Evidence map›Paper›PMID 27099438›Full record

ArticleWorld journal of gastroenterology2016

Gallic acid induced apoptotic events in HCT-15 colon cancer cells.

Aruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Mahitosh Mandal, Eko Supriyanto, Ida Idayu Muhamad

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

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  18. How gallic acid regulates molecular signaling: role in cancer drug resistance.Medical oncology (Northwood, London, England) · 2023
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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

5 authors at 2 institutions in 2 countries.

Aruna Priyadharshni SubramanianAruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Eko Supriyanto, Ida Idayu Muhamad, IJN-UTM Cardiovascular Engineering Centre, Faculty of Biosciences and Medical Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia.
Saravana Kumar JaganathanAruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Eko Supriyanto, Ida Idayu Muhamad, IJN-UTM Cardiovascular Engineering Centre, Faculty of Biosciences and Medical Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia.
Mahitosh MandalAruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Eko Supriyanto, Ida Idayu Muhamad, IJN-UTM Cardiovascular Engineering Centre, Faculty of Biosciences and Medical Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia.
Eko SupriyantoAruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Eko Supriyanto, Ida Idayu Muhamad, IJN-UTM Cardiovascular Engineering Centre, Faculty of Biosciences and Medical Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia.
Ida Idayu MuhamadAruna Priyadharshni Subramanian, Saravana Kumar Jaganathan, Eko Supriyanto, Ida Idayu Muhamad, IJN-UTM Cardiovascular Engineering Centre, Faculty of Biosciences and Medical Engineering, Universiti Teknologi Malaysia, Johor Bahru 81310, Malaysia.
University of Technology Malaysia · MYIndian Institute of Technology Kharagpur · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the inhibitory action of diet-derived phenolic compound gallic acid (GA) against HCT-15 colon cancer cells.

methodsThe antiproliferative effect of GA against colon cancer cells was determined by performing thiazolyl blue tetrazolium bromide (MTT) assay. The colony forming ability of GA treated colon cancer cells was evaluated using the colony forming assay. The cell cycle changes induced by GA in HCT-15 cells were analyzed by propidium iodide staining. Levels of reactive oxygen species (ROS) and mitochondrial membrane potential of HCT-15 exposed to GA was assessed using 2',7'-dichlorfluorescein-diacetate and rhodamine-123 respectively, with the help of flow cytometry. Morphological changes caused by GA treatment in the colon cancer cells were identified by scanning electron microscope and photomicrograph examination. Apoptosis was confirmed using flow cytometric analysis of GA treated HCT-15 cells after staining with Yo-Pro-1.

resultsMTT assay results illustrated that GA has an inhibitory effect on HCT-15 cells with IC50 value of 740 μmol/L. A time-dependent inhibition of colony formation was evident with GA treatment. Cell cycle arrest was evident from the accumulation of GA treated HCT-15 cells at sub-G1 phase (0.98 ± 1.03 vs 58.01 ± 2.05) with increasing exposure time. Flow cytometric analysis of GA treated HCT-15 cells depicted early events associated with apoptosis like lipid layer breakage and fall in mitochondrial membrane potential apart from an increase in the generation of ROS which were in a time dependent manner. SEM and photomicrograph images of the GA-treated cells displayed membrane blebbing and cell shrinking characteristics of apoptosis. Further apoptosis confirmation by Yo-Pro-1 staining also showed the time-dependent increase of apoptotic cells after treatment.

conclusionThese results show that GA induced ROS dependent apoptosis and inhibited the growth of colon cancer cells.

Indexed as

AdenocarcinomaAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsDose-Response Relationship, DrugG1 Phase Cell Cycle CheckpointsGallic AcidHumansInhibitory Concentration 50Membrane Potential, MitochondrialOxidative StressReactive Oxygen SpeciesTime FactorsAntineoplastic AgentsGallic AcidReactive Oxygen SpeciesApoptosisCell cycleColon cancerGallic acidLipid layer breakReactive oxygen species

Identifiers

PMID27099438
PMCPMC4823245
OpenAlexW2417264979

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.