Evidence map›Paper›PMID 29190639›Full record

ArticlePloS one2017

Induction of colon and cervical cancer cell death by cinnamic acid derivatives is mediated through the inhibition of Histone Deacetylases (HDAC).

Preethi G Anantharaju, Deepa B Reddy, Mahesh A Padukudru, Ch M Kumari Chitturi, Manjunath G Vimalambike, SubbaRao V Madhunapantula

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-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

37 citing papers in PubMed, 77 citations in OpenAlex.

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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 2 institutions in 1 country.

Preethi G AnantharajuDepartment of Biochemistry, Center of Excellence in Molecular Biology and Regenerative Medicine, JSS Medical College, Jagadguru Sri Shivarathreeshwara University,Mysuru, Karnataka, India.
Deepa B ReddyDepartment of Applied Microbiology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, Andhra Pradesh, India.
Mahesh A PadukudruDepartment of Pulmonary Medicine, JSS Medical College, Jagadguru Sri Shivarathreeshwara University, Mysuru, Karnataka, India.
Ch M Kumari ChitturiDepartment of Applied Microbiology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, Andhra Pradesh, India.
Manjunath G VimalambikeDepartment of Pathology, JSS Medical College, Jagadguru Sri Shivarathreeshwara University, Mysuru, Karnataka, India.
SubbaRao V MadhunapantulaDepartment of Biochemistry, Center of Excellence in Molecular Biology and Regenerative Medicine, JSS Medical College, Jagadguru Sri Shivarathreeshwara University,Mysuru, Karnataka, India.ORCID http://orcid.org/0000-0001-9167-9271
JSS Academy of Higher Education and Research · INSri Padmavati Mahila Visvavidyalayam · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies from our group and many others have shown the ability of histone deacetylase (HDAC) inhibitors for retarding the growth of carcinomas of cervix, colon and rectum in vitro. A search for naturally occurring HDAC inhibitors continues due to the adverse effects associated with known HDAC inhibitors like SAHA and TSA. Therefore in the current study, naturally occurring cinnamic acids derivatives were screened for HDAC inhibitory effect using in silico docking method which identified cinnamic acids as potential candidates. Cinnamic acids (CA) are naturally occurring phenolic compounds known to exhibit anticancer properties. However, it is not clearly known whether the anticancer properties of CA derivatives are due to the inhibition of oncogenic HDACs, if so how the efficacy varies among various CA derivatives. Hence, the HDAC inhibitory potential of CA derivatives containing increasing number of hydroxylic groups or methoxy moieties was determined using Discovery Studio software and the most potent CA derivatives tested ex vivo (biochemical assay) as well as in vitro (using cell based assay). Among CA derivatives tested, dihydroxy cinnamic acid (DHCA, commonly known as caffeic acid) exhibited better interactions with HDAC2 (compared to other isoforms) in silico and inhibited its activity ex vivo as well as in vitro. Targeted reduction of HDAC activity using DHCA induced death of cancer cells by (a) generating reactive oxygen species, (b) arresting cells in S and G2/M phases; and (c) induction of caspase-3 mediated apoptosis. In conclusion, we demonstrated that DHCA inhibited cancer cell growth by binding to HDAC followed by the induction of apoptosis.

Indexed as

ApoptosisBinding SitesButyric AcidCell Line, TumorCinnamatesColorectal NeoplasmsFemaleHistone Deacetylase InhibitorsHumansHydroxamic AcidsUterine Cervical NeoplasmsButyric AcidCinnamatescinnamic acidHistone Deacetylase InhibitorsHydroxamic Acidstrichostatin A

Identifiers

PMID29190639
PMCPMC5708809
OpenAlexW2772670881

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.