Evidence map›Paper›PMID 40668612›Full record

Observational studyBlood advances2025

Targeting bone marrow mesenchymal stromal cell-derived IL-6 to overcome acute myeloid leukemia chemoresistance.

Diyu Hou, Danni Cai, Wei Dai, Xinai Liao, Maoqing Tan, Xiaoming Zheng, Liuhuan Wang, Jingru Liu, Jin Wang, Xiaoting Wang and 2 more

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06486350 (Bone Marrow Supernatant IL-6 as a Predictor of Chemotherapy Sensitivity in AML Patients), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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.

NCT06486350 unknown statusnot on this map

Bone Marrow Supernatant IL-6 as a Predictor of Chemotherapy Sensitivity in AML Patients

TypeobservationalSponsorFujian Medical University Union HospitalRan2023 to 2025Enrolled72ConditionsAML, Adult
3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
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  8. 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

12 authors.

Diyu HouCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0009-0009-8561-7424
Danni CaiCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0000-0001-9254-1207
Wei DaiCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0000-0002-9657-6121
Xinai LiaoCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Maoqing TanCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Xiaoming ZhengCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Liuhuan WangCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Jingru LiuCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Jin WangCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0009-0007-8702-6420
Xiaoting WangCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.
Qiang FuFujian Institute of Hematology, Fujian Provincial Key Laboratory on Hematology, Fujian Medical University Union Hospital, Fuzhou, China.
Huifang HuangCentral Laboratory, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0000-0002-8548-028X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractIn acute myeloid leukemia (AML), elevated interleukin 6 (IL-6) levels in the bone marrow (BM) are linked to poor prognosis. However, the mechanisms driving this elevation and its role in chemoresistance remain unclear. Using the Prrx1-Cre system, we selectively deleted Il6 in BM mesenchymal stromal cells (MSCs) and established an AML mouse model. Our results show that MSCs are a major source of IL-6 in AML BM. Importantly, Il6 deletion in MSCs reduced oxidative phosphorylation (OXPHOS) activity in AML cells, slowed disease progression, and enhanced chemosensitivity to cytarabine (Ara-C). Similarly, the OXPHOS inhibitor IACS-010759 improved chemosensitivity in AML mice. Exogenous recombinant IL-6 reversed the chemosensitivity gains from Il6 deletion, confirming its role in chemoresistance. We further demonstrated that Il6 absence in MSCs inhibits mitochondria transfer to AML cells, dampening OXPHOS and enhancing Ara-C efficacy. In summary, our study underscores the critical role of Il6 from MSCs in AML progression and chemoresistance. Targeting IL-6 in MSCs may offer a promising therapeutic strategy for AML. This trial was registered at www.clinicaltrials.gov as #NCT06486350.

Indexed as

Drug Resistance, NeoplasmInterleukin-6Leukemia, Myeloid, AcuteMesenchymal Stem CellsAnimalsCytarabineDisease Models, AnimalHumansMiceOxidative PhosphorylationCytarabineInterleukin-6

Identifiers

PMID40668612
PMCPMC12495097

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Registered trials

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.