Evidence map›Paper›PMID 33650674›Full record

ArticleOncology reports2021

Acanthopanax senticosus Harms extract causes G0/G1 cell cycle arrest and autophagy via inhibition of Rubicon in human liver cancer cells.

Yutaka Kawano, Maki Tanaka, Masaki Fujishima, Eri Okumura, Hideo Takekoshi, Kohichi Takada, Osamu Uehara, Yoshihiro Abiko, Hidekatsu Takeda

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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 2 institutions in 1 country.

Yutaka KawanoDepartment of Gastroenterology, Health Sciences University of Hokkaido Hospital, Sapporo, Hokkaido 002‑8072, Japan.
Maki TanakaDepartment of Clinical Laboratory Science, Health Sciences University of Hokkaido Hospital, Sapporo, Hokkaido 002‑8072, Japan.
Masaki FujishimaProduction and Development Department, Sun Chlorella Co., Ltd., Kyoto 600‑8177, Japan.
Eri OkumuraProduction and Development Department, Sun Chlorella Co., Ltd., Kyoto 600‑8177, Japan.
Hideo TakekoshiProduction and Development Department, Sun Chlorella Co., Ltd., Kyoto 600‑8177, Japan.
Kohichi TakadaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido 060‑8543, Japan.
Osamu UeharaDivision of Disease Control and Molecular Epidemiology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Tobetsu, Hokkaido 061‑0293, Japan.
Yoshihiro AbikoDivision of Oral Medicine and Pathology, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido, Tobetsu, Hokkaido 061‑0293, Japan.
Hidekatsu TakedaDepartment of Physical Therapy, Sapporo Medical University School of Medicine, Sapporo, Hokkaido 060‑8543, Japan.
Health Sciences University of Hokkaido · JPSapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acanthopanax senticosus (Rupr. et Maxim) Harms (ASH), also known as Siberian ginseng or eleuthero, is a hardy shrub native to China, Korea, Russia and the northern region of Japan. ASH is used for the treatment of several diseases such as heart disease, hypertension, rheumatoid arthritis, allergies, chronic bronchitis, diabetes and cancer. In the present study, the inhibitory effect of the root extract of ASH (ASHE) on HuH‑7 and HepG2 liver cancer cells was examined. ASHE suppressed liver cancer cell proliferation by inducing cell cycle arrest at the G0/G1 phase, as well as apoptosis, as indicated by the increased number of Annexin V and 7‑AAD‑positive cells. Furthermore, the expression of LC3‑II, an autophagy marker, in these cells also increased post treatment with ASHE. LC3‑II induction was further enhanced by co‑treatment with chloroquine. Fluorescence and transmission electron micrographs of ASHE‑treated liver cancer cells showed the presence of an increased number of autophagic vesicles. A decreased protein expression level of run domain Beclin‑1‑interacting and cysteine‑rich domain‑containing, an autophagy inhibitor, with no change in RUBCN mRNA expression was observed, indicating activation of the autophagosome‑lysosome fusion step of autophagy. In conclusion, ASHE exerts cytostatic activity on liver cancer cells via both apoptosis and autophagy, and may serve as a potential therapeutic agent for management of liver cancer and autophagy‑related diseases.

Indexed as

Antineoplastic AgentsApoptosisAutophagyAutophagy-Related ProteinsCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalEleutherococcusHumansLiver NeoplasmsPlant ExtractsPlant RootsAntineoplastic AgentsAutophagy-Related ProteinsPlant ExtractsRUBCN protein, humanAcanthopanax senticosus Harmsautophagyliver cancerrun domain Beclin-1-interacting and cysteine-rich domain-containing

Identifiers

PMID33650674
PMCPMC7859978
OpenAlexW3125038451

What OpenQuestion holds

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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.