Evidence map›Paper›PMID 33437165›Full record

ArticleJournal of ginseng research2021

Ginsenosides Rk1 and Rg5 inhibit transforming growth factor-β1-induced epithelial-mesenchymal transition and suppress migration, invasion, anoikis resistance, and development of stem-like features in lung cancer.

Hyunhee Kim, Pilju Choi, Taejung Kim, Youngseok Kim, Bong Geun Song, Young-Tae Park, Seon-Jun Choi, Cheol Hee Yoon, Won-Chul Lim, Hyeonseok Ko and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of ginseng research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 71 citations in OpenAlex.

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  16. Recent trends in ginseng research.Journal of natural medicines · 2024
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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

11 authors at 4 institutions in 1 country.

Hyunhee KimDepartment of Biomedical Sciences, Asan Medical Center, AMIST, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Pilju ChoiNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Taejung KimNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Youngseok KimNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Bong Geun SongNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Young-Tae ParkNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Seon-Jun ChoiNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Cheol Hee YoonNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Won-Chul LimTraditional Food Research Group, Korea Food Research Institute, Wanju, Republic of Korea.
Hyeonseok KoBiomedical Research Center, Asan Institute for Life Sciences, Seoul, Republic of Korea.
Jungyeob HamNatural Products Research Institute, Korea Institute of Science and Technology (KIST), 679 Saimdang-ro, Gangneung, Republic of Korea.
Korea Institute of Science and Technology · KRAsan Medical Center · KRKorea Food Research Institute · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer has a high incidence worldwide, and most lung cancer-associated deaths are attributable to cancer metastasis. Although several medicinal properties of

methodsWe treated TGF-β1 or alternatively Rk1 and Rg5 in A549 cells. We used western blot analysis, real-time polymerase chain reaction (qPCR), wound healing assay, Matrigel invasion assay, and anoikis assays to determine the effect of Rk1 and Rg5 on TGF-mediated EMT in lung cancer cell. In addition, we performed tumorsphere formation assays and real-time PCR to evaluate the stem-like properties.

resultsEMT is induced by TGF-β1 in A549 cells causing the development of cancer stem-like features. Expression of E-cadherin, an epithelial marker, decreased and an increase in vimentin expression was noted. Cell mobility, invasiveness, and anoikis resistance were enhanced with TGF-β1 treatment. In addition, the expression of stem cell markers, CD44, and CD133, was also increased. Treatment with Rk1 and Rg5 suppressed EMT by TGF-β1 and the development of stemness in a dose-dependent manner. Additionally, Rk1 and Rg5 markedly suppressed TGF-β1-induced metalloproteinase-2/9 (MMP2/9) activity, and activation of Smad2/3 and nuclear factor kappa B/extra-cellular signal regulated kinases (NF-kB/ERK) pathways in lung cancer cells.

conclusionsRk1 and Rg5 regulate the EMT inducing TGF-β1 by suppressing the Smad and NF-κB/ERK pathways (non-Smad pathway).

Indexed as

Epithelial-mesenchymal transitionGinsenosidesLung cancerPanax ginseng MeyerTransforming growth factor β1

Identifiers

PMID33437165
PMCPMC7790904
OpenAlexW3014434964

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.