Evidence map›Paper›PMID 24676394›Full record

ArticleInternational journal of molecular medicine2014

Celecoxib regulates apoptosis and autophagy via the PI3K/Akt signaling pathway in SGC-7901 gastric cancer cells.

Min Liu, Chun-Mei Li, Zhao-Feng Chen, Ri Ji, Qing-Hong Guo, Qiang Li, Hong-Ling Zhang, Yong-Ning Zhou

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

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  8. Role of autophagy in gastric carcinogenesis.World journal of gastrointestinal oncology · 2021
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  13. C21 Fraction Refined fromACS omega · 2020
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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

8 authors at 2 institutions in 1 country.

Min LiuDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Chun-Mei LiDivision of Oncology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Zhao-Feng ChenDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Ri JiDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Qing-Hong GuoDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Qiang LiDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Hong-Ling ZhangDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Yong-Ning ZhouDivision of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Lanzhou University · CNFirst Hospital of Lanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer, one of the most common malignancies worldwide, typically has a poor prognosis and poor survival rate. Previous studies have investigated the chemopreventive effect of celecoxib. In the present study, the SGC-7901 human gastric cancer cell line was utilized to examine the chemopreventive mechanisms of celecoxib. The inhibition of cell proliferation was determined using MTT assay, cell apoptosis was monitored by terminal deoxynucleotidyl transferase-mediated dUTP nick end‑labeling (TUNEL) and flow cytometry, and cell ultrastructural changes were assessed via transmission electron microscopy. The mRNA expression of Akt, caspase-8 and -9 was examined using quantitative reverse-transcription-polymerase chain reaction (qRT-PCR) and p-Akt, procaspase-8 and -9 were analyzed via western blotting. The results showed that celecoxib inhibited the proliferation of SGC-7901 cells in a time- and dose-dependent manner. Additionally, celecoxib induced apoptosis as substantiated by typical apoptotic bodies, autophagosomes and an increased apoptotic rate. It was found that following celecoxib treatment, Akt mRNA expression was not significantly altered, and that p-Akt protein levels decreased in a time- and dose‑dependent manner. Additionally, caspase-8 and -9 mRNA expression was significantly increased, while procaspase-8 and -9 protein expression decreased relative to the time- and dose-dependent effects. These results demonstrated that celecoxib induced apoptosis and autophagy of gastric cancer cells in vitro through the PI3K/Akt signaling pathway. Moreover, our findings suggested that celecoxib induces apoptosis in gastric cancer cells through the mitochondrial and death receptor pathways, providing additional understanding regarding the chemopreventive behaviors of celecoxib and its uses in cancer therapy.

Indexed as

ApoptosisAutophagyBlotting, WesternCaspase 8Caspase 9CelecoxibCell Line, TumorCell ProliferationFlow CytometryHumansIn Situ Nick-End LabelingMicroscopy, Electron, TransmissionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazolesReverse Transcriptase Polymerase Chain ReactionCaspase 8Caspase 9CelecoxibPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazolesSulfonamides

Identifiers

PMID24676394
PMCPMC4055439
OpenAlexW2056339946

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.