Objective: Oral squamous cell carcinoma (OSCC) exhibits the highest lethality among head and neck cancers. Treatment for OSCC is limited due to diverse side effects. Quercetin is a natural flavonoid compound found in many kinds of plants and foods. Quercetin has been reported to be a modulator of proliferation and survival in various types of cancers due to its cytotoxic effects. We aimed to investigating chemopreventative roles of quercetin in YD10B and YD38 OSCC cells. Methods: For our study, two different types of OSCC cells were used. YD10B cells are tongue SCC cells with the p53 mutation and YD38 cells are lower gingiva SCC cells without the p53 mutation, respectively. The anticancer effects of quercetin were examined by cell viability, cell cycle, annexin-PI staining, and western blot. Result: Our results showed that quercetin decreased cell viability and induced G1 cell cycle arrest in YD10B and YD38 OSCC cells. Moreover, quercetin remarkably decreased the expression of cell cycle upregulating proteins and increased the expression of a CDK inhibitor. Quercetin also significantly increased the number of annexin-V-positive cells in a dose-dependent manner in both types of OSCC cells. This apoptotic potential of quercetin triggered cleavage of PARP followed by activation of p38 MAPK signaling pathway. Conclusion: In conclusion, this study demonstrates that quercetin shows different anti-cancer responses in OSCC with and without p53 mutation, respectively. Despite different p53 status in OSCC cells, quercetin led to apoptotic signals in both cells. Quercetin repressed cell proliferation with G1 cell cycle arrest and apoptosis by activating the p38 signaling pathway in two OSCC cells with different p53 status. These findings might provide new strategy for OSCC therapy by quercetin.

Mulberry leaves extract (Morus alba extracts; MAE) is known to have therapeutic potentials for numerous human diseases, including diabetes, neurological disorders, cardiovascular diseases, and cancers. However, there has not been sufficient research proving therapeutic effects on oral disease and its related oral risk factors. Thus, we investigated whether MAE has any anti-inflammatory and anti-bacterial effects on risk factors causing oral infectious diseases. To examine the anti-inflammatory response and bacterial inhibition of MAE, we measured intracellular reactive oxygen species (ROS) generation, production of pro-inflammatory cytokines, and the bacterial growth rate. Our study showed that MAE has anti-inflammatory activities, which inhibit the ROS generation and suppressed the production of pro-inflammatory cytokines (TNF-α and IL-6) in human monocyte THP-1 cells by stimulating lipopolysaccharide (LPS) and/or F. nucleatum, which are the virulent factors in periodontal diseases. Furthermore, MAE inhibited the bacterial growth on oral microorganisms (F. nucleatum and S. mutans) infected THP-1 cells. These findings suggested that MAE could be a potential natural source for therapeutic drugs in oral infectious disease.

Gelatin, a natural polymer, provides excellent tissue compatibility for use in tissue rehabilitation. Bioactive glasses (BAG) offer superior capacity in stimulating a bioactive response but show high variability in uptake and solubility. To tackle these drawbacks, a combination of gelatin with BAG is proposed to form composites, which then offer a synergistic response. The cross-linked gelatin structure’s mechanical properties are enhanced by the incorporation of the inorganic BAG, and the rate of BAG ionic supplementation responsible for bioactivity and regenerative potential is better controlled by a protective gelatin layer. Several studies have demonstrated the cellular benefits of these composites in different forms of functional modification such as doping with zinc or incorporation of zinc such as ions directly into the BAG matrix. This review presents a comprehensive perspective on the individual characteristics of BAG and gelatin, including the synthesis and mechanism of action. Further, adaptation of the composite into various applications for bone tissue engineering is discussed and future challenges are highlighted.

