Evidence map›Paper›PMID 42704369›Full record

ArticleApoptosis : an international journal on programmed cell death2026

Activating a novel cell death pathway to target PI-resistant multiple myeloma and enhance immunogenic cell death.

Xinyun Zhang, Zhiming Wang, Yilei Shi, Qi Li, Si Chen, Lexin He, Yali Chai, Hao Xu, Yuchen Zhang, Meifang Zhao and 2 more

Abstract read
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In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Xinyun ZhangDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Zhiming WangDepartment of Cell Biology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, 215123, Ren Ai Road 199, Suzhou, China.
Yilei ShiDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Qi LiDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Si ChenSuzhou Sano Precision Medicine Ltd, Suzhou, China.
Lexin HeSuzhou Sano Precision Medicine Ltd, Suzhou, China.
Yali ChaiDepartment of Cell Biology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, 215123, Ren Ai Road 199, Suzhou, China.
Hao XuDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Yuchen ZhangDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Meifang ZhaoDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China.
Wenzhuo ZhuangDepartment of Cell Biology, School of Biology & Basic Medical Sciences, Suzhou Medical College of Soochow University, 215123, Ren Ai Road 199, Suzhou, China. zhuangwenzhuo@suda.edu.cn.
Bingzong LiDepartment of Hematology, the Second Affiliated Hospital of Soochow University, San Xiang Road 1055, Suzhou, China. lbzwz0907@hotmail.com.ORCID http://orcid.org/0000-0002-2732-9354

Funding

National Natural Science Foundation of China 82270197
6 · The paper itself

Abstract

Resistance to proteasome inhibitors (PIs) and inadequate engagement of anti-tumor immunity remain major barriers to effective treatment of multiple myeloma (MM). Here, we identified anwulignan, a bioactive natural product, as a translationally promising agent that retains activity in PI-resistant MM cells and promotes anti-myeloma immune responses. Anwulignan demonstrated potent cytotoxic activity against MM cells and exhibited strong synergy with proteasome inhibitors both in vitro and in vivo. In mouse MM models, anwulignan significantly suppressed tumor growth while maintaining favorable tolerability and safety profiles. Mechanistically, nucleophosmin 1 (NPM1) has been identified as a direct molecular target of anwulignan. Elevated NPM1 expression correlates with poor clinical outcomes in MM, and its inhibition by anwulignan induces cell cycle arrest and apoptosis. In addition to its tumor-intrinsic cytotoxic effects, anwulignan activated the caspase-1-dependent gasdermin D (GSDMD) pyroptosis pathway, thereby inducing immunogenic cell death. Genetic silencing of GSDMD markedly impaired anwulignan-mediated tumor suppression in vitro and in vivo, highlighting pyroptosis as a critical effector mechanism. In immunocompetent syngeneic MM models, anwulignan treatment increased bone marrow and splenic T-cell proportions and achieved superior tumor control compared with GSDMD-deficient tumors. Collectively, these findings establish anwulignan as a dual-function therapeutic that directly targets MM cell survival while simultaneously promoting anti-tumor immunity through pyroptosis-driven immunogenic cell death. This study provides a strong translational rationale for leveraging natural products as immune-engaging strategies to target drug-resistant multiple myeloma and improve therapeutic outcomes.

Indexed as

Drug Resistance, NeoplasmImmunogenic Cell DeathMultiple MyelomaProteasome InhibitorsAnimalsApoptosisCell Line, TumorHumansMiceNucleophosminPyroptosisNPM1 protein, humanNpm1 protein, mouseNucleophosminProteasome InhibitorsAnwulignanImmunogenic cell deathMultiple myelomaProteasome inhibitorsPyroptosis

Identifiers

What Socratic holds

Textmetadata
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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 Socratic graph.