Intensity-modulated radiotherapy (IMRT) is gradually replacing conventional radiation therapy and has become the mainstream radical treatment for patients with nasopharyngeal carcinoma (NPC). IMRT can conform and increase radiation doses to tu-mor-associated regions as well as decrease exposure doses and volumes on normal organs and tissues to avoid damage on critical or-gans. Aside from system and setup errors, other factors, such as the gradual reduction of the primary NPC lesion and the decrease in vol-ume of involved neck lymph nodes as well as body weight loss and changes in the head and neck shape during IMRT, may cause devia-tions in the radiation doses and volume delivered to the NPC targets and the organs at risk. These factors may affect the accuracy of IMRT. Several researchers have attempted to correct such deviations during IMRT for NPC patients by using adaptive radiotherapy (ART). The results indicate that ART is feasible to a certain degree and can correct the deviations, including decrease in tumor volume, body weight loss, and changes in head and neck shape of NPC patients.

Cancer stands as one of the predominant causes of mortality globally, necessitating ongoing efforts to develop innovative therapeutics. Historically, natural products have been foundational in the quest for anticancer agents. Bulbocodin D (BD) and Bulbocodin C (BC), two bibenzyls derived from Pleione bulbocodioides (Franch.) Rolfe, have demonstrated notable in vitro anticancer activity. In human lung cancer A549 cells, the IC_50s for BD and BC were 11.63 and 11.71 μmol·L^-1, respectively. BD triggered apoptosis, as evidenced by an upsurge in Annexin V-positive cells and elevated protein expression of cleaved-PARP in cancer cells. Furthermore, BD and BC markedly inhibited the migratory and invasive potentials of A549 cells. The altered genes identified through RNA-sequencing analysis were integrated into the CMap dataset, suggesting BD's role as a potential signal transducer and activator of transcription 3 (STAT3) inhibitor. SwissDock and MOE analyses further revealed that both BD and BC exhibited a commendable binding affinity with STAT3. Additionally, a surface plasmon resonance assay confirmed the direct binding affinity between these compounds and STAT3. Notably, treatment with either BD or BC led to a significant reduction in p-STAT3 (Tyr 705) protein levels, regardless of interleukin-6 stimulation in A549 cells. In addition, the extracellular signal-regulated kinase (ERK) was activated after BD or BC treatment. An enhancement in cancer cell mortality was observed upon combined treatment of BD and U0126, the MEK1/2 inhibitor. In conclusion, BD and BC emerge as promising novel STAT3 inhibitors with potential implications in cancer therapy.
Humans ; Lung Neoplasms/metabolism* ; STAT3 Transcription Factor/metabolism* ; Antineoplastic Agents/chemistry* ; A549 Cells ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation