Abstract. Sinonasal inverted papilloma (SIP) is a benign tumor of the nasal cavity and sinus. SIP is characterized by aggressive malignant transformation and a high rate of recurrence. Inadequate removal of the tumor during surgery is one of the most significant contributors to SIP recurrence. A growing body of evidence suggests that molecular alteration in SIP, including human papilloma virus infections, single nucleotide polymorphisms of key genes, deregulation of signaling pathways and immunological changes, may lead to SIP occurrence and malignant transformation. However, the extent to which these molecular mechanisms contribute to SIP pathology and transformation remains unclear due to limited research. Further studies are warranted to elucidate the primary dependent factors that contribute to SIP etiology. The present article reviewed risk factors of progression and recurrence of SIP, including outdoor and industrial occupational exposure, smoking, septal deviation, SIP location, recurrent cases, stage of SIP-associated squamous cell carcinoma and choice of surgical method.

Hypoxia promotes the radioresistance of laryngeal carcinomas and CD133 is one of the markers expressed by tumor-initiating, human laryngeal carcinoma cells. In order to investigate whether CD133-positive Hep-2 cells exhibit a radioresistant phenotype and to determine whether hypoxia promotes this phenotype, we performed a series of experiments. Hep-2 cells, and Hep-2 cells stably expressing hypoxia-inducible factor (HIF)-targeted small interfering RNA (siRNA) were cultured under hypoxic and normoxic conditions and were treated with varying doses of γ-rays (0, 5, 10, 15 and 20 Gy). MTT and cell cycle assays were subsequently performed. Using fluorescence-activated cell sorting (FACS), CD133-positive Hep-2 cells and CD133-positive HIF-siRNA Hep-2 cells were isolated. These cells were grown as spheres under hypoxic and normoxic conditions for MTT and soft agar colony formation assays. The expression levels of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), survivin, p53 and ataxia-telangiectasia mutated (ATM) were also assayed using flow cytometry. The data showed that the growth of Hep-2 cells exposed to hypoxic conditions and treated with 10 Gy radiation (group A) was less compared to that of groups B-D (P<0.05). In addition, more cells in group A were arrested in the G1 phase of the cell cycle compared to groups B-D (P<0.05). The percentage of CD133+ cells detected after radiation increased and was the highest for group A (P<0.05). In sphere formation assays, significantly more CD133+ cells grew in spheres than CD133- cells (P<0.001). Moreover, sphere formation was the highest for CD133+ Hep-2 cells grown under hypoxic conditions and exposed to irradiation (group E) (P<0.05). Lastly, expression of DNA-PKcs and survivin for group E was the highest (P<0.05), while ATM and p53 levels remained largely unchanged (P>0.05). In conclusion, CD133-positive Hep-2 cells exhibited a radioresistant phenotype that was enhanced with hypoxia. Furthermore, an increase in DNA-PK activity was associated with this enhancement.

Electrocatalytic 2e − oxygen reduction reaction (2e − ORR) is a promising approach to producing H 2 O 2 at ambient temperature and pressure especially in acidic media, which, however, is hindered by the high cost of precious metal-based electrocatalysts. Hence, the development of efficient earth-abundant electrocatalysts and reaction mechanism exploration for H 2 O 2 production by 2e − ORR in acidic solution are critically important but remain challenging at present. In this work, NiSe 2 has been developed as a novel and high-performance 2e − ORR electrocatalyst in acidic media, moreover, using nickel chalcogenides as the models, the influence of different anion species (Se 2 2− , S 2 2− , and O 2− ) on 2e − ORR electrocatalytic performance of the catalysts has been investigated. The synthesized NiSe 2 exhibits outstanding 2e − ORR performance of high selectivity (90%) and long-term durability (12 h). The maximum H 2 O 2 concentration of NiSe 2 reaches 988 ppm, which is the highest among all the reported transition metal chalcogenides. This work demonstrates a novel point of view in anion tuning for designing high-efficiency transition-metal-based electrocatalysts for 2e − ORR. Electronic Supplementary Material Supplementary material (additional experimental procedures, characterizations, and computational details) is available in the online version of this article at 10.1007/s12274-022-5160-2.

Abstract. The present study evaluated the regulation of glucose transporter protein-1 (Glut-1) and vascular endothelial growth factor (VEGF) by hypoxia inducible factor 1α (HIF-1α) under hypoxic conditions in Hep-2 human cells to explore the feasibility of these three genes as tumor markers. Hep-2 cells were cultured under hypoxic and normoxic conditions for 6, 12, 24, 36 and 48 h. The proliferation of Hep-2 cells was evaluated using an MTT assay. The protein and mRNA expression levels of HIF-1α, Glut-1 and VEGF were detected using the S-P immunocytochemical method, western blotting and reverse transcription polymerase chain reaction (RT-PCR). The results revealed that the expression levels of HIF-1α, Glut-1 and VEGF protein in Hep-2 cells were significantly elevated under hypoxic conditions compared with those under normoxic conditions over 36 h. Under hypoxic conditions, mRNA levels of HIF-1α were stable, while mRNA levels of Glut-1 and VEGF changed over time. In conclusion, Glut-1 and VEGF were upregulated by HIF-1α under hypoxic conditions in a time-dependent manner in Hep-2 cells and their co-expression serves as a tumor marker. IntroductionHead and neck squamous cell carcinoma (HNSCC) is the sixth most common malignant tumor worldwide (1). Its clinicopathological characteristics include an insidious onset, strong invasiveness and the liability of recurrence and metastasis with poor prognosis. Although improvements in therapeutic strategies have been made in the past 2-3 decades, the overall five-year survival rate remains almost unchanged. The main reasons for this are considered to be post-treatment locoregional recurrence, distant metastasis and inherent therapeutic resistance to chemoradiation and newly developed molecularly targeted therapy, which is affected by numerous tumoral microenvironmental factors. Among these factors, hypoxia in tumors is thought to be closely correlated with the therapeutic resistance of various types of human cancer.Hypoxia inducible factor 1α (HIF-1α), a key regulator of hypoxia, promotes the expression of more than 100 genes related to angiogenesis, cell proliferation, glucose metabolism, erythropoiesis and cell survival rate (2). Previous studies have demonstrated that the expression of HIF-1α in HNSCC is associated with a poor response to radiotherapy and an adverse prognosis (3). As a downstream factor of HIF-1α, glucose transporter protein-1 (Glut-1; encoded by the SLC2A1 gene in humans) is ubiquitously expressed in a number of solid tumors. Previous studies have demonstrated that the suppression of SLC2A1 expression by antisense oligodeoxynucleotides decreases glucose uptake and inhibits the proliferation of Hep-2 cells. The expression level of Glut-1 has been correlated with poor prognosis in a variety of tumors and is responsible for resistance to therapy (4). The study by Sullu et al demonstrated that vascular endothelial growth factor (VEGF) appears to be vital in the metastatic process of HNSCC (5).Although the expression of HIF-1α, Glut-1 and VEGF has been inves...