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Zhang et al. Cancer Drug Resist 2024;7:34  https://dx.doi.org/10.20517/cdr.2024.59  Page 11 of 20

               Table 4. HNC cell drug resistance-related circRNAs
                Tumor   circRNA Cell line        Expression  Target              Functions  Corresponding  Ref.
                type                             level                                drugs
                NPC    IPO7   CNE2, HNE1, HONE1,   Up       YBX1      Promote cell migration,  CDDP  [138]
                              SUNE1, HK1, C666-1                      invasion, and cisplatin
                                                                      resistance
                NPC    WDR37  S18, S26           Up         PKR       CCND1           CDDP, gemcitabine  [139]
                NPC    CRIM1  S18, S26           Up         miR-422a  Promote metastasis and  Docetaxel  [80]
                                                                      EMT
                OSCC   AP1M2  CAL27/CDDP         Up         miR-1249-3p  modulate miR-1249-3p- CDDP  [51]
                                                                      ATG9A axis
                LSCC   PARD3  Tu 177, HOK, FD-LSC-1  Up     miR-145-5p w  Activate the Akt-mTOR  CDDP  [142]
                                                                      axis
                ATC    EIF6   TPC1, BHT101       Up         miR-144-3p  Regulate miR144-  CDDP      [143]
                                                                      3p/TGF-α axis

               HNC: Head and neck cancer; NPC: nasopharyngeal carcinoma; CDDP: cisplatin; CCND1: stimulate cyclin D1; EMT: epithelial-mesenchymal
               transition; OSCC: oral squamous cell carcinoma; LSCC: laryngeal squamous cell carcinoma; ATC: anaplastic thyroid carcinoma.




































                     Figure 3. Overview of the main molecular mechanisms of circRNAs in HNC drug resistance. HNC: Head and neck cancer.


               SLC7A11 transcription. Inhibition of HMGA1 has been shown to enhance the sensitivity of ESCC to
               ferroptosis . Multiple studies have now established that regulating ferroptosis can impact the effectiveness
                        [158]
               of cancer treatment and potentially overcome resistance to chemotherapy, targeted therapy, and
               immunotherapy [159-164] . Several  non-coding  RNAs,  including  miR-324-3p,  miR-375,  miR-144-3p,
               miR-27a-3p, miR-3173-5p, circRNA-101093, and lncRNA-PMAN, have been implicated in the regulation of
               tumor ferroptosis [165-168] . Currently, there are no relevant studies investigating the role of non-coding RNAs
               in tumor drug resistance through the regulation of ferroptosis specifically in HNC.
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