Background: Gliosarcoma (GS) is a rare variant of glioblastoma (GBM), characterized by biphasic glial and sarcomatous histology and poor prognosis. Despite its distinct clinical features, GS remains underrepresented in glioma research due to the lack of biologically faithful and experimentally tractable models. Methods: We established patient-derived gliosarcoma organoids (GSOs) from freshly resected tumors using a suspension culture system without enzymatic dissociation. Histological, molecular, and functional properties were evaluated using H&E staining, immunohistochemistry, whole-exome sequencing, 3D invasion assays, and single-cell RNA sequencing (scRNA-seq). Drug response assays were performed using temozolomide and ANA-12 (NTRK2 inhibitor). Results: GSOs preserved key histological features, genetic alterations, and tumor microenvironmental cell populations from the original tumors. They stable growth and viability over extended culture periods and maintained integrity following cryopreservation and recovery, supporting their long-term utility. 3D invasion assays further revealed infiltrative behavior, consistent with the aggressive nature of GS. Histological and molecular analyses revealed that GSOs retained glial and mesenchymal differentiation, diverse non-malignant stromal cells, and case-specific somatic alterations. Comparative scRNA-seq revealed distinct transcriptional programs: GSOs were enriched for fibroblast-like and oligodendrocyte progenitor-like states, while glioblastoma organoids (GBOs) displayed astrocyte-like differentiation and high connectivity signatures. Functional assays confirmed consistent sensitivity of GSOs to temozolomide, and selective therapeutic response to NTRK2 inhibition was observed in the GSO harboring an NTRK2 alteration, supporting the utility for genomic-context-guided therapy. Conclusion: Together, GSOs constitute a tractable and translationally relevant model that faithfully reflects the cellular complexity, genetic landscape, and tumor-specific heterogeneity. This model addresses a critical gap in GS biology and supports its integration into precision oncology.

Background: Osbeckia octandra is a plant endemic to Sri Lanka and is used in ethnomedicine for treating various diseases. However, the anti-cancer properties of O. octandra are yet to be fully investigated. In the present study, we evaluated the anti-cancer effects of O. octandra on oral cancer cells. Methods: Human oral cancer cell lines (HSC2, YD10B, YD38, YD9, and YD32) were used in this study. BrdU incorporation, cell cycle and annexin-V/PI staining were all evaluated using flow cytometry to determine the extent to which O. octandra leaf extract inhibits cell proliferation and induces apoptosis. Cell viability and reactive oxygen species (ROS) were also measured in order to investigate the anti-cancer effects of O. octandra extracts. Western blotting was performed to detect cell cycle related protein such as cyclin d1 and cdk4, and to detect apoptosis-related proteins such as Bcl-2, Bcl-X_L, Bax, Caspase-9, Cleaved caspase-3, Fas, Caspase-8, and Bid. Results: Leaf extract of O. octandra reduced oral squamous cell carcinoma (OSCC) cell viability in a dose-dependent manner. Leaf extract of O. octandra has non-toxic in normal keratinocytes. Also, O. octandra extract interrupted the DNA replication via G1 phase arrests, and this effect was independent of ROS generation. In the apoptosis-related experiments, the population of annexin V-positive cells increased upon treatment with O. octandra extract. Furthermore, the expression of anti-apoptotic protein (Bcl-2 and Bcl-xL) was decreased, whereas the expression of cleaved caspase-3 protein was increased in O. octandra-treated OSCC cells. Conclusions: The results suggest that a leaf extract of O. octandra inhibited the proliferation of OSCC cells through G₁ phase arrest and interrupting DNA replication. The leaf extract of O. octandra could trigger the apoptotic response via caspase 3 activation in OSCC cells. These results suggest that O. octandra has the potential to be developed as an alternative medicine for treating OSCC.

Objective: Angiopoietin-like proteins (ANGPTLs) have emerged as both important regulator of lipid and glucose metabolism as well as insulin sensitivity. In particular, ANGPTL3 activity is one of the most important factors in cancer growth and invasion. Although ANGPTL3 have been studied in OSCC, but the role of ANGPTL3 between OSCC and CAFs has yet to be clearly defined. Thus, this study aimed to investigate the roles of ANGPTL3 in the differentiation of CAFs. Methods: For our study, we used hTERT-hNOFs to replace CAFs by coculturing them with oral squamous cell carcinoma (OSCC) cells. We did a microarray dataset analysis to investigate what factors secreted from OSCC cells can induce cancer associated fibroblastic phenotype in surrounding fibroblasts. The secreted factors were confirmed by RT-PCR, real-time PCR, and Western blot. Result: ANGPTL3 has the most secreted factor derived from various oral cancer cells. To investigate the role of ANGPTL3 in CAFs, we treated rhANGPTL3 in hTERT-hNOFs. The fibroblasts showed an increase of tumor-promoting cytokines (IL-6 and IL-8) and myofibroblastic markers, such as α-SMA and FAP. Conclusion: In conclusion, our study reports the first evidence that ANGPTL3 plays a crucial role in tumor microenvironments by inducing CAF. Therefore, targeting ANGPTL3 may be promising treatment strategy for CAF-targeted therapy in CAF-rich tumors.