icaritin has been researched along with Nasopharyngeal-Neoplasms* in 2 studies
2 other study(ies) available for icaritin and Nasopharyngeal-Neoplasms
| Article | Year |
|---|---|
[Icaritin increases radiosensitivity of nasopharyngeal carcinoma cells by regulating iron death].
To explore the radiosensitizing effect of icaritin on nasopharyngeal carcinoma (NPC) cells and the underlying mechanism.. MTT assay and clonal formation assay were used to evaluate the effect of icaritin on proliferation of human NPC HONE1 and HNE1 cells. The effects of icaritin treatment, γ-ray radiation, or both on production of reactive oxygen species (ROS), cell cycle distribution and apoptosis of the NPC cells were assessed using flow cytometry. The expressions of DNA damage markers γ-H2AX, cycle-related proteins CDC25C, p-CDC25C and cyclin B1, and ferroptosis markers ACSL4 and GXP4 were detected using Western blotting. A nude mouse model bearing subcutaneous HONE1 cell xenograft was used to observe the effect of icaritin and radiation on tumor growth.. Icaritin dose-dependently inhibited the viability of the NPC cells and enhanced the inhibitory effect of radiation on cell proliferation. Flow cytometry and Western blotting showed that icaritin treatment prior to radiation significantly promoted ROS production and γ-H2AX expression in the NPC cells (. Icaritin can enhance radiosensitivity of NPC cells both Topics: Animals; Apoptosis; Carcinoma; Cell Line, Tumor; Cell Proliferation; Cyclin B1; Humans; Mice; Mice, Nude; Nasopharyngeal Carcinoma; Nasopharyngeal Neoplasms; Radiation Tolerance; Reactive Oxygen Species | 2023 |
Inhibitory effect of icaritin on proliferation, migration, and invasion of human nasopharyngeal carcinoma cell CNE2 by regulating STAT3 activation.
The influence of icaritin on the proliferation, migration, and invasion of human nasopharyngeal carcinoma cell CNE2 and the influencing mechanisms were discussed. Results indicated that icaritin can realize dosage-dependent inhibition of CNE2 cell proliferation, migration, and invasion and inhibit the expression levels of VEGF, KDR, bFGF, MMP2, and MMP9. It can also inhibit STAT3 phosphorylation without affecting STAT3 expression. Icaritin exerts multiple bonding effects on the SH2 structural domain of STAT3. Therefore, icaritin can become a candidate drug for resisting nasopharyngeal carcinoma, and its mechanism is related to the blocking of STAT3 signaling pathway activation. Topics: Cell Line, Tumor; Cell Movement; Cell Proliferation; Dose-Response Relationship, Drug; Flavonoids; Gene Expression Regulation, Neoplastic; Humans; Nasopharyngeal Carcinoma; Nasopharyngeal Neoplasms; Neoplasm Invasiveness; Signal Transduction; STAT3 Transcription Factor | 2019 |