Three-dimensional finite element analysis of the biomechanical behaviour of different dental implants under immediate loading during three masticatory cycles.

The study aimed to evaluate the impact of varying modulus of elasticity (MOE) values of dental implants on the deformation and von Mises stress distribution in implant systems and peri-implant bone tissues under dynamic cyclic loading. The implant-bone interface was characterised as frictional contact, and the initial stress was induced using the interference fit method to effectively develop a finite element model for an immediately loaded implant-supported denture. Using the Ansys Workbench 2021 R2 software, an analysis was conducted to examine the deformation and von Mises stress experienced by the implant-supported dentures, peri-implant bone tissue, and implants under dynamic loading across three simulated masticatory cycles. These findings were subsequently evaluated through a comparative analysis. The suprastructures showed varying degrees of maximum deformation across zirconia (Zr), titanium (Ti), low-MOE-Ti, and polyetheretherketone (PEEK) implant systems, registering values of 103.1 µm, 125.68 µm, 169.52 µm, and 844.06 µm, respectively. The Zr implant system demonstrated the lowest values for both maximum deformation and von Mises stress (14.96 µm, 86.71 MPa) in cortical bone. As the MOE increased, the maximum deformation in cancellous bone decreased. The PEEK implant system exhibited the highest maximum von Mises stress (59.12 MPa), whereas the Ti implant system exhibited the lowest stress (22.48 MPa). Elevating the MOE resulted in reductions in both maximum deformation and maximum von Mises stress experienced by the implant. Based on this research, adjusting the MOE of the implant emerged as a viable approach to effectively modify the biomechanical characteristics of the implant system. The Zr implant system demonstrated the least maximum von Mises stress and deformation, presenting a more favourable quality for preserving the stability of the implant-bone interface under immediate loading.

Radical meta-C-H Halogenation of Azines via N-Benzyl Activation Strategy.

Regioselective halogenation of six-membered N-heteroarenes is crucial for precise functional derivatization. We present a meta-selective halogenation method for pyridines, quinolines, and isoquinolines via electrophilic halogen radical addition utilizing an N-benzyl activation strategy. This method achieves C3- and C5-dihalogenation in pyridines, C3- and C6-dihalogenation in quinolines, and C3-monohalogenation in isoquinolines. The feasibility and potential applications of this method were validated through scale-up reactions and the bromination of quinoline derivatives with biomolecular fragments.

The role of neutrophil extracellular traps in ß-methylamino L-alanine-induced liver injury in mice.

The non-protein amino acid ß-N-methylamino-L-alanine (BMAA), produced by cyanobacteria, has been recognized as a neurotoxin. L-serine as an antagonist of BMAA can effectively alleviate BMAA-induced neurotoxicity. Although BMAA has long been emphasized as a neurotoxin, with the emergence of BMAA detected in a variety of algae in freshwater around the world and its clear biological enrichment effect, it is particularly important to study the non-neurotoxic adverse effects of BMAA. However, there is only limited evidence to support the ability of BMAA to cause oxidative damage in the liver. The exact molecular mechanism of BMAA-induced liver injury is still unclear. The formation of neutrophil extracellular traps (NETs) is a 'double-edged sword' for the organism, excessive formation of NETs is associated with inflammatory diseases of the liver. Our results innovatively confirmed that BMAA was able to cause the formation of NETs in the liver during the liver injury. The possible mechanism may associated with the regulation of ERK/p38 and cGAS/STING signaling pathways. The massive formation of NETs was able to exacerbate the BMAA-induced oxidative stress and release of inflammatory factors in the mice liver. And the removal of NETs could alleviate this injury. This article will bring a new laboratory evidence for BMAA-induced non-neurotoxicity and immunotoxicity.

In silico mining and identification of a novel lipase from Paenibacillus larvae: Rational protein design for improving catalytic performance.

