ArticleOncogene2026
HERC1 oncogene enhances stemness and tumorigenic potential in CD44
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
HECT and RCC1-like domain-containing protein 1 (HERC1), a large E3 ubiquitin ligase, has been implicated in neural development and genome stability, but its role in cancer remains unclear. This study identifies HERC1 as a critical regulator of cancer stemness, metastasis, and chemoresistance in head and neck squamous cell carcinoma (HNSCC). CD44⁺ HNSCC organoids with shRNA-mediated HERC1 knockdown were assessed for stemness, EMT, and IL-6/STAT3/HERC1 signaling using molecular assays, CAF co-culture, xenografts, and tissue immunohistochemistry. High HERC1 expression in TCGA-HNSCC datasets was associated with enrichment of stemness signatures. HERC1 knockdown in CD44⁺ cells reduced Sox2, and Slug expression, suppressed EMT, and impaired metastatic potential in Transwell assays and in vivo models. CD44⁺ cells formed organoids in a HERC1-dependent manner. CAF co-culture showed that IL-6 promoted organoid invasiveness through STAT3 activation and HERC1 upregulation. Mechanistic validation revealed that HERC1 modulation altered p-STAT3, p-ERK, CD44, and Slug levels, and STAT3 inhibition reduced HERC1 expression, defining a p-STAT3-HERC1-p-ERK axis. IL-6 neutralization or HERC1 inhibition sensitized organoids to 5-fluorouracil and cisplatin, and combined HERC1 knockdown with 5-FU markedly reduced tumor growth and increased apoptosis. Tissue arrays confirmed elevated HERC1 and pathway markers in advanced HNSCC. These findings define an p-STAT3-HERC1-p-ERK signaling axis that promotes cancer stemness and chemoresistance through CD44
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Registered trials
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