PFKP is required for chemoresistant phenotype of breast cancer through modulating the formation of CD133

Kai Fang, Yue Ma, Lihua Li, Yan Yue, Hang Ruan, Sidong Xiong

Abstract read

In one paragraph

Article in Molecular biomedicine, 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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5 · Who and what money

Authors and funding

6 authors.

Kai Fang *The Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, 215123, China.

Yue Ma *The Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, 215123, China.

Lihua LiDepartment of Oncology Institute, The Affiliated Hospital of Jiangnan University, Wuxi, 214000, China. LLHWXSY@aliyun.com.

Yan YueThe Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, 215123, China. yueyan@suda.edu.cn.

Hang RuanThe Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, 215123, China. hangruan@suda.edu.cn.ORCID http://orcid.org/0000-0001-7506-3805

Sidong XiongThe Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, 215123, China. sdxiong@suda.edu.cn.

Funding

Interdisciplinary Basic Frontier Innovation Program of Suzhou Medical College of Soochow University YXY2303026National Natural Science Foundation of China 32100523

6 · The paper itself

Abstract

Breast cancer is the foremost cause of cancer-related death in women globally, and taxane-anthracycline (TA) combination regimens represent standard frontline chemotherapy. Although widely administered, the pathological complete response rate to TA therapy is less than 30%, and chemoresistance remains a major barrier to effective disease control, frequently leading to relapse and poor survival. Both metabolic reprogramming and tumor microenvironmental remodeling are closely associated with treatment failure, yet how they interact to drive TA resistance remains largely unclear. Here we show that phosphofructokinase platelet (PFKP), a key glycolytic enzyme, is highly expressed in breast cancer. PFKP drives glycolysis and promotes CD133

Indexed as

AC133 AntigenBreast NeoplasmsDrug Resistance, NeoplasmNeoplastic Stem CellsPhosphofructokinase-1, Type CAnimalsCancer-Associated FibroblastsCell Line, TumorFemaleGlycolysisHumansMetabolic ReprogrammingPhenotypeTumor MicroenvironmentAC133 AntigenPFKP protein, humanPhosphofructokinase-1, Type CPROM1 protein, humanBreast cancerCancer-associated fibroblastsCancer stem-like cellsChemoresistanceGlycolysisPFKP

Identifiers

PMID42024199

DOI10.1186/s43556-026-00454-z

PMCPMC13106758

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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.