidence map›Paper›PMID 22415137›Full record

ArticleCancer biology & therapy2012

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells.

Yan Shen, Masanobu Takahashi, Hyang-Min Byun, Alexander Link, Nupur Sharma, Francesc Balaguer, Hon-Chiu E Leung, C Richard Boland, Ajay Goel

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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  7. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
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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

9 authors at 3 institutions in 1 country.

Yan ShenGI Cancer Research Laboratory, Charles A. Sammons Cancer Center and Baylor Research Institute, Baylor University Medical Center, Dallas, TX, USA.
Masanobu Takahashi
Hyang-Min Byun
Alexander Link
Nupur Sharma
Francesc Balaguer
Hon-Chiu E Leung
C Richard Boland
Ajay Goel
Baylor University Medical Center · USDan L Duncan Comprehensive Cancer CenterHarvard University · US

Funding

The Biology and Diagnosis of HNPCCR01CA072851 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GOEL, AJAY · 1996 to 2019
$6.6M
Measuring Methylation Kinetics in Cancer Cells: Computations and ExperimentsR01CA129286 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KOMAROVA, NATALIA L · 2008 to 2012
$1.5M
NCI NIH HHS CA129286NCI NIH HHS R01 CA072851NCI NIH HHS R01 CA129286NCI NIH HHS R01 CA72851
6 · The paper itself

Abstract

Accumulating evidence suggests that chemopreventive effects of some dietary polyphenols may in part be mediated by their ability to influence epigenetic mechanisms in cancer cells. Boswellic acids, derived from the plant Boswellia serrata, have long been used for the treatment of various inflammatory diseases due to their potent anti-inflammatory activities. Recent preclinical studies have also suggested that this compound has anti-cancer potential against various malignancies. However, the precise molecular mechanisms underlying their anti-cancer effects remain elusive. Herein, we report that boswellic acids modulate DNA methylation status of several tumor suppressor genes in colorectal cancer (CRC) cells. We treated RKO, SW48 and SW480 CRC cell lines with the active principle present in boswellic acids, acetyl-keto-β-boswellic acid (AKBA). Using genome-wide DNA methylation and gene expression microarray analyses, we discovered that AKBA induced a modest genome-wide demethylation that permitted simultaneous re-activation of the corresponding tumor suppressor genes. The quantitative methylation-specific PCR and RT-PCR validated the gene demethylation and re-expression in several putative tumor suppressor genes including SAMD14 and SMPD3. Furthermore, AKBA inhibited DNMT activity in CRC cells. Taken together, these results lend further support to the growing notion that anti-cancer effect of boswellic acids may in part be due to its ability to demethylate and reactivate methylation-silenced tumor suppressor genes. These results suggest that not only boswellic acid might be a promising epigenetic modulator in the chemoprevention and treatment of CRC, but also provide a rationale for future investigations on the usefulness of such botanicals for epigenetic therapy in other human malignancies.

Indexed as

DNA MethylationAnti-Inflammatory AgentsApoptosisCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsCpG IslandsDNA (Cytosine-5-)-MethyltransferasesEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticSignal TransductionTriterpenesAnti-Inflammatory Agentsboswellic acidDNA (Cytosine-5-)-MethyltransferasesTriterpenes

Identifiers

PMID22415137
PMCPMC3364790
OpenAlexW2145393955

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.