Dendrobium (commonly known as Shihu in China), a traditional Chinese medicinal herb recognized in the Pharmacopoeia of China (2020 edition), boasts a rich history of medicinal application. Extensive research has been conducted on its Chinese medicinal prescription due to its demonstrated anti-tumour effects in clinical settings. Dendrobium is comprised of a diverse range of chemical compounds, notably the Bibenzyls, Erianin, and Gigantol, which have exhibited significant inhibitory and therapeutic effects on cervical cancer, thereby suggesting potential therapeutic value. However, the comprehensive investigation of Chrysotoxine, a naturally occurring active ingredient of Bibenzyls in Dendrobium, remains incomplete in treatment of cervical cancer. This study aimed to conduct a comprehensive investigation of Chrysotoxine and its regulatory impact on ferroptosis in cervical cancer. Initially, the effects of chrysotoxine on the cervical cancer cell line HeLa were assessed using CCK-8, transwell, colony formation, and flow cytometry to evaluate cell proliferation, invasion, migration, and apoptosis. Subsequently, network pharmacology and molecular docking techniques were employed to identify the molecular targets of chrysotoxine in cervical cancer. Finally, confocal microscopy assessed the expression levels of ROS and lipid compounds in response to chrysotoxine treatment, and the influence of chrysotoxine on signaling pathways was investigated using Western blot analysis, guided by KEGG pathway analysis. Our cell-based experiments revealed that CTX effectively suppresses the cell proliferation, migration, invasion, and apoptosis in CC. Subsequently, we comprehensively analyzed that HSP90AA1, ESR1, PIK3CA, mTOR and MAPK1 may be the possible targets of CTX in CC by combining network pharmacology with molecular docking techniques. Finally, we observed that CTX enhances the production of intracellular ROS and excessive lipid peroxides. Simultaneously, we detected that CTX promotes ferroptosis-based p53/GPX4/SLC7A11 pathway and inhibits PI3K/AKT/mTOR pathway-induced cell death of CC by Western blot. Our study indicates that chrysotoxine shows promise as a novel medication for treating CC. The findings provide a scientific foundation for the regulation of cervical cancer by chrysotoxine, presenting new insights into the application of traditional Chinese medicine for fighting CC.

Nasopharyngeal carcinoma (NPC) is a cancer with a high metastatic rate and poor prognosis. Growing studies suggest that ferroptosis take part in the development of tumours. At the same time, the connection between ferroptosis-related genes (FRGs) and the prognosis of NPC remains unclear. In this study, we explored the dysregulated FRGs between normal control and tumour samples of NPC. Firstly, 14 of 36 differentially expressed FRGs were identified in NPC tissues compared to normal tissues, among which ABCC1, GLS2, CS and HMGCR were associated with poor prognosis for patients. The four ferroptosis genes were used for consensus cluster analysis and two risk-related FRGs (ABCC1 and GLS2) were used in a risk model. The ROC curve revealed the good predictive performance of this risk signature. Multivariate analysis revealed that risk score and intratumoral TILs were independent risk factors linked to prognosis. Additionally, our results suggested that the risk signature was attached to the immune microenvironment. Moreover, the NPC patients with high risk were sensitive to chemotherapeutic drugs including axitinib, docetaxel, embelin, epothilone.B, parthenolide, thapsigargin, tipifarnib, vinorelbine. Finally, the expression of ABCC1 and GLS2 was validated in NPC tissues using immunohistochemistry. Together, these results revealed ferroptosis may be a potential biomarker in NPC and representing a promising future direction in prognosis and therapeutic strategy for the treatment of NPC.

Background. Linc00312 is downregulated in nasopharyngeal carcinoma (NPC) and associates with poor treatment efficacy. Genetic variations are the main cause of individual differences in treatment response. The objective of this study is to explore the relationship between genetic variations of linc00312 and the risk of chemoradiotherapy induced toxic reactions in NPC patients. Methods. We used a bioinformatics approach to select 3 single nucleotide polymorphisms (SNPs) with regulatory feature in linc00312 (rs12497104, rs15734, and rs164966). 505 NPC patients receiving chemoradiotherapy with complete follow-up data were recruited. Genotyping was carried out by MassARRAY iPLEX platform. Univariate logistic and multivariate logistic regression were used to analyze the risk factors responsible for toxic reactions of NPC patients. Results. Our result demonstrated that linc00312 rs15734 ( ) was significantly associated with severe leukopenia in NPC patients underwent chemoradiotherapy (AA vs. GG, , ). In addition, the risk of severe leukopenia was remarkably increased to 5.635 times ( ) in female with rs15734 AA genotype compared to male with rs15734 GG genotype. Moreover, patients with rs12497104 ( ) AA genotype showed a 67.5% lower risk of thrombocytopenia than those with GG genotype ( ). Remarkably, the younger patients ( ) with rs12497104 AA genotype displayed a 90% decreased risk of thrombocytopenia compared with older patients ( ) carrying rs12497104 GG genotype ( ). Conclusions. Genetic variations of linc00312 affect the risk of chemoradiotherapy induced hematotoxicity in nasopharyngeal carcinoma patients and may serve as biomarkers for personalized medicine.