Exploring the therapeutic potential of curcumin in oral squamous cell carcinoma (HSC-3 cells): Molecular insights into hypoxia-mediated angiogenesis.

BACKGROUND: Oral cancer represents a substantial global health burden, often associate with hypoxia-induced angiogenesis as a critical factor in its progression. Curcumin, a naturally occurring bioactive compounds, has gained increasing attention for its potential anticancer properties. OBJECTIVE: To assess the impact of curcumin on oral cancer, particularly its role in modulating HIF-1α-mediated angiogenesis in HSC-3 cells. METHODS: Our investigation involved multiple experimental approaches, including MTT assay, aerobic glycolysis by metabolic kit, cell cycle, and apoptosis assessment via flow cytometry. Furthermore, we employed molecular docking techniques to examine the interactions between curcumin and key angiogenesis related proteins, including HIF-1α, VEGF-B, MMP-3, and STAT3. RESULTS: Our results demonstrate that curcumin exerts significant effects on the cell survivability, cell cycle regulation, and apoptosis induction in oral cancer cells. These effects were particularly pronounced under the conditions of HIF-1α mediated angiogenesis. Computational binding analysis revealed strong binding interactions with curcumin and the selected proteins, implying a plausible mechanism through which curcumin may modulate the angiogenic pathways in oral cancer. CONCLUSION: Our research sheds light on the diverse effects of curcumin on oral cancer cells, emphasizing its potential as a promising therapeutic tool for addressing hypoxia-induced angiogenesis. However, further investigation is essential to comprehensively understand the molecular mechanisms underlying these effects in in vitro models. This deeper comprehension is crucial for translating these findings into clinical applications aimed at improving oral cancer treatment.

Unlocking the potential of beta sitosterol: Augmenting the suppression of oral cancer cells through extrinsic and intrinsic signalling mechanisms.

The global increase in the prevalence of oral neoplasms and related deaths can be attributed to social development and lifestyle factors, leading to poor prognosis and a lack of early clinical detection. Oral cancer ranks ranked sixth mostly diagnosed cancer and is a leading cause of cancer-related deaths. In light of these circumstances, our objective was to assess the potential of ß-sitosterol, a naturally occurring herbal compound, as an anticancer agent against KB cells, a representative cell line for oral cancer. Our study primarily focused on evaluating the cytotoxic effect and mRNA expression of apoptotic proteins by ß-sitosterol on KB cells. The results demonstrated a remarkable cytotoxic effect, leading to cell death. Further investigation using flow cytometric analysis revealed that this cell death was mediated through the initiation of the apoptotic signalling by ß-sitosterol. The use of the bioinformatic tool, STITCH, supported our study by predicting drug-protein interactions and suggesting that ß-sitosterol may play a significant role in targeting apoptotic pathways. Additionally, docking results were employed to validate the findings demonstrating high binding affinity of ß-sitosterol with apoptotic-mediated signalling targets. To gain deeper insights into the molecular insights, we measured mRNA levels for BAX, BCL-2, MCL-1, P53, P21, MDM2, caspase3, and caspase9. Based on our comprehensive findings, our study concludes that ß-sitosterol holds significant therapeutic potential against oral cancer cells. These results strongly suggest that this herbal compound should be further explored as a potential treatment option for oral cancer for clinical trial.

Unveiling the anti-cancer mechanisms of calotropin: Insights into cell growth inhibition, cell cycle arrest, and metabolic regulation in human oral squamous carcinoma cells (HSC-3).

Background: Calotropin, a cardiac glycoside obtained from the plant Calotropis gigantea, has demonstrated promising potential as an anti-tumorigenesis compound. Objective: The main objective of this study was to investigate the potential anti-cancer properties of calotropin against HSC-3 oral squamous cancer cells and to elucidate the underlying mechanisms involved in its action. Material and method: Calotropin were treated in HSC-3 to evaluate cell viability by MTT assay. Flow cytometry analysis divulged that calotropin G0/G1 phase cell cycle arrest and apoptosis in HSC-3 cells. Calotropin displayed inhibitory properties against aerobic glycolysis, a metabolic alteration using glucose uptaken, lactose production and LDHA activity assays. Furthermore, migration and invasion assays help that calotropin has ability to reduce the migratory and invasive of HSC-3 cells, using transwell and Matrigel assay. Validation of mRNA expression through RT-PCR. Molecular docking was implemented to validate the binding association of calotropin with apoptosis and metastatic regulating targets. Result: The results exemplify that increasing doses of calotropin effectively hold back the HSC-3 cell progression. Migration and invasion assays help that calotropin has ability to reduce the migratory and invasive of HSC-3 cells, indicating its potential to inhibit cancer metastasis. These results imply that calotropin may influence genes linked to metastasis and apoptosis in order to achieve its beneficial effects on cancer. Docking results provided further support, showing a high binding energy between calotropin and metastasis-mediated pathways. Conclusion: Overall, our findings shed an experimental evidence on how calotropin inhibits the HSC-3 oral squamous cancer cell growth, highlighting the drug's potential as a treatment for oral cancer. Further, investigation on in-vivo experiment is warranted to explore its potential mechanism of action and to develop a novel drug towards clinical trial.

Quantitative assessment of platelet rich fibrin for the repair of extraction socket in a rat model.

