Evidence map›Paper›PMID 35211843›Full record

ArticleHepatology international2022

Abnormal bile acid-microbiota crosstalk promotes the development of hepatocellular carcinoma.

Rui Shen, Lixin Ke, Qiao Li, Xi Dang, Shunli Shen, Jianming Shen, Shaoqiang Li, Lijian Liang, Baogang Peng, Ming Kuang and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.9field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Dysregulation of serum bile acids in liver cancer: a systematic review and meta-analysis.Metabolomics : Official journal of the Metabolomic Society · 2025
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
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

13 authors at 3 institutions in 1 country.

Rui Shen *Hepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Lixin Ke *Hepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Qiao Li *Department of Liver Surgery, Guangdong Provincial People's Hospital, Guangzhou, People's Republic of China.
Xi Dang *Hepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Shunli Shen *Hepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Jianming ShenHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Shaoqiang LiHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Lijian LiangHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China.
Baogang PengHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China. pengbg@mail.sysu.edu.cn.
Ming KuangHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China. kuangminda@hotmail.com.
Yi MaDepartment of Organ Transplantation, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People's Republic of China. anhuimayi2002@163.com.
Zhonghan YangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China. yangzhh@mail.sysu.edu.cn.
Yunpeng HuaHepatobiliary and Pancreatic Surgery Center, First Affiliated Hospital, Sun Yat-Sen University, 58 Zhongshan 2nd Road, Guangzhou, 510080, People's Republic of China. hyp0427@163.com.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNGuangdong Provincial People's Hospital · CN

Funding

Guangzhou Science, Technology and Innovation Commission 201707010387Medical Science and Technology Foundation of Guangdong Province 2014A020212626National Natural Science Foundation of China 81501677National Natural Science Foundation of China 81873591
6 · The paper itself

Abstract

backgroundGut microbiota and microbe-derived metabolites are involved in the development of HCC. Bile acids (BAs) are the most important gut microbiota-modulated endogenous signaling molecules.

methodsWe tested serum bile acid levels and gut microbiome compositions in patients with HCC, chemical-induced HCC mouse models (DEN-HCC mice) and mouse orthotopic implanted liver tumor models with vancomycin treatment (vancomycin-treated mice). Then, we screened an important kind of HCC-related BAs, and verified its effect on the growth of HCC in vivo and in vitro.

resultsWe found that the remarkably decreasing percentages of serum secondary BAs in the total bile acids of patients and DEN-HCC mice, especially, conjugated deoxycholic acids (DCA). The relative abundance of the bile salt hydrolase (BSH)-rich bacteria (Bifidobacteriales, Lactobacillales, Bacteroidales, and Clostridiales) was decreased in the feces of patients and DEN-HCC mice. Then, in vancomycin-treated mice, vancomycin treatment induced a reduction in the BSH-rich bacteria and promoted the growth of liver tumors. Similarly, the percentage of conjugated DCA after vancomycin treatment was significantly declined. We used a kind of conjugated DCA, Glyco-deoxycholic acid (GDCA), and found that GDCA remarkably inhibited the growth of HCC in vivo and in vitro.

conclusionsWe conclude that the remarkably decreasing percentages of serum conjugated DCA may be closely associated with HCC, which may be induced by the reducing gut BSH-rich bacteria. The mechanisms may be correlated with conjugated DCA directly inhibiting the growth and migration of HCC cells.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicrobiotaAnimalsBile Acids and SaltsHumansMiceVancomycinBile Acids and SaltsVancomycinBacteroidalesBifidobacterialesBile salt hydrolaseClostridialesGlyco-deoxycholic acidGut microbiotaLactobacillalesPrimary bile acidsSecondary bile acidsTumorigenesis

Identifiers

PMID35211843
PMCPMC9013324
OpenAlexW4214613491

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.