Evidence map›Paper›PMID 35505354›Full record

ArticleJournal of cardiothoracic surgery2022

Ginsenoside compound K inhibits the proliferation, migration and invasion of Eca109 cell via VEGF-A/Pi3k/Akt pathway.

Jianhou Huang, Dinglong Pan, Feng Liu, Yiting Hong, Gang Huang, Xiaowei Huang, Xinwen Wang, Zhiqiang Lin

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiothoracic surgery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 10 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

8 authors at 3 institutions in 1 country.

Jianhou HuangDepartment of Pharmacy, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Dinglong PanDepartment of Radiotherapy, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Feng LiuDepartment of Orthopedics, Dongguan People's Hospital, Southern Medical University, Dongguan, China.
Yiting HongDepartment of Gynaecology and Obstetrics, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Gang HuangDepartment of Pharmacology, Quanzhou Medical College, Quanzhou, China.
Xiaowei HuangDepartment of Pharmacy, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China.
Xinwen WangDepartment of Orthopedics, Dongguan People's Hospital, Southern Medical University, Dongguan, China. andrewbread@163.com.
Zhiqiang LinDepartment of Pharmacy, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou, China. fmulzq@163.com.ORCID http://orcid.org/0000-0002-4880-8899
Fujian Medical University · CNDongguan People’s Hospital · CNQuanzhou Normal University · CN

Funding

quanzhou bureau of science and technology 2018N052S
6 · The paper itself

Abstract

objectiveEsophageal cancer, one of the most common cancers in the upper digestive tract and is one of the leading cancer-related mortality worldwide. Accumulating studies found that Ginsenoside compound K (CK) has significantly anti-tumor effects, especially in the suppression of proliferation, migration, as well as invasion in various human cancers. While the effects of Ginsenoside CK in esophageal cancer have not been well studied. In our present study, we aim to explore the functions and mechanisms of Ginsenoside CK in the progression of esophageal cancer cells (Eca109).

methodsCell Counting Kit-8 (CCK-8), wound healing, transwell and flow cytometry assays were applied to analyze the effects of Ginsenoside CK in the progression of Eca109 cell, western blot assay was used to investigate the potential downstream signaling pathway after Ginsenoside CK treatment.

resultsOur study found that Ginsenoside CK can suppress cell proliferation, migration and invasion of Eca109 cell. Furthermore, the flow cytometry showed that Ginsenoside CK increased of apoptosis rates in Eca109 cell. The western blot results indicated that Ginsenoside CK decreased the expression of VEGF-A, P-Pi3k and P-Akt proteins. Moreover, the knockdown of VEGF-A gene could suppress cell proliferation, migration, invasion and induce apoptosis in Eca109 cell, and the expression of P-Pi3k and P-Akt proteins were significantly downregulated.

conclusionsOur study suggests that Ginsenoside CK inhibits the proliferation, migration, invasion, and induced apoptosis of Eca109 cell by blocking VEGF-A/Pi3k/Akt signaling pathway.

Indexed as

Esophageal NeoplasmsPhosphatidylinositol 3-KinasesCell MovementCell ProliferationGinsenosidesHumansProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor Aginsenoside compound KGinsenosidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AEca109Ginsenoside CKKnockdownProgressionVEGF-A

Identifiers

PMID35505354
PMCPMC9066758
OpenAlexW4225314857

What OpenQuestion holds

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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.