Evidence map›Paper›PMID 34016944›Full record

ArticleOncogenesis2021

High expression of PSMC2 promotes gallbladder cancer through regulation of GNG4 and predicts poor prognosis.

Dawei Zhu, Xing Gu, Zhengyu Lin, Dandan Yu, Jing Wang

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Research progress on prognostic factors of gallbladder carcinoma.Journal of cancer research and clinical oncology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Expression ofTranslational cancer research · 2022
    Article
  12. Article
  13. MLN2238 exerts its anti-tumor effectsFrontiers in pharmacology · 2022
    Article
  14. Article
  15. 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

5 authors at 2 institutions in 1 country.

Dawei Zhu *Department of Gynaecology and Obstetrics, Daping Hospital, Army Medical University, Chongqing, China.
Xing Gu *Department of Gynaecology and Obstetrics, Daping Hospital, Army Medical University, Chongqing, China.
Zhengyu LinCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dandan YuCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jing WangCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. littlespirit1980@hotmail.com.ORCID http://orcid.org/0000-0003-1010-8579
Union Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gallbladder cancer (GBC) is a common malignant tumor of the biliary tract, which accounts for 80-95% of biliary tumors worldwide, and is the leading cause of biliary malignant tumor-related death. This study identified PSMC2 as a potential regulator in the development of GBC. We showed that PSMC2 expression in GBC tissues is significantly higher than that in normal tissues, while high PSMC2 expression was correlated with more advanced tumor grade and poorer prognosis. The knockdown of PSMC2 in GBC cells induced significant inhibition of cell proliferation, colony formation and cell motility, while the promotion of cell apoptosis. The construction and observation of the mice xenograft model also confirmed the inhibitory effects of PSMC2 knockdown on GBC development. Moreover, our mechanistic study recognized GNG4 as a potential downstream target of PSMC2, knockdown of which could aggravate the tumor suppression induced by PSMC2 knockdown in vitro and in vivo. In conclusion, for the first time, PSMC2 was revealed as a tumor promotor in the development of GBC, which could regulate cell phenotypes of GBC cells through the interaction with GNG4, and maybe a promising therapeutic target in GBC treatment.

Identifiers

PMID34016944
PMCPMC8138011
OpenAlexW3183633834

What OpenQuestion holds

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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.