Evidence map›Paper›PMID 40560034›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Adipocytes Promote Cisplatin Resistance through Secreting A1BG and Regulating NAMPT/PARP1 Axis-Mediated DNA Repair in Osteosarcoma.

Yonghui Liang, Zhaohui Li, Lina Tang, Zhen Pan, Xiang Fei, Chen Tan, Aina He, Qingcheng Yang, Dongdong Cheng

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. SOCS3 Stabilizes PARP1 to Suppress Adipogenic Transcription and Abdominal Adipogenesis in Avian.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

9 authors.

Yonghui LiangDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0009-0003-7126-1822
Zhaohui LiDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0002-6447-1675
Lina TangDepartment of Oncology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0003-4763-9832
Zhen PanDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0003-1492-7619
Xiang FeiInstitute of Clinical Chemistry and Laboratory Medicine, Section Mass Spectrometry and Proteomics, University Medical Center Hamburg-Eppendorf (UKE), 20246, Hamburg, Germany.ORCID https://orcid.org/0009-0004-3773-550X
Chen TanDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0009-0006-4695-0441
Aina HeDepartment of Oncology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0001-6442-3975
Qingcheng YangDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0002-4539-8791
Dongdong ChengDepartment of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID https://orcid.org/0000-0002-4411-9949

Funding

National Natural Science Foundation of China 82173343National Natural Science Foundation of China 82403167National Natural Science Foundation of China 82472645
6 · The paper itself

Abstract

Obesity is increasingly recognized as a negative prognostic factor for cancers, including osteosarcoma. However, the mechanisms linking obesity to chemoresistance in osteosarcoma remain unclear. This study found obesity is significantly associated with poor responses to cisplatin-based chemotherapy in osteosarcoma patients. In vitro, adipocyte-conditioned medium (Adi-CM) induced cisplatin resistance, while peritumoral adipocytes and diet-induced obesity (DIO) reduce the cisplatin efficacy in vivo. Mechanistically, Adi-CM enhanced DNA repair by the PARP1/ATM pathway activation. Proteomic analysis identified A1BG, a secreted protein upregulated in adipocytes from chemoresistant patients, as a key mediator of this effect. A1BG depletion in adipocytes restored cisplatin sensitivity, whereas recombinant A1BG enhanced resistance and promoted DNA repair. Further investigation revealed a direct interaction between A1BG and NAMPT, leading to the stabilization of NAMPT and an increased NAD

Indexed as

AdipocytesBone NeoplasmsCisplatinCytokinesDNA RepairDrug Resistance, NeoplasmNicotinamide PhosphoribosyltransferaseOsteosarcomaPoly (ADP-Ribose) Polymerase-1AnimalsAntineoplastic AgentsCell Line, TumorHumansMaleMiceObesityAntineoplastic AgentsCisplatinCytokinesNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1adipocytescisplatin resistancedna repairosteosarcoma

Identifiers

PMID40560034
PMCPMC12463075

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.