ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
S100A10 promotes glycolysis and malignant progression of CCA by activating the HK2/ERK signaling pathway.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsCholangiocarcinoma (CCA) is a highly aggressive malignancy characterized by late diagnosis and poor prognosis. The molecular mechanisms driving CCA progression and metabolic reprogramming remain incompletely understood. This study aimed to elucidate the clinical significance, biological function, and underlying mechanisms of the calcium-binding protein S100A10 in CCA pathogenesis.
methodsS100A10 expression was analyzed using TCGA and Human Protein Atlas datasets and validated in a clinical cohort of 46 CCA patients. The diagnostic value and prognostic associations were evaluated statistically. Loss-of-function assays (shRNA knockdown) were performed in HuCCT1 cells to assess proliferation, migration, invasion, and apoptosis. Mechanistic investigations involved metabolic assays (glucose uptake/lactate release), Western blotting, and rescue experiments targeting the Hexokinase 2 (HK2) and ERK signaling pathways.
resultsBioinformatic analysis and clinical validation revealed that S100A10 is significantly upregulated in CCA tissues compared to normal controls, with a high diagnostic accuracy (AUC = 0.917). Elevated S100A10 expression correlated significantly with advanced tumor stage and shortened overall survival. Functionally, S100A10 silencing markedly attenuated CCA cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, S100A10 was found to orchestrate metabolic reprogramming by enhancing aerobic glycolysis. This effect was mediated through the regulation of key glycolytic enzymes, particularly HK2, and the activation of the ERK signaling cascade. Notably, the suppression of malignant phenotypes induced by S100A10 depletion was partially reversed by either HK2 overexpression or pharmacological ERK activation.
conclusionsThis study identifies S100A10 as a critical oncogenic driver in CCA that links metabolic reprogramming to tumor progression via the HK2/ERK signaling axis. These findings suggest S100A10 is a robust prognostic biomarker and a potential therapeutic target for disrupting the metabolic adaptability of cholangiocarcinoma.
Indexed as
Identifiers
41701476What 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.