Evidence map›Paper›PMID 41793503›Full record

ArticleApoptosis : an international journal on programmed cell death2026

Superenhancer-driven SMC4 promotes myeloma growth by epigenetically enhancing IFI16-dependent STING signaling.

Jiayun Guan, Xuanyi Lin, Zhenfeng Dai, Jianbiao Zhou, Zhen Cai, Tze King Tan, Tae-Hoon Chung, Xiaochen Zhang, Wee-Joo Chng, Xiaoxiang Rong and 1 more

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Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Jiayun Guan *Department of Medical Oncology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Xuanyi Lin *Department of Medical Oncology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Zhenfeng Dai *Bone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jianbiao ZhouCancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Republic of Singapore.
Zhen CaiBone Marrow Transplantation Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Tze King TanCancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Republic of Singapore.
Tae-Hoon ChungCancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Republic of Singapore.
Xiaochen ZhangDepartment of Medical Oncology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Wee-Joo ChngCancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Republic of Singapore. mdccwj@nus.edu.sg.
Xiaoxiang RongDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. rongxx@smu.edu.cn.
Yunlu JiaDepartment of Medical Oncology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China. jiayunlu@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a complex hematological malignancy characterized by the uncontrolled proliferation of plasma cells in the bone marrow. Emerging evidence suggests that the aberrant activation of specific gene regulatory elements known as SE plays a crucial role in driving oncogenic gene expression programs in cancer. In this study, we investigated the role of the SE-driven SMC4 in promoting myeloma growth. Depletion of SMC4 resulted in a significant impairment of myeloma cell proliferation and clonogenicity. Mechanistically, we identified that SMC4 orchestrates the epigenetic modulation of the IFI16-dependent STING signaling pathway. This epigenetic enhancement of the IFI16-STING axis led to increased production of pro-inflammatory cytokines, creating a favorable microenvironment for myeloma cell growth. Furthermore, we established a direct link between the SE-driven SMC4 and the upregulation of IFI16 and STING gene expression in MM cells. Importantly, pharmacological inhibition of the IFI16-STING pathway abrogated the oncogenic effects mediated by SMC4. Our findings uncover a novel regulatory circuit involving SMC4 and the IFI16-STING signaling axis that promotes myeloma growth. Targeting this epigenetic network may hold therapeutic potential to intervene in myeloma progression and improve patient outcomes.

Indexed as

Cell Cycle ProteinsChromosomal Proteins, Non-HistoneEpigenesis, GeneticMembrane ProteinsMultiple MyelomaNuclear ProteinsPhosphoproteinsAnimalsCell Line, TumorCell ProliferationcGAS-STING Signaling PathwayGene Expression Regulation, NeoplasticHumansSignal TransductionSTING ProteinSuper EnhancersCell Cycle ProteinsChromosomal Proteins, Non-HistoneIFI16 protein, humanMembrane ProteinsNuclear ProteinsPhosphoproteinsSTING1 protein, humanSTING ProteinIFI16Multiple myelomaSMC4STINGSuper enhancer

Identifiers

PMID41793503

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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.