Evidence map›Paper›PMID 25889185›Full record

ArticleBMC complementary and alternative medicine2015

So-Cheong-Ryong-Tang induces apoptosis through activation of the intrinsic and extrinsic apoptosis pathways, and inhibition of the PI3K/Akt signaling pathway in non-small-cell lung cancer A549 cells.

Cheol Park, Su Hyun Hong, Gi-Young Kim, Yung Hyun Choi

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 14 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

4 authors at 2 institutions in 1 country.

Cheol ParkDepartment of Molecular Biology, College of Natural Sciences, Dongeui University, 176 Eomgwangno Busanjin-gu, Busan, 614-714, Republic of Korea. parkch@deu.ac.kr.
Su Hyun HongDepartment of Biochemistry, Dongeui University College of Korean Medicine, 52-57, Yangjeong-ro, Busanjin, Busan, 614-052, Republic of Korea. hongsh@deu.ac.kr.
Gi-Young KimLaboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, 102 Jejudaehak-ro, Jeju, 690-756, Republic of Korea. immunkim@cheju.ac.kr.
Yung Hyun ChoiDepartment of Biochemistry, Dongeui University College of Korean Medicine, 52-57, Yangjeong-ro, Busanjin, Busan, 614-052, Republic of Korea. choiyh@deu.ac.kr.
Dong-Eui University · KRJeju National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSo-Cheong-Ryong-Tang (SCRT), a traditional Korean medicine containing eight species of medicinal plant, has been used to treat patients with bronchial asthma and allergic rhinitis for hundreds of years; however, its anti-cancer potential is poorly understood. The present study was designed to evaluate the apoptotic effect of SCRT against human non-small-cell lung cancer (NSCLC) A549 cells.

methodsThe effects of SCRT on cell growth and viability were evaluated by trypan blue dye exclusion and 3-(4, 5-dimethyl-thiazol-2-yl)-2, 5-diphenyl tetrazoliumbromide (MTT) assays, respectively. Apoptosis was detected using 4,6-diamidino-2-phenyllindile (DAPI) staining, agarose gel electrophoresis and flow cytometry. The protein levels were determined by Western blot analysis. Caspase activity was measured using a colorimetric assay.

resultsSCRT treatment resulted in significantly decreased A549 cell growth and viability by induction of apoptosis. SCRT induced the translocation of pro-apoptotic Bax to the mitochondria, mitochondrial membrane permeabilization, cytochrome c release from mitochondria to cytosol, and activated caspase-9 and caspase-3. SCRT also increased death receptor-associated ligands and enhanced the activation of caspase-8 and cleavage of its substrate Bid. However, the pan-caspases inhibitor significantly blocked the SCRT-induced apoptosis, suggesting that it is a caspase-dependent pathway. In addition, SCRT suppressed the phosphorylation of phosphoinositide 3-kinase (PI3K) and Akt, and treatment with a potent inhibitor of PI3K further increased the apoptotic activity of SCRT.

conclusionsThese findings suggest that SCRT may play its anti-cancer actions partly through a suppression of the PI3K/Akt signal pathway in A549 cells, and further in vivo studies on the potential of SCRT for prevention and therapy of NSCLCs are warranted.

Indexed as

PhytotherapyAntineoplastic Agents, PhytogenicApoptosisCarcinoma, Non-Small-Cell LungCaspase 3Caspase 9Cell ProliferationCytochromes cDrugs, Chinese HerbalHumansMitochondriaPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionAntineoplastic Agents, PhytogenicCaspase 3Caspase 9Cytochromes cDrugs, Chinese HerbalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25889185
PMCPMC4397677
OpenAlexW1980044195

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Registered trials

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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.