Lipases play a vital role in various biological processes, from lipid metabolism to industrial applications. However, the ever-evolving challenges and diverse substrates necessitate the continual exploration of novel high-performance lipases. In this study, we employed an in silico mining approach to search for lipases with potential high sn-1,3 selectivity and catalytic activity. The identified novel lipase, PLL, from Paenibacillus larvae subsp. larvae B-3650 exhibited a specific activity of 111.2 ± 5.5 U/mg towards the substrate p-nitrophenyl palmitate (pNPP) and 6.9 ± 0.8 U/mg towards the substrate olive oil when expressed in Escherichia coli (E. coli). Computational design of cysteine mutations was employed to enhance the catalytic performance of PLL. Superior stability was achieved with the mutant K7C/A386C/H159C/K108C (2M3/2M4), showing an increase in melting temperature (Tm) by 1.9°C, a 2.05-fold prolonged half-life at 45°C, and no decrease in enzyme activity. Another mutant, K7C/A386C/A174C/A243C (2M1/2M3), showed a 4.9-fold enhancement in specific activity without compromising stability. Molecular dynamics simulations were conducted to explore the mechanisms of these two mutants. Mutant 2M3/2M4 forms putative disulfide bonds in the loop region, connecting the N- and C-termini of PLL, thus enhancing overall structural rigidity without impacting catalytic activity. The cysteines introduced in mutant 2M1/2M3 not only form new intramolecular hydrogen bonds but also alter the polarity and volume of the substrate-binding pocket, facilitating the entry of large substrate pNPP. These results highlight an efficient in silico exploration approach for novel lipases, offering a rapid and efficient method for enhancing catalytic performance through rational protein design.

Suppression of GATA3 promotes epithelial-mesenchymal transition and simultaneous cellular senescence in human extravillous trophoblasts.

The regulatory mechanism of the transcription factor GATA3 in the differentiation and maturation process of extravillous trophoblasts (EVT) in early pregnancy placenta, as well as its relevance to the occurrence of pregnancy disorders, remains poorly understood. This study leveraged single-cell RNA sequencing data from placental organoid models and placental tissue to explore the dynamic changes in GATA3 expression during EVT maturation. The expression pattern exhibited an initial upregulation followed by subsequent downregulation, with aberrant GATA3 localization observed in cases of recurrent miscarriage (RM). By identifying global targets regulated by GATA3 in primary placental EVT cells, JEG3, and HTR8/SVneo cell lines, this study offered insights into its regulatory mechanisms across different EVT cell models. Shared regulatory targets among these cell types and activation of trophoblast cell marker genes emphasized the importance of GATA3 in EVT differentiation and maturation. Knockdown of GATA3 in JEG3 cells led to repression of GATA3-induced epithelial-mesenchymal transition (EMT), as evidenced by changes in marker gene expression levels and enhanced migration ability. Additionally, interference with GATA3 accelerated cellular senescence, as indicated by reduced proliferation rates and increased activity levels for senescence-associated ß-galactosidase enzyme, along with elevated expression levels for senescence-associated genes. This study provides comprehensive insights into the dual role of GATA3 in regulating EMT and cellular senescence during EVT differentiation, shedding light on the dynamic changes in GATA3 expression in normal and pathological placental conditions.

The tumor-associated fibrotic reactions in microenvironment aggravate glioma chemoresistance.

Malignant gliomas are one of the most common and lethal brain tumors with poor prognosis. Most patients with glioblastoma (GBM) die within 2 years of diagnosis, even after receiving standard treatments including surgery combined with concomitant radiotherapy and chemotherapy. Temozolomide (TMZ) is the first-line chemotherapeutic agent for gliomas, but the frequent acquisition of chemoresistance generally leads to its treatment failure. Thus, it's urgent to investigate the strategies for overcoming glioma chemoresistance. Currently, many studies have elucidated that cancer chemoresistance is not only associated with the high expression of drug-resistance genes in glioma cells but also can be induced by the alterations of the tumor microenvironment (TME). Numerous studies have explored the use of antifibrosis drugs to sensitize chemotherapy in solid tumors, and surprisingly, these preclinical and clinical attempts have exhibited promising efficacy in treating certain types of cancer. However, it remains unclear how tumor-associated fibrotic alterations in the glioma microenvironment (GME) mediate chemoresistance. Furthermore, the possible mechanisms behind this phenomenon are yet to be determined. In this review, we have summarized the molecular mechanisms by which tumor-associated fibrotic reactions drive glioma transformation from a chemosensitive to a chemoresistant state. Additionally, we have outlined antitumor drugs with antifibrosis functions, suggesting that antifibrosis strategies may be effective in overcoming glioma chemoresistance through TME normalization.

Highly selective and additive-free Pd(OAc)2/CPP catalyzed hydroaminocarbonylation of alkynes.

Herein, the synthesis of branched α,ß-unsaturated amides by a hydroaminocarbonylation reaction of alkynes with various amine substrates such as aromatic amines, aliphatic amines, solid amine sources like NH4HCO3, and even strongly basic piperidines is reported, using a Pd(OAc)2/hybrid N-heterocyclic carbene-phosphine-phosphine (CPP) catalytic system. The reactions feature no additives, wide substrate scope, high selectivity (b/l > 99 : 1) and excellent yields. Mechanistic studies have disclosed that the reaction takes place via a palladium hydride pathway. CPP adopts a hybrid bidentate ligand conformation with a carbene-phosphine coordination mode, wherein one phosphorus atom remains externally accessible, potentially serving as a stabilizing auxiliary during catalytic cycles.

