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Laryngeal squamous cell carcinoma (LSCC) is a common head and neck cancer. Despite recently improved management of LSCC, chemotherapy resistance of patients remains a challenge. In this study, we identified that long noncoding RNA  FOXD2-AS1  regulates LSCC therapeutic resistance by augmenting LSCC stemness. LSCC chemotherapy-resistant patients showed increased  FOXD2-AS1  expression compared with that in chemotherapy-sensitive patients, which predicted poor prognosis. Gain- or loss-of-function experiments showed that upregulated  FOXD2-AS1  maintained cancer stemness, reducing the response to chemotherapy, while  FOXD2-AS1  downregulation had the opposite effects.  FOXD2-AS1  acted as a scaffold for STAT3 and PRMT5, promoting STAT3 transcriptional activity, which is essential to maintain cancer stemness and promote chemotherapeutic resistance. Interfering with  FOXD2-AS1  using short hairpin RNA rescued LSCC’s chemotherapeutic sensitivity. Thus,  FOXD2-AS1  promotes LSCC chemotherapeutic resistance and is an upstream activator of  STAT3 , making  FOXD2-AS1  a potential therapeutic target to improve the chemotherapy effect in LSCC patients.

Long noncoding RNA FOXD2-AS1 enhances chemotherapeutic resistance of laryngeal squamous cell carcinoma via STAT3 activation