Evidence map›Paper›PMID 33889569›Full record

ArticleFrontiers in cell and developmental biology2021

The Nuclear Farnesoid X Receptor Reduces p53 Ubiquitination and Inhibits Cervical Cancer Cell Proliferation.

Xiaohua Huang, Bin Wang, Runji Chen, Shuping Zhong, Fenfei Gao, Yanmei Zhang, Yongdong Niu, Congzhu Li, Ganggang Shi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 13% 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, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

9 authors at 3 institutions in 2 countries.

Xiaohua HuangDepartment of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, China.
Bin WangDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Runji ChenDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Shuping ZhongDepartment of Biochemistry and Molecular Biology, University of Southern California, Los Angeles, Los Angeles, CA, United States.
Fenfei GaoDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Yanmei ZhangDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Yongdong NiuDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Congzhu LiDepartment of Gynecology, Cancer Hospital, Shantou University Medical College, Shantou, China.
Ganggang ShiDepartment of Pharmacology, Shantou University Medical College, Shantou, China.
Shantou University · CNShantou University Medical College · CNUniversity of Southern California · US

Funding

Molecular mechanism of alcohol-associated liver tumor developmentR01AA024169 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZHONG, SHUPING · 2017 to 2021
$1.9M
NIAAA NIH HHS R01 AA024169
6 · The paper itself

Abstract

The role of farnesoid X receptor (FXR) in cervical cancer and the underlying molecular mechanism remain largely unknown. Therefore, this study aimed to assess the mechanism of FXR in cervical cancer. Western blot, qRT-PCR, and immunohistochemistry demonstrated that FXR was significantly reduced in squamous cell carcinoma tissues, although there were no associations of metastasis and TNM stage with FXR. In Lenti-FXR cells obtained by lentiviral transfection, the overexpression of FXR reduced cell viability and colony formation. Compared with the Lenti-Vector groups, the overexpression of FXR induced early and late apoptosis and promoted G1 arrest. With time, early apoptosis decreased, and late apoptosis increased. In tumor xenograft experiments, overexpression of FXR upregulated small heterodimer partner (SHP), murine double minute-2 (MDM2), and p53 in the nucleus. Co-immunoprecipitation (Co-IP) showed that SHP directly interacted with MDM2, which is important to protect p53 from ubiquitination. Nutlin3a increased MDM2 and p53 amounts in the Lenti-Vector groups, without effects in the Lenti-FXR groups. Silencing SHP reduced MDM2 and p53 levels in the Lenti-FXR groups, and Nutlin3a counteracted these effects. Taken together, these findings suggest that FXR inhibits cervical cancer via upregulation of SHP, MDM2, and p53.

Indexed as

cervical cancerFXRMDM2p53ubiquitination

Identifiers

PMID33889569
PMCPMC8056046
OpenAlexW3148981625

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.