Evidence map›Paper›PMID 42871472›Full record

ReviewGenes & diseases2027

Molecular mechanisms and targeted therapeutic strategies for glycolytic reprogramming in osteosarcoma.

Xuewen Ni, Ping Xia, Mengxue Liang, Li Zhang, Jiaqi Chen, Zhuojia He, Hua Huang, Jing Feng, Xun Niu, Feifei Pu

Abstract readReview
In one paragraph

Review in Genes & diseases, 2027. 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

10 authors.

Xuewen NiFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Ping XiaDepartment of Orthopedics, Wuhan Fourth Hospital, Wuhan, Hubei 430030, China.
Mengxue LiangFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Li ZhangFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Jiaqi ChenFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Zhuojia HeFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Hua HuangFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Jing FengFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.
Xun NiuDepartment of Otorhinolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.
Feifei PuFirst Clinical College, Hubei University of Chinese Medicine, Wuhan, Hubei 430060, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma, a highly invasive and metastatic malignant bone tumor, has a poor prognosis primarily because of early pulmonary metastasis and resistance to conventional treatments. The malignant progression of osteosarcoma cells significantly depends on glycometabolic reprogramming, a process characterized by enhanced aerobic glycolysis. This review begins by mapping the multi-dimensional networks driving sugar metabolism reprogramming, which revealed that functional abnormalities in core glycolytic enzymes, including hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A (LDHA), are driven by a multi-level regulatory network that includes altered transcription factor activity, epigenetic modifications, and interactions mediated by non-coding RNAs. Mitochondrial dysfunction leads to succinate and reactive oxygen species accumulation, synergistically promoting the remodeling of metabolic pathways. Furthermore, the synergistic interaction between the pentose phosphate pathway and glutamine metabolism accelerates the energy supply and biosynthesis, whereas lactate accumulation shapes the immunosuppressive microenvironment by inhibiting immune cell function. This review focuses on dissecting the core mechanisms of glucose metabolism reprogramming in osteosarcoma pathogenesis, including promoting proliferation, inhibiting apoptosis, enhancing invasion and metastasis, regulating immune metabolism, and mediating chemotherapy resistance. Additionally, it evaluates novel therapeutic strategies targeting key nodes of glucose metabolism in osteosarcoma, including advances in preclinical research on specific small-molecule inhibitors and gene regulatory approaches. Finally, it delves into the major challenges in translational research, such as metabolic heterogeneity, targeting selectivity, and compensatory resistance, as well as prospects for future research, including multi-omics analysis, smart delivery systems, organoid models, and combination immunotherapy. This study offers novel insights into overcoming the therapeutic bottlenecks in osteosarcoma treatment.

Indexed as

ChemoresistanceGlycolysisLactylationMetabolic reprogrammingOsteosarcomaTherapeutic targeting

Identifiers

PMID42871472
PMCPMC13659329

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.