Evidence map›Paper›PMID 35641480›Full record

ArticleOncogenesis2022

Calreticulin enhances gastric cancer metastasis by dimethylating H3K9 in the E-cadherin promoter region mediating by G9a.

Lina Wang, Jun Chen, Qianfei Zuo, Chunmei Wu, Ting Yu, Pengfei Zheng, Hui Huang, Jun Deng, Lichao Fang, Huamin Liu and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogenesis, 2022. 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
2.4field-weighted citation impact, top 10% 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, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023
    Review
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

14 authors at 1 institution in 2 countries.

Lina Wang *Department of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.ORCID http://orcid.org/0000-0002-2003-0659
Jun Chen *Department of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Qianfei ZuoNational Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Chunmei WuDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Ting YuNational Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Pengfei ZhengDepartment of medicinal chemistry, College of Pharmacy, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Hui HuangDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Jun DengDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Lichao FangDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Huamin LiuDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Chenghong LiDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China.
Peiwu YuDepartment of General Surgery and Center of Minimal Invasive Gastrointestinal Surgery, Southwest Hospital, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China. yupeiwu0l@sina.com.ORCID http://orcid.org/0000-0001-8243-2963
Quanming ZouNational Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China. qmzou2007@163.com.ORCID http://orcid.org/0000-0002-6971-0786
Junsong ZhengDepartment of Clinical and Military Laboratory Medicine, College of Medical Laboratory Science, Army Medical University, No. 30 Gaotanyan Street, 400038, Chongqing, China. zhengalpha@sina.com.ORCID http://orcid.org/0000-0002-5248-4209
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The latest study shows that gastric cancer (GC) ranked the fifth most common cancer (5.6%) with over 1 million estimated new cases annually and the fourth most common cause of cancer death (7.7%) globally in 2020. Metastasis is the leading cause of GC treatment failure. Therefore, clarifying the regulatory mechanisms for GC metastatic process is necessary. In the current study, we discovered that calreticulin (CALR) was highly expressed in GC tissues and related to lymph node metastasis and patient's terrible prognosis. The introduction of CALR dramatically promoted GC cell migration in vitro and in vivo, while the repression of CALR got the opposite effects. Cell migration is a functional consequence of the epithelial-mesenchymal transition (EMT) and is related to adhesion of cells. Additionally, we observed that CALR inhibition or overexpression regulated the expression of EMT markers (E-cadherin, ZO-1, Snail, N-cadherin, and ZEB1) and cellular adhesive moleculars (Fibronectin, integrin β1and MMP2). Mechanistically, our data indicated that CALR could mediate DNA methylation of E-cadherin promoter by interacting with G9a, a major euchromatin methyltransferase responsible for methylation of histone H3 on lysine 9(H3K9me2) and recruiting G9a to the E-cadherin promoter. Knockdown of G9a in CALR overexpressing models restored E-cadherin expression and blocked the stimulatory effects of CALR on GC cell migration. Taken together, these findings not only reveal critical roles of CALR medicated GC metastasis but also provide novel treatment strategies for GC.

Identifiers

PMID35641480
PMCPMC9156786
OpenAlexW4281705288

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.