BackgroundHead and neck squamous cell carcinoma (HNSCC) is the sixth most common malignant tumor in the world. Studies in recent years have demonstrated that cancer stem cells (CSCs) are present in many tumor tissues, including HNSCC, and CSCs are the root cause of tumor recurrence and metastasis. Thus, taking new treatment measures to target the killing of CSCs that are resistant to chemotherapy and radiotherapy is key to the success of cancer treatment.MethodsWe explored a method for preparing anti-CD44 antibody-modified superparamagnetic iron oxide nanoparticles (SPIONPs). Biocompatibility was evaluated by a CCK-8 assay. The CSCs were obtained by a 3D cell culture technique from Cal-27 (human oral squamous cell carcinoma) cells, and then the CSCs were identified by quantitative real-time polymerase chain reaction (qRT-PCR). The targeting efficiency of the CD44-SPIONPs to CSCs was confirmed by Prussian blue staining and visualized by laser scanning confocal microscopy (LSCM). Flow cytometry was used to detect the apoptosis of CSCs after alternating magnetic field (AMF) treatment. The efficacy of tumor growth inhibition by CD44-SPIONP-mediated magnetic hyperthermia therapy was evaluated with tumor xenografts in nude mice.ResultsThe CD44-SPIONPs exhibited no negative effect on CSCs, indicating good biocompatibility. After SPIONPs were cocultured with stem cells, the majority of CD44-SPIONPs labeled with FITC penetrated the cell membrane into the cytoplasm. After AMF treatment, CD44-SPIONPs induced CSCs to undergo programmed death. The inhibitory ratio of the treated group was 33.43%, and necrotic areas in the tumor tissue were mainly distributed around the magnetic fluid.ConclusionThese results demonstrate that it is possible to kill CSCs using targeted magnetic nanoparticles and an AMF and that magnetic fluid hyperthermia significantly inhibited the growth of grafted Cal-27 tumors in mice.

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Background: Evidence has indicated that dysregulation of long noncoding RNAs (lncRNA) is a critical factor in the occurrence of many diseases, including cancer. The lncRNA AFAP1-AS1 has been shown to participate in oncogenesis, metastasis, or drug resistance in many types of cancer. However, the potential role of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. Methods: Bioinformatics analysis was performed to compare AFAP1-AS1 expression levels in OSCC cancer samples and in normal controls. The biological function of AFAP1-AS1 was studied through loss-of-function assays. To study the potential mechanisms, high-throughput sequencing was applied to OSCC cancer samples and a series of bioinformatics analyses were performed. The effects of AFAP1-AS1 on OSCC tumor growth was evaluated by in vivo xenograft tumor formation assays. Results: Bioinformatics analyses indicated that AFAP1-AS1 was upregulated in OSCC. Overexpression of AFAP1-AS1 was positively correlated with lymph node metastasis, tumor stage, and pathological grade. Down-regulation of AFAP1-AS1 in OSCC led to decreased proliferation in vitro and, notably, inhibition of tumor growth in vivo. Further research indicated that AFAP1-AS1 regulated OSCC cell proliferation by targeting CCNA2. Conclusion: AFAP1-AS1 promotes tumor proliferation and indicates a poor prognosis in OSCC, providing a potential therapeutic strategy.