A Simplified GBR Treatment and Evaluation of Posterior Seibert Class I Ridge Defects via Bio-collagen and Platelet-Rich Fibrin: A Retrospective Study.

BACKGROUND: Classical guided bone regeneration (GBR) treatments can achieve favorable clinical results for ridge defects. However, extensive bone augmentation in the non-esthetic area in the posterior region for minor ridge defects is unnecessary. Therefore, this study used a collagen and Platelet-rich fibrin (PRF) mixture for bone augmentation on minor posterior ridge defects and evaluated the effects. METHODS: 22 Seibert Class I ridge defects were treated with BC and covered with a PRF membrane (simplified guided bone regeneration, simplified GBR) and other 22 were treated with Bio-Oss and covered with Bio-Gide (classical GBR). Cone-beam computed tomography imaging was conducted 6 months post-surgery to compare the ridge's horizontal width (HW) and buccal ridge's horizontal width to assess the osteogenic effect. In addition, the buccal ridge contour morphology was studied and classified. RESULTS: The buccal ridge contour of simplified GBR was Type A in 14 cases, Type B in 7 cases, and Type C in 1 case and it of classical GBR was Type A in 11 cases, Type B in 8 cases, and Type C in 3 cases. The mean HW significantly increased by 1.50 mm of simplified GBR treatment, while it increased by 1.83 mm in classical GBR treatment. CONCLUSION: The combined use of BC and PRF had a significant effect on bone augmentation and this treatment exhibited promising clinical results for correcting posterior Seibert Class I ridge defects. The morphological classification of the reconstructive effect in this study can be utilized in future clinical work.

Enhancing the Thermostability and Catalytic Activity of the Lipase from Rhizopus oryzae via Introducing N-Glycosylation.

Lipase from Rhizopus oryzae (ROL) exhibits remarkable sn-1,3 stereoselectivity and catalytic activity, but its poor thermostability limits its applications in the production of 1,3-dioleoyl-2-palmitoyl glycerol (OPO, a high-quality substitute for human milk fat). In this work, a semirational method was proposed to engineer the thermostability and catalytic activity of 4M (ROL mutant in our previous study). First, a computer-aided design is performed using 4M as a template, and N-glycosylation mutants are then recombinantly expressed and screened in Pichia pastoris, the optimal mutant N227 exhibited a half-life of 298.8 h at 45 °C, which is 7.23-folds longer than that of 4M. Its catalytic activity also reached 1043.80 ± 61.98 U/mg, representing a 29.2% increase compared to 4M (808.02 ± 47.02 U/mg). Molecular dynamics simulations of N227 suggested that the introduction of glycan enhanced the protein rigidity, while the strong hydrogen bonds formed between the glycan and the protein stabilized the lipase structure, thereby improving its thermostability. The acidolysis reaction between oleic acid (OA) and glycerol tripalmitate (PPP) was successfully carried out using immobilized N227, achieving a molar conversion rate of 90.2% for PPP. This engineering strategy guides the modification of lipases, while the glycomutants obtained in this study have potential applications in the biosynthesis of OPO.

Selective biosorption of Li+ in aqueous solution by lithium ion-imprinted material on the surface of chitosan/attapulgite.

The extraction of Li+ from liquid lithium resources is a pivotal focus of current research endeavors. Attapulgite (ATP), characterized by its distinctive layered structure and inherent ion exchange properties, emerges as an exceptional material for fabricating lithium-ion sieve. Ion-imprinted chitosan/ATP composite materials are successfully synthesized, demonstrating efficacy in selectively absorbing Li+. The results emphasize the rich functional groups present in H-CTP-2, enhancing its absorbability and selectivity, with an adsorption capacity of 37.56 mg•g-1. The adsorption conforms to the Langmuir and pseudo-second-order kinetic model. Li+ coordination involves amino and hydroxyl group, indicating a chemisorption process. Furthermore, the substantial pore structure and significant specific surface area of ATP significantly promote Li+ adsorption, suggesting its participation not only in chemisorption but also in physical adsorption. The fabricated ion-imprinted materials boast substantial adsorption capacity, exceptional selectivity, and rapid kinetics, highlighting their potential for effectively separating Li+ from aqueous solution.

Reduction in Serum Concentrations of Uremic Toxins Driven by Bifidobacterium Longum Subsp. Longum BL21 is Associated with Gut Microbiota Changes in a Rat Model of Chronic Kidney Disease.

