Evidence map›Paper›PMID 37076815›Full record

ArticleCellular & molecular biology letters2023

KIAA1429-mediated m6A modification of CHST11 promotes progression of diffuse large B-cell lymphoma by regulating Hippo-YAP pathway.

Xiaomin Chen, Tiange Lu, Yiqing Cai, Yang Han, Mengfei Ding, Yurou Chu, Xiangxiang Zhou, Xin Wang

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. mFrontiers in cell and developmental biology · 2026
    Review
  4. KIAA1429-mediated ZFPM2-AS1 mOncology letters · 2025
    Article
  5. Article
  6. Article
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  8. Article
  9. Regulation and application of mScience China. Life sciences · 2025
    Review
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  11. Article
  12. Article
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  14. Article
  15. Article
  16. Review
  17. Article
  18. Downregulation of the mThe Journal of biological chemistry · 2024
    Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Xiaomin ChenDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Tiange LuDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Yiqing CaiDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Yang HanDepartment of Hematology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Mengfei DingDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Yurou ChuDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China.
Xiangxiang ZhouDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China. xiangxiangzhou@sdu.edu.cn.
Xin WangDepartment of Hematology, Shandong Provincial Hospital, Shandong University, No.324, Jingwu Road, Jinan, 250021, Shandong, China. xinw007@126.com.
Shandong Provincial Hospital · CNFirst Affiliated Hospital of Soochow University · CN

Funding

China Postdoctoral Science Foundation No. 2020M672103China Postdoctoral Science Foundation No. 2021T140422Development Project of Youth Innovation Teams in Colleges and Universities of Shandong Province No. 2020KJL006Key Research and Development Program of Shandong Province No.2018CXGC1213National Natural Science Foundation of China No. 81770210National Natural Science Foundation of China No. 81800194National Natural Science Foundation of China No. 82070203National Natural Science Foundation of China No. 82170189National Natural Science Foundation of China No. 82270200Shandong Provincial Natural Science Foundation ZR2021YQ51Taishan Scholars Program of Shandong Province; Shandong Provincial Engineering Research Center of Lymphoma; Academic Promotion Programme of Shandong First Medical University No. 2019QL018Taishan Scholars Program of Shandong Province; Shandong Provincial Engineering Research Center of Lymphoma; Academic Promotion Programme of Shandong First Medical University No. 2020RC006Technology Development Project of Jinan City No. 202134034Translational Research Grant of NCRCH No. 2020ZKMB01Translational Research Grant of NCRCH No. 2021WWB02
6 · The paper itself

Abstract

backgroundN

methodsThe expression and clinical significance of KIAA1429 were verified by our clinical data. CRISPR/Cas9 mediated KIAA1429 deletion, and CRISPR/dCas9-VP64 for activating endogenous KIAA1429 was used to evaluate its biological function. RNA sequencing (RNA-seq), methylated RNA immunoprecipitation sequencing (MeRIP-seq), RNA immunoprecipitation (RIP) assays, luciferase activity assay, RNA stability experiments, and co-immunoprecipitation were performed to investigate the regulatory mechanism of KIAA1429 in DLBCL. Tumor xenograft models were established for in vivo experiments.

resultsDysregulated expression of m6A regulators was observed, and a novel predictive model based on m6A score was established in DLBCL. Additionally, elevated KIAA1429 expression was associated with poor prognosis of patients with DLBCL. Knockout of KIAA1429 repressed DLBCL cell proliferation, facilitated cell cycle arrest in the G2/M phase, induced apoptosis in vitro, and inhibited tumor growth in vivo. Furthermore, carbohydrate sulfotransferase 11 (CHST11) was identified as a downstream target of KIAA1429, which mediated m6A modification of CHST11 mRNA and then recruited YTHDF2 for reducing CHST11 stability and expression. Inhibition of CHST11 diminished MOB1B expression, resulting in inactivation of Hippo-YAP signaling, reprogramming the expression of Hippo target genes.

conclusionsOur results revealed a new mechanism by which the Hippo-YAP pathway in DLBCL is inactivated by KIAA1429/YTHDF2-coupled epitranscriptional repression of CHST11, highlighting the potential of KIAA1429 as a novel predictive biomarker and therapeutic target for DLBCL progression.

Indexed as

Lymphoma, Large B-Cell, DiffuseMethyltransferasesBiomarkersCell ProliferationGene Expression Regulation, NeoplasticHumansRNASulfotransferasesTranscription FactorsBiomarkersCHST11 protein, humanMethyltransferasesRNASulfotransferasesTranscription FactorsCHST11Diffuse large B-cell lymphomaHippo–YAPKIAA1429N 6-methyladenosineYTHDF2

Identifiers

PMID37076815
PMCPMC10114474
OpenAlexW4366413066

What OpenQuestion holds

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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.