Evidence map›Paper›PMID 41492119›Full record

ArticleClinical and translational medicine2026

HBx hijacks the miR-19a-3p/BAMBI/TGF-β1 axis to impair the anti-tumour activity of CD4

Xuecong Guo, Jianguo Li, Xiaofei Bai, Yinghui Huang, Xu Xu, Jiabang Yang, Zhenghao Sun, Wangcheng Zhu, Xudong Guo, Jie Chen and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Xuecong GuoClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Jianguo LiClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xiaofei BaiClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Yinghui HuangClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xu XuDepartment of Hematology, Changhai Hospital, Naval Medical University, Shanghai, China.
Jiabang YangDepartment of Hematology, Changhai Hospital, Naval Medical University, Shanghai, China.
Zhenghao SunClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Wangcheng ZhuDepartment of Life Sciences, Imperial College London, London, UK.
Xudong GuoClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Jie ChenDepartment of Hematology, Changhai Hospital, Naval Medical University, Shanghai, China.
Jiuhong KangClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, National Stem Cell Translational Resource Center, School of Life Sciences and Technology, Tongji University, Shanghai, China.

Funding

Fundamental Research Funds for the Central Universities 22120250258Fundamental Research Funds for the Central Universities 22120250374Ministry of Science and Technology of the People's Republic of China 2021YFA1100400National Natural Science Foundation of China 31721003National Natural Science Foundation of China 32170575Natural Science Foundation of Shanghai Municipality 23ZR1465500The Peak Disciplines of Institutions of Higher Learning in Shanghai
6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) is clinically associated with poor prognosis in diffuse large B-cell lymphoma (DLBCL), while cellular communication in the tumour microenvironment (TME) is recognized as a critical driver of tumour progression. Nevertheless, whether HBV infection mediates DLBCL cell-immune cell crosstalk remains undefined, with the precise mechanisms and associated key molecules remaining elusive.

methodsSsGSEA, Cox regression (univariate/multivariate), WGCNA, and Kaplan-Meier analyses identified prognostic immune subsets and miRNAs in HBV

resultsTME profiling identified diminished CD4⁺ T cell infiltration as an independent predictor of poor survival in HBV⁺ DLBCL. Mechanistically, HBx-mediated down-regulation of miR-19a-3p activated the BAMBI/Wnt signalling pathway, thereby enhancing TGF-β1 secretion and suppressing the anti-tumour activity of CD4

conclusionsHBx promoted TGF-β1 hypersecretion via miR-19a-3p repression-mediated Wnt/β-catenin activation, directly driving CD4 HIGHLIGHTS: Reduced CD4

Indexed as

CD4-Positive T-LymphocytesLymphoma, Large B-Cell, DiffuseMicroRNAsTrans-ActivatorsTransforming Growth Factor beta1Viral Regulatory and Accessory ProteinsAnimalsFemaleHepatitis BHepatitis B virusHumansMaleMiceTumor Microenvironmenthepatitis B virus X proteinMicroRNAsMIRN19A microRNA, humanTrans-ActivatorsTransforming Growth Factor beta1Viral Regulatory and Accessory ProteinsCD4+ T cellsdiffuse large B‐cell lymphoma (DLBCL)hepatitis B virus (HBV)prognosis

Identifiers

PMID41492119
PMCPMC12771663

What OpenQuestion holds

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Registered trials

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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.