Evidence map›Paper›PMID 38086844›Full record

ArticleCell death discovery2023

Cepharanthine, a regulator of keap1-Nrf2, inhibits gastric cancer growth through oxidative stress and energy metabolism pathway.

Yang-Yang Lu, Chun-Yang Zhu, Yi-Xin Ding, Bing Wang, Shu-Fen Zhao, Jing Lv, Shu-Ming Chen, Sha-Sha Wang, Yan Wang, Rui Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.5field-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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  17. Cepharanthine Promotes CaInternational journal of molecular sciences · 2025
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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

12 authors at 1 institution in 1 country.

Yang-Yang Lu *Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Chun-Yang Zhu *Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Yi-Xin DingDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Bing WangBiomedical Centre, Qingdao University, Qingdao, China.
Shu-Fen ZhaoDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Jing LvDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Shu-Ming ChenDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Sha-Sha WangDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Yan WangDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Rui WangDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Wen-Sheng QiuDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China. wsqiuqd@163.com.ORCID http://orcid.org/0000-0002-9817-1857
Wei-Wei QiDepartment of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, China. qwwqdfy@126.com.ORCID http://orcid.org/0000-0001-6608-2799
Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cepharanthine (CEP), a bioactive compound derived from Stephania Cephalantha Hayata, is cytotoxic to various malignancies. However, the underlying mechanism of gastric cancer is unknown. CEP inhibited the cellular activity of gastric cancer AGS, HGC27 and MFC cell lines in this study. CEP-induced apoptosis reduced Bcl-2 expression and increased cleaved caspase 3, cleaved caspase 9, Bax, and Bad expression. CEP caused a G2 cell cycle arrest and reduced cyclin D1 and cyclin-dependent kinases 2 (CDK2) expression. Meanwhile, it increased oxidative stress, decreased mitochondrial membrane potential, and enhanced reactive oxygen species (ROS) accumulation in gastric cancer cell lines. Mechanistically, CEP inhibited Kelch-like ECH-associated protein (Keap1) expression while activating NF-E2 related factor 2 (Nrf2) nuclear translocations, increasing transcription of Nrf2 target genes quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HMOX1), and glutamate-cysteine ligase modifier subunit (GCLM). Furthermore, a combined analysis of targeted energy metabolism and RNA sequencing revealed that CEP could alter the levels of metabolic substances such as D (+) - Glucose, D-Fructose 6-phosphate, citric acid, succinic acid, and pyruvic acid, thereby altering energy metabolism in AGS cells. In addition, CEP significantly inhibited tumor growth in MFC BALB/c nude mice in vivo, consistent with the in vitro findings. Overall, CEP can induce oxidative stress by regulating Nrf2/Keap1 and alter energy metabolism, resulting in anti-gastric cancer effects. Our findings suggest a potential application of CEP in gastric cancer treatment.

Identifiers

PMID38086844
PMCPMC10716385
OpenAlexW4389624403

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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.