Multimodal imaging in the diagnosis of bone giant cell tumors: A retrospective study.

BACKGROUND: Giant cell tumor of bone is a locally aggressive and rarely metastasizing tumor, and also a potential malignant tumor that may develop into a primary malignant giant cell tumor. AIM: To evaluate the role of multimodal imaging in the diagnosis of giant cell tumors of bone. METHODS: The data of 32 patients with giant cell tumor of bone confirmed by core-needle biopsy or surgical pathology at our hospital between March 2018 and March 2023 were retrospectively selected. All the patients with giant cell tumors of the bone were examined by X-ray, computed tomography (CT) and magnetic resonance imaging (MRI), and 7 of them were examined by positron emission tomography (PET)-CT. RESULTS: X-ray imaging can provide overall information on giant cell tumor lesions. CT and MRI can reveal the characteristics of the internal structure of the tumor as well as the adjacent relationships of the tumor, and these methods have unique advantages for diagnosing tumors and determining the scope of surgery. PET-CT can detect small lesions and is highly valuable for identifying benign and malignant tumors to aid in the early diagnosis of metastasis. CONCLUSION: Multimodal imaging plays an important role in the diagnosis of giant cell tumor of bone and can provide a reference for the treatment of giant cell tumors.

Costunolide enhances cisplatin-induced cytotoxicity in hypopharyngeal SCC FaDu cells by increasing the production of reactive oxygen species.

OBJECTIVE: The sesquiterpene lactone costunolide (CTL) has attracted much attention due to its antitumor effect on a variety of malignant tumors. However, the effect of CTL on hypopharyngeal squamous cell carcinoma (HSCC) remains unclear. This study aimed to examine the effects of this sesquiterpene lactone on HSCC FaDu cells. METHODS: The FaDu cell line was treated with CTL and/or cisplatin. CCK-8 was used to examine cell viability. Annexin-FITC/PI and Hoechst 33258 staining were used to measure apoptosis. Reactive oxygen species (ROS) were analysed by MitoSOX Red staining. Protein expression was examined by Western blotting. RESULTS: CTL (0, 2, 4, 6, 8, 10, 20, 30, and 40 µM) dose-dependently induced cytotoxicity in FaDu cells. CTL increased ROS production and induced apoptosis in FaDu cells. Moreover, CTL synergized with cisplatin to induce apoptosis in FaDu cells. In addition, the caspase inhibitor Z-DEVD-FMK attenuated CTL-induced apoptosis. Western blot analysis showed that CTL increased the expression levels of cleaved caspase-3 and Bax and decreased the expression levels of Bcl-2, phospho-AKT and phospho-NF-κB. CONCLUSION: In conclusion, these data demonstrate that CTL induced apoptosis and enhanced cisplatin-induced cytotoxicity in HSCC FaDu cells.

Puerarin attenuates cisplatin-induced apoptosis of hair cells through the mitochondrial apoptotic pathway.

Puerarin, one of the main components of Pueraria lobata, has been reported to possess a wide range of pharmacological activities, including anti-inflammatory, antioxidative and anti-apoptotic effects. However, the role of puerarin in ototoxic drug-induced hair cell injury has not been well characterized. This study explored whether puerarin protects against cisplatin-induced hair cell damage and its potential mechanisms. The viability of puerarin-treated HEI-OC1 cells was assessed by CCK8 assay. Reactive oxygen species (ROS) was estimated with flow cytometric analysis using Cellrox Green fluorescent probe. Apoptosis-related protein levels were detected by western blot analysis. Immunostaining of the organ of Corti was performed to determine mice cochlear hair cell survival. Our results showed that puerarin improved cell viability and suppressed apoptosis in the cisplatin-damaged HEI-OC1 cells and cochlear hair cells. Mechanistic studies revealed that puerarin attenuated mitochondrial apoptosis pathway by regulating apoptotic related proteins, such as Bax and cleaved caspase-3, and attenuated ROS accumulation after cisplatin damage. Moreover, puerarin was involved in regulating the Akt pathway in HEI-OC1 cells in response to cisplatin. Our results demonstrated that puerarin administration decreased the sensitivity to apoptosis dependent on the mitochondrial apoptotic pathway by reducing ROS generation, which could be used as a new protective agent against cisplatin-induced ototoxicity.

NaF reduces KLK4 expression by decreasing Foxo1/Runx2 expression in LS8 cells.

OBJECTIVE: This study aimed to investigate the effect of high fluoride on runt-related transcription factor 2 (Runx2) expression and to explore the possible relationship among Runx2, forkhead box o1 (Foxo1) and kallikrein 4 (KLK4) in high fluoride-treated ameloblasts. DESIGN: Ameloblast-like cells (LS8 cells) were exposed to various concentrations of sodium fluoride (NaF) for up to 48 h. Runx2 expression was downregulated by gene silencing, and Foxo1 expression was up- and downregulated by gene overexpression and silencing, respectively. The mRNA and protein levels of Runx2, Foxo1, KLK4 and matrix metalloproteinase 20 (MMP20) were detected by qRT-PCR and western blotting. RESULTS: Runx2 expression was decreased in a dose- and time-dependent manner in NaF-treated LS8 cells. The knockdown of Runx2 markedly decreased KLK4 expression in LS8 cells under NaF conditions. However, the variation trend of MMP20 was unclear. In addition, forced Foxo1 expression led to significant upregulation of Runx2 in LS8 cells under NaF conditions. In contrast, the knockdown of Foxo1 markedly decreased the Runx2 protein levels under NaF conditions. Moreover, Foxo1 downregulation markedly decreased runx2 mRNA levels, and this inhibition in LS8 cells was intensified when combined with NaF treatment. CONCLUSION: The results indicated that NaF reduces Runx2 expression in LS8 cells and that decreased Foxo1/Runx2 expression induced by high fluoride is a cause of low KLK4 expression.