ArticleCancer medicine2025
SPARC Promotes Aerobic Glycolysis and 5-Fluorouracil Resistance in Colorectal Cancer Through the STAT3/HK2 Axis.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Glucose Metabolism Regulating Colorectal Cancer Initiation and Progression.Cancer science · 2026Review
- Integrative single-cell and bulk transcriptomic analyses identify DRAM1 as a candidate gene from fibroblast-associated transcriptional programs in colorectal cancer.Frontiers in oncology · 2026Article
- Mechanical stress, metabolic reprogramming and stromal remodeling: an emerging paradigm in the bladder cancer mechano-micro-environment.Frontiers in genetics · 2026Review
- New Dihalogenated Derivatives of Condensed Benzimidazole Diones Promotes Cancer Cell Death Through Regulating STAT3/HK2 Axis/Pathway.Molecules (Basel, Switzerland) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
backgroundChemotherapy has been used extensively in the clinic to treat colorectal cancer (CRC). Nevertheless, cancer cells usually develop chemoresistance under chemotherapy stress, leading to treatment failure. At present, the mechanism of chemoresistance in patients with CRC is not fully understood.
methodsFirstly, Secreted protein acidic and rich in cysteine (SPARC) expression and prognosis in CRC clinical samples were investigated using tissue microarray (TMAs) and GEPIA databases. Subsequently in vitro, SPARC knockdown or overexpression was used to explore the role of SPARC in 5-fluorouracil (5-FU) resistance in CRC cell lines. Western blot or RT-qPCR was used to analyze the downstream molecules and pathways regulated by SPARC. The contents of glucose and lactic acid were determined by Elisa. In vivo a xenograft tumor model was constructed to verify the function of SPARC in 5-FU chemoresistance.
resultsThis study revealed a correlation between 5-FU resistance in CRC and the expression of SPARC. The elevated SPARC expression in CRC tissues was linked to a poor prognosis for CRC patients. SPARC knockdown in CRC cells significantly suppressed aerobic glycolysis and 5-FU resistance, whereas SPARC overexpression had cancer-promoting effects. Additionally, SPARC increased 5-FU resistance through the Signal transducer and activator of transcription 3 (STAT3)/Hexokinase-2 (HK2) pathway. The impact of SPARC on 5-FU resistance was eliminated both in vitro and in vivo by blocking HK2 or STAT3 signaling.
conclusionOur results confirmed that SPARC affects the chemoresistance of CRC to 5-FU through the STAT3/HK2 axis and is one of the indispensable factors affecting the development of 5-FU resistance in CRC.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.