Evidence map›Paper›PMID 37907575›Full record

ArticleCell death discovery2023

METTL3-mediated m6A methylation of C1qA regulates the Rituximab resistance of diffuse large B-cell lymphoma cells.

Junping Li, Zhigang Zhu, Yuan Zhu, Jinqing Li, Kangbao Li, Weijie Zhong

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Targeting intracellular mRNA mJournal of advanced research · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. 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

6 authors at 2 institutions in 1 country.

Junping LiDepartment of Geriatrics, Hematology & Oncology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0009-1674-7196
Zhigang ZhuDepartment of Geriatrics, Hematology & Oncology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0001-8038-2798
Yuan ZhuDepartment of Geriatrics, Hematology & Oncology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0002-1388-0628
Jinqing LiDepartment of Geriatrics, Hematology & Oncology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0007-8855-919X
Kangbao LiDepartment of Geriatrics, Gastroenterology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China. canblelee@163.com.ORCID http://orcid.org/0000-0002-5294-9571
Weijie ZhongDepartment of Geriatrics, Hematology & Oncology Ward, the Second Affiliated Hospital, School of Medicine, South China University of Technology, 510180, Guangzhou, Guangdong, China. eyweijiezhong@scut.edu.cn.ORCID http://orcid.org/0000-0002-4710-3870
South China University of Technology · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rituximab has been incorporated into the standard treatment regimen for diffuse large B-cell lymphoma (DLBCL), and induces the death of tumor cells via complement-dependent cytotoxicity (CDC). Unfortunately, the resistance of DLBCL cells to Rituximab limits its clinical usefulness. It remains unclear whether the complement system is related to Rituximab resistance in DLBCL. A Rituximab-resistant DLBCL cell line (Farage/R) was generated under the stress of Rituximab. Constituent proteins of the complement system in wild-type Farage cells (Farage/S) and Farage/R cells were analyzed by qPCR, western blotting, and immunofluorescence. In vitro and in vivo knockdown and overexpression studies confirmed that the complement 1Q subcomponent A chain (C1qA) was a regulator of Rituximab resistance. Finally, the mechanism by which C1qA is regulated by m

Identifiers

PMID37907575
PMCPMC10618261
OpenAlexW4388135180

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.