Evidence map›Paper›PMID 35725485›Full record

ArticleChinese medicine2022

Metabolomics and integrated network pharmacology analysis reveal SNKAF decoction suppresses cell proliferation and induced cell apoptisis in hepatocellular carcinoma via PI3K/Akt/P53/FoxO signaling axis.

Wei Guo, Xiaohui Yao, Siyuan Lan, Chi Zhang, Hanhan Li, Zhuangzhong Chen, Ling Yu, Guanxian Liu, Yuan Lin, Shan Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Chinese medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 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

11 authors at 4 institutions in 1 country.

Wei Guo *The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Xiaohui Yao *The Research Center for Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Siyuan LanThe Research Center for Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Chi ZhangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Hanhan LiThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Zhuangzhong ChenThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Ling YuThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China.
Guanxian LiuDepartment of Nephrology, Huizhou Municipal Central Hospital, Huizhou, 510006, Guangdong, People's Republic of China.
Yuan LinDepartment of Pathology, The First Affiliated Hospital of Sun Yat Sen University, Guangzhou, 510080, Guangdong, People's Republic of China. liny36@mail.sysu.edu.cn.
Shan LiuThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China. liushan@gzucm.edu.cn.
Hanrui ChenThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, People's Republic of China. chenhanrui1689@gzucm.edu.cn.ORCID http://orcid.org/0000-0002-0058-6609
First Affiliated Hospital of Guangzhou University of Chinese Medicine · CNGuangzhou University of Chinese Medicine · CNHuizhou Central People's Hospital · CNSun Yat-sen University · CN

Funding

Guangdong Bureau of traditional Chinese Medicine 20212051Guangdong Natural Science Foundation 2021A1515011489Science and Technology Planning Project of Guangzhou 202002030376the First Affiliated Hospital of Guangzhou University of traditional Chinese medicine, Youth Scientific Research Fund Project 2019QN20University Science and technology project of Guangdong Provincial Department of Education 2020KTSCX028
6 · The paper itself

Abstract

backgroundThere is no comprehensive treatment method for hepatocellular carcinoma (HCC); hence, research and development are still focused on systemic therapies, including drugs. Sinikangai fang (SNKAF) decoction, a classic Chinese herbal prescription, has been widely used to treat liver cancer. However, there is no research on its core active component and target.

methodsMouse models were established to measure the anticancer effect of SNKAF decoction on HCC. Further, we investigated the effect of SNKAF decoction on inhibition of hepatoma cells proliferation using cell viability, cloning and invasion assays in vitro. The components of SNKAF were collected from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database and TCM@Taiwan database. Metabolomic analysis was used to identify the potential genes and pathways in HCC treated with SNKAF decoction. Then, the expression of phosphoinositide 3-kinase (PI3K), Akt, P53, FoxO proteins of the potential signal pathways were detected using Western blot.

resultsThe animal experiments showed that SNKAF decoction inhibited tumor growth (P < 0.05) and induced no weight loss in the mice. In vitro data showed that HCCLM3 and MHCC97H cell proliferation was inhibited by SNKAF serum in a time- and concentration dependent manner. Further combined analysis network pharmacology with metabonomics showed that 217 target genes overlapped. The core target genes included BCL2, MCL1, Myc, PTEN, gsk3b, CASP9, CREB1, MDM2, pt53 and CCND1. Cancer-associated pathways were largely involved in SNKAF mechanisms, including P53, FoxO, and PI3K/Akt signaling pathways, which are closely related to induced-tumor cell apoptosis. In addition, Western bolt verified that 10% SNKAF serum significantly affected the main proteins of PI3K/Akt/P53/FoxO signaling pathway in both cell lines.

conclusionSNKAF decoction-containing serum inhibited HCCLM3 and MHCC97H cell proliferation, migration, invasion, and induced-tumor cell apoptosis in-vivo. We confirmed that SNKAF decoction is a promising alternative treatments for HCC patients.

Indexed as

Hepatocellular carcinomaMetabolomic analysisNetwork pharmacologyPI3K/Akt/P53/FoxO signaling pathway axisSNKAF decoction

Identifiers

PMID35725485
PMCPMC9208213
OpenAlexW4283169956

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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.