Evidence map›Paper›PMID 28927141›Full record

ArticleOncology letters2017

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway.

Lan Liu, Hongwei Gao, Hongbo Wang, Yuan Zhang, Weihua Xu, Sen Lin, Hongjuan Wang, Qiong Wu, Jianqiang Guo

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.6field-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

16 citing papers in PubMed, 41 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

9 authors at 1 institution in 1 country.

Lan LiuDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Hongwei GaoDepartment of Trauma and Orthopedics, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Hongbo WangDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Yuan ZhangDepartment of Evidence-Based Medicine, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Weihua XuDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Sen LinDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Hongjuan WangDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Qiong WuDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Jianqiang GuoDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China.
Second Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Catalpol is an effective active ingredient that functions as a diuretic and laxative, and exhibits blood sugar-lowering, liver protective, anti-aging and anticancer effects. In traditional Chinese medicine, catalpol is believed to be Yin nourishing. The anticancer effect of catalpol on human HCT116 colorectal cancer cells were investigated and the mechanism of action was evaluated. Cellular viability was detected using an MTT assay. Caspase-3 and caspase-9 activity, cellular apoptosis and nucleic morphology were analyzed using caspase-3 and caspase-9 activity assay kits, flow cytometric assays and DAPI staining assay, respectively. Western blot analysis was used to measure the protein expressions of phosphatidylinositol 3-kinase (PI3K), phosphorylated-protein kinase B (p-Akt) and Akt. Expression of microRNA-200 was detected using the reverse transcription-quantitative polymerase chain reaction. HCT116 cells were incubated with PI3K inhibitors in order to analyze the effect of catalpol on cell proliferation. Catalpol was able to inhibit HCT116 cell proliferation. Furthermore, catalpol induced apoptosis in HCT116 cells, which depended on the increased activities of caspase-3 and -9. In addition, catalpol reduced the expression of PI3K, p-Akt and Akt in HCT116 cells. However, downregulation of PI3K/Akt decreased the viability of HCT116 cells following treatment with catalpol and enhanced microRNA-200 expression. Catalpol promoted cellular apoptosis in human HCT116 colorectal cancer cells through upregulation of microRNA-200 expression, which depended on a downregulation of the phosphatase and tensin homolog/PI3K-Akt signaling pathway.

Indexed as

catalpolhuman colorectal cancermicroRNA-200phosphatidylinositol 3-kinaseprotein kinase B

Identifiers

PMID28927141
PMCPMC5588014
OpenAlexW2734547801

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.