Search

Chemoresistance poses a significant challenge in the treatment of advanced head and neck squamous cell cancer (HNSCC). The role and mechanism of circular RNAs (circRNAs) in HNSCC chemoresistance remain understudied. We conducted circRNA microarray analysis to identify differentially expressed circRNAs in HNSCC. The expression of circRNAs from the tyrosylprotein sulfotransferase 2 (TPST2) gene and miRNAs was evaluated through qPCR, while the circular structure of circTPST2 was verified using Sanger sequencing and RNase R. Through Western blotting, biotin-labeled RNA pulldown, RNA immunoprecipitation, mass spectrometry, and rescue experiments, we discovered miR-770-5p and nucleolin as downstream targets of circTPST2. Functional tests, including CCK8 assays and flow cytometry, assessed the chemoresistance ability of circTPST2, miR-770-5p, and Nucleolin. Additionally, FISH assays determined the subcellular localization of circTPST2, miR-770-5p, and Nucleolin. IHC staining was employed to detect circTPST2 and Nucleolin expression in HNSCC patients. circTPST2 expression was inversely correlated with cisplatin sensitivity in HNSCC cell lines. Remarkably, high circTPST2 expression correlated with lower overall survival rates in chemotherapeutic HNSCC patients. Mechanistically, circTPST2 reduced chemosensitivity through sponge-like adsorption of miR-770-5p and upregulation of the downstream protein Nucleolin in HNSCC cells. The TCGA database revealed improved prognosis for patients with low circTPST2 expression after chemotherapy. Moreover, analysis of HNSCC cohorts demonstrated better prognosis for patients with low Nucleolin protein expression after chemotherapy. We unveil circTPST2 as a circRNA associated with chemoresistance in HNSCC, suggesting its potential as a marker for selecting chemotherapy regimens in HNSCC patients. Further exploration of the downstream targets of circTPST2 advanced our understanding and improved treatment strategies for HNSCC.

Oral potentially malignant disorders (OPMDs) are linked with an escalated risk of developing cancers, particularly oral squamous cell carcinoma (OSCC). Since prevailing therapies cannot effectively forestall the exacerbation and recurrence of OPMDs, halting their malignant progression is paramount. The immune checkpoint serves as a cardinal regulator of the immune response and the primary cause of adaptive immunological resistance. Although the exact mechanism remains elusive, elevated expression of multiple immune checkpoints in OPMDs and OSCC relative to healthy oral mucosa has been ascertained. This review delves into the immunosuppressive microenvironment of OPMDs, the expression of diverse immune checkpoints such as programmed death receptor-1 (PD-1) and programmed death receptor-1 ligand (PD-L1) in OPMDs, and the potential application of corresponding inhibitors. In addition, synergistic strategies incorporating combined immune checkpoint inhibitors, such as cGAS-STING, costimulatory molecules, cancer vaccines, and hydrogels, are discussed to gain a more comprehensive understanding of the role and application of immune checkpoint inhibitors (ICIs) in oral carcinogenesis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

In this paper, we report our numerical simulation on the symmetry distortion and mechanism of the vortex-shaped momentum distribution of hydrogen atom by taking into account of the dynamic Stark effect. By deploying the strong field approximation (SFA) theory, we performed extensive simulation on the momentum pattern of hydrogen ionized by two time-delayed oppositely circularly polarized attosecond pulses. We deciphered that this distortion is originated from the temporal characteristics of the dynamic Stark phase which is nonlinear in time.