Value of cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy to treat malignant peritoneal mesothelioma.

OBJECTIVE: To investigate the clinical efficacy of cytoreductive surgery (CRS) combined with hyperthermic intraperitoneal chemotherapy (HIPEC) for treating malignant peritoneal mesothelioma (MPM) and to assess the impact of this approach on patient prognosis. METHODS: A retrospective analysis of 44 patients with MPM was performed. The control group (CNG, N = 23) was treated with CRS combined with postoperative intraperitoneal (IP) chemotherapy, while the observation group (OG, N = 21) was treated with CRS combined with HIPEC. The treatment efficacy, volume of blood loss, operation time, postoperative length of stay, and 3-year survival rate (SR) were compared, and the factors affecting the prognosis of MPM patients were analyzed by multivariate analysis. RESULTS: The OG showed decreased volume of blood loss and operation time, while also showing increased overall treatment efficacy compared with the CNG. The SR in the OG was 65.22% compared with a rate of 33.33% in the CNG, and the 3-year SR in the OG was significantly higher than that in the CNG. Multivariate analysis revealed that tumor-node-metastasis (TNM) stage, Eastern Cooperative Oncology Group (ECOG) score, and treatment modality were independent risk factors for the prognosis of MPM patients. CONCLUSION: CRS combined with HIPEC for MPM has a favorable treatment efficacy and prolongs the survival of MPM patients. Additionally, TNM stage, ECOG score, and treatment modality are independent risk factors for the prognosis of MPM patients.

FTO-stabilized lncRNA HOXC13-AS epigenetically upregulated FZD6 and activated Wnt/ß-catenin signaling to drive cervical cancer proliferation, invasion, and EMT.

PURPOSE: Cervical cancer (CC) is the third most prevalent malignancy in women. Frizzled class receptor 6 (FZD6) is demonstrated to either activate or repress the activity of Wnt/ß-catenin pathway, a crucial signaling involved in cancer development. However, the role of FZD6 in CC is unknown. The present study explored the function of FZD6 and its mechanism in CC. METHODS: The levels of FZD6, HOXC13-AS were detected in CC specimens and CC cell lines via qRT-PCR. Cell proliferation and invasion was explored via CCK-8 assay, colony formation assay and transwell assay. Luciferase reporter analysis, FISH, subcellular fractionation, chromatin immunoprecipitation and RNA immunoprecipitation were performed for investigating the molecular mechanism. RESULTS: FZD6 was up-regulated in CC. FZD6 silence retarded proliferation, invasion, and epithelial-to-mesenchymal transition (EMT), and inactivated Wnt/ß-catenin. HOXC13 antisense RNA (HOXC13-AS) was up-regulated in CC and positively correlated with FZD6. Mechanistically, HOCX13-AS1 augmented FZD through cAMP-response element binding protein-binding protein (CBP)-modulated histone H3 on lysine 27 acetylation (H3K27ac). Additionally, fat mass and obesity-associated protein (FTO) reduced N6-methyladenosine (m6A) and stabilized HOXC13-AS in CC. CONCLUSIONS: In conclusion, this study firstly showed that FTO-stabilized HOXC13-AS epigenetically up-regulated FZD6 and activated Wnt/ß-catenin signaling to drive CC proliferation, invasion, and EMT, suggesting HOXC13-AS as a potential target for CC treatment.