The present study evaluated the quantitative effects of platelet-rich fibrin (PRF) for the repair of extraction socket in Sprague Dawley (SD) rat model by assessing several key clinical parameters. Seventy two male SD rats were subjected to surgical extraction of the maxillary right incisor. Rats were randomly divided into four groups with eighteen rats in each group based on the treatment received: extraction socket without treatment of PRF was taken as control (group I). Extraction socket implanted with 0.1, 0.2, and 0.4 mL of PRF was taken as study groups (groups II, III, and IV). The obtained results demonstrated that, low dose of PRF efficiently enhanced the natural healing cascade. Whereas, high dose interfered with native tissue contribution and altered the natural healing process. The beneficial effects of quantity-based application of PRF may raise the possibility of a new approach as complementary therapy besides conventional treatment.

Architectural and Ultrastructural Variations of Human Leukocyte-Rich Platelet-Rich Fibrin and Injectable Platelet-Rich Fibrin.

BACKGROUND: Platelet-rich fibrin (PRF) architecture and ultrastructure plays a crucial role in regulating and coordinating the cellular functions and provides a physical architecture, mechanical stability, and biochemical cues necessary for tissue morphogenesis and homeostasis. No study consciously reported the variation in architecture, ultrastructure, and morphology of leukocyte-rich PRF (L-PRF) and injectable PRF (i-PRF). OBJECTIVE: Hence, the present study was aimed to evaluate the fibrin architecture, ultrastructure, and cell contents of autologous L-PRF and i-PRF. MATERIALS AND METHODS: The autologous L-PRF and i-PRF were prepared from blood samples of healthy donors. The morphological and structural variations were assessed by histopathology, atomic force microscopy, confocal laser scanning microscope, and field emission scanning electron microscope. RESULTS: Disparity was found on architecture and ultrastructure of L-PRF and i-PRF fibrin network. The variation in platelet and leukocyte concentration attributed to the fibrin conformational changes. L-PRF shows thick fibrins with rough surface, whereas in i-PRF, smooth thin fibrins. CONCLUSIONS: The current study revealed that there is heterogeneity between L-PRF and i-PRF fibrin matrix architecture, ultrastructure, platelets, leukocytes, and the fibrin content. These speculate that the diameter, width, roughness, and smoothness of fibrin fibers, pore size, and shapes of L-PRF and i-PRF matrix may initiate and mediate the scaffold functions differently.

Cytokine Expression Pattern and Protein-Protein interaction network analysis of Leucocyte Rich Platelet Rich Fibrin and Injectable Form of Platelet Rich Fibrin.

PURPOSE: Platelet-rich fibrin (PRF) such as leucocyte-rich PRF (L-PRF) and injectable form of PRF (i-PRF) are widely used in various surgical applications. L-PRF- and i-PRF-derived cytokine variations and functional pathways are still unexplored. The aim of the study was to evaluate the expression pattern of Th1-, Th2-, and Th17-related cytokines by L-PRF and i-PRF under in vitro. METHODS: Cytokine levels were evaluated using multi-analyte ELISArray kit. Using elevated level of cytokines, the protein-protein interaction and pathway were predicted by computational method. RESULTS: The expressed cytokine levels were higher in L-PRF than in i-PRF. Specifically in L-PRF, IL8, IL2, IL6, and IL1A were expressed abundantly, whereas IL4, IL10, and IL6 were significantly high in i-PRF. Furthermore, protein-protein interaction (PPI) networks (cytokine-cytokine interactions) and pathway analyses were predicted using higher-order cytokines. PPI networks and gene ontology enrichment analysis showed functional variations between L-PRF and i-PRF. Kyoto Encyclopedia of Gene and Genome pathway analysis found that L-PRF mediates NF-k B signaling, Toll-like receptor signaling (TLR), and MAPK signaling via T-cell receptor signaling pathway. i-PRF is significantly involved in JAK-STAT signaling pathway through upregulation of STAT1. CONCLUSION: Our study concludes that L-PRF and i-PRF act via different pathways that confirm functional variations between them. Therefore, we speculate that L-PRF may be effective in acute phase of chronic wounds such as in diabetes mellitus and immunocompromised patients whereas i-PRF may have a better outcome in acute wounds.

Antimicrobial and antibiofilm potential of injectable platelet rich fibrin-a second-generation platelet concentrate-against biofilm producing oral staphylococcus isolates.

Injectable Platelet rich fibrin (i-PRF) is a platelet concentrate that has been extensively used for multiple medical purposes and is a valuable adjunct for the regeneration of damaged tissues in surgical procedures. The enriched bioactive substances in i-PRF are responsible for speeding the wound healing process. Infection of biofilm producing bacteria in surgical wounds is becoming a serious threat. Research in this field is focused on new strategies to fight infections and to reduce the healing time. The present study was aimed to evaluate the in vitro antimicrobial and antibiofilm effects of i-PRF against oral pathogenic biofilm producing staphylococcus bacteria isolated from patient with dental and oral abscess. The antibacterial activity of i-PRF, was determined through broth microdilution as minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC). i-PRF exhibited bactericidal activity against both non biofilm and biofilm producing bacteria. i-PRF could be potential antimicrobial peptide used to combat postoperative infections caused by biofilm producing staphylococcus.