Evidence map›Paper›PMID 32668392›Full record

ArticleMolecular therapy. Nucleic acids2020

The Role and Underlying Mechanism of Exosomal CA1 in Chemotherapy Resistance in Diffuse Large B Cell Lymphoma.

Yuhua Feng, Meizuo Zhong, Youhong Tang, Xianling Liu, Yiping Liu, Leyuan Wang, Hui Zhou

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  11. Extracellular vesicles in malignant and normal B lymphocyte growth and development.Extracellular vesicles and circulating nucleic acids · 2025
    Review
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  13. Article
  14. Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Review
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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

7 authors at 3 institutions in 1 country.

Yuhua FengDepartment of Oncology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, People's Republic of China.
Meizuo ZhongDepartment of Oncology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, People's Republic of China.
Youhong TangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, People's Republic of China.
Xianling LiuDepartment of Oncology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, People's Republic of China.
Yiping LiuDepartment of Oncology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, People's Republic of China.
Leyuan WangDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha 410008, Hunan, People's Republic of China.
Hui ZhouDepartment of Lymphoma & Hematology, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha 410013, Hunan, People's Republic of China. Electronic address: zhouhui9403@126.com.
Central South University · CNXiangya Hospital Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy resistance plays a major role in treatment failure of diffuse large B cell lymphoma (DLBCL). Exosomes are closely related to tumor drug resistance. Herein, the expression of exosomal proteins in DLBCL and their roles in chemotherapy resistance of DLBCL are explored. Tandem mass tag labeling proteomics was used to perform proteomic profiling in exosomes from DLBCL patients' serum. The expression of carbonic anhydrase 1 (CA1) in parental, chemo-resistant DLBCL cells and DLBCL patient exosomes was detected. Proliferation of DLBCL following CA1 knockdown was investigated both in vitro and in vivo, along with the effects on nuclear factor κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) pathways. We identified 54 differentially expressed proteins. We validated that the expression level of exosomal CA1 was higher in chemo-resistant DLBCL cells than in chemo-sensitive counterparts. Knockdown of CA1 inhibited the growth of DLBCL via inhibiting the activation of NF-κB and STAT3 signaling pathways both in vitro and in vivo. An increased expression level of exosomal CA1 was associated with poorer prognosis, and exosomal CA1 could be used as a biomarker to predict chemotherapeutic efficacy. Our study suggests that exosomal CA1 can promote chemotherapy resistance in DLBCL via the NF-κB and STAT3 pathways, and it can serve as a biomarker for DLBCL prognosis.

Indexed as

CA1chemotherapy resistancediffuse large B cell lymphomaexosomes

Identifiers

PMID32668392
PMCPMC7358223
OpenAlexW3037936273

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.