Long non-coding RNA HOXC-AS3 promotes proliferation and metastasis of esophageal squamous carcinoma by targeting WNT3A through binding to YBX1.
[UNLABELLED] Esophageal squamous cell carcinoma (ESCC) is one of the malignancies with high morbidity and mortality rates.
APA
Hu S, Wang Q, et al. (2026). Long non-coding RNA HOXC-AS3 promotes proliferation and metastasis of esophageal squamous carcinoma by targeting WNT3A through binding to YBX1.. BMC cancer, 26(1). https://doi.org/10.1186/s12885-026-15672-5
MLA
Hu S, et al.. "Long non-coding RNA HOXC-AS3 promotes proliferation and metastasis of esophageal squamous carcinoma by targeting WNT3A through binding to YBX1.." BMC cancer, vol. 26, no. 1, 2026.
PMID
41691198
Abstract
[UNLABELLED] Esophageal squamous cell carcinoma (ESCC) is one of the malignancies with high morbidity and mortality rates. Previous studies have demonstrated the critical roles of long non-coding RNAs (lncRNAs) in cell differentiation, embryonic development and cancer progression. The lncRNA HOXC-AS3 has been shown to exert pro-carcinogenic effects in adenocarcinoma, gastric cancer and breast cancer; however, its biological function in ESCC remains unclear. In the present study, HOXC-AS3 expression was found to be elevated in ESCC tissues. We discovered that HOXC-AS3 regulates the proliferation and migration of ESCC cells. Flow cytometry assays indicated that knockdown of HOXC-AS3 led to increased apoptosis and cell cycle arrest in ESCC cells. RNA sequencing and Gene Ontology findings revealed that the downstream genes regulated by HOXC-AS3 were primarily enriched in signaling pathways associated with cell proliferation and migration. RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (CHIP) experiments confirmed that HOXC-AS3 can be recruited to the promoter region of the WNT3A gene by binding to YBX1. These findings provide evidence of lncRNA HOXC-AS3 functions as a novel oncogene in ESCC.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12885-026-15672-5.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12885-026-15672-5.
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