Gut microbiota dysbiosis and consequent impairment of gut barrier function, culminating in elevated levels of uremic toxins, are prevalent in chronic kidney disease (CKD) patients. These toxins, notably indoxyl sulphate (IS), indole-3-acetic acid (IAA), and trimethylamine oxide (TMAO), are implicated in a spectrum of CKD-related complications, including cardiovascular disease, bone and mineral disorders, and inflammation. The specific impacts of various probiotics on these CKD manifestations remain unexplored. This study delved into the potential of dietary probiotic interventions, particularly Bifidobacterium longum subsp. longum BL21, to modulate gut microbiota and mitigate metabolic disorders in a CKD rat model. Over a six-week period, we administered a dietary regimen of BL21 and conducted comprehensive analyses, including serum uremic toxin quantification and 16S rRNA gene sequencing, to systematically profile gut microbial alterations at the phylogenetic level. Our findings reveal that BL21 intervention significantly ameliorated CKD-induced disruptions in gut microbial populations, enhancing both microbial richness and the relative abundance of key taxa. Importantly, BL21 appeared to exert its beneficial effects by modulating the abundance of crucial species such as Barnesiella and Helicobacter. Functionally, the intervention markedly normalized serum levels of IS, IAA, and TMAO, while potentially attenuating p-cresol sulphate (PCS) and p-cresol glucuronide (PCG) concentrations. Consequently, BL21 demonstrated efficacy in regulating gut microbiota and curtailing the accumulation of uremic toxins. Our results advocate for the utilization of BL21 as a dietary intervention to diminish serum uremic toxins and re-establish gut microbiota equilibrium at the phylogenetic level, underscoring the promise of probiotic strategies in the management of CKD.

TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation.

BACKGROUND: Ovarian cancer is a common gynecological tumor with high malignant potential and poor prognosis. TRIM8, is involved in the development of various tumors, but its precise regulatory role in ovarian cancer is still unknown. AIMS: The aim of this study was to explore the specific mechanism by which TRIM8 regulates ovarian cancer. MATERIALS AND METHODS: We used bioinformatics analysis to screen for high expression of TRIM8 in ovarian cancer. The expression of TRIM8 in healthy and cancerous ovarian tissues was assessed by immunofluorescence. TRIM8 was silenced or overexpressed in ovarian cancer cell lines, with cell proliferation and migration evaluated by CCK8, transwell and clonal formation assays. The effect of TRIM8 on ovarian cancer cells in vivo was assessed by subcutaneous tumor formation experiments in nude mice. The potential interacting protein VDAC2 was identified by mass spectrometry. The mechanism underlying TRIM8 regulation of VDAC2 was evaluated by co-immunoprecipitation and western blotting. RESULTS: TRIM8 was overexpressed in ovarian cancer. TRIM8 promoted the proliferation and migration of ovarian cancer cells in vitro and the growth of subcutaneous tumors in mice in vivo. TRIM8 interacted with VDAC2, weakened the stability of the protein, and promoted its polyubiquitination and subsequent degradation. Knockdown of VDAC2 increased the resistance of ovarian cancer cells to iron death, whereas overexpression of VDAC2 attenuated ovarian cancer progression induced by TRIM8 overexpression. DISCUSSION: TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation, these finding may provide new targets for the treatment of ovarian cancer. CONCLUSION: TRIM8 degraded VDAC2 through the ubiquitination pathway, increased the resistance of ovarian cancer cells to iron death, and promoted the proliferation and migration of ovarian cancer.

Exercise therapy in postoperative patients with temporomandibular joint internal derangement: A systematic review.

OBJECTIVE: Postoperative patients with temporomandibular joint internal derangement (ID) often have problems such as limited mouth opening and pain. Exercise therapy can be advantageous for improving the recovery of patients following surgery. However, there is continuing discussion on the precise aspects of the exercise program, including the optimal timing, length, intensity, and use of assistive equipment. Hence, this study aimed to incorporate pre-existing exercise treatment regimens and investigate their impact. METHODS: Publications that detailed the clinical treatment of patients with temporomandibular joint ID who received postoperative exercise therapy interventions were included. Nine databases were searched until October 1st, 2023. The JBI critical appraisal tools were used to assess the methodological quality of the included studies. RESULTS: Five studies were finally included for subsequent analysis; two were randomised controlled studies, and three were quasi-experimental. Exercises suitable for such patients encompass vertical, transverse, and horizontal stretching, among which vertical stretch can be divided into active and passive movements. The start time ranged from the first to the fifth week after surgery, with a duration of 1-6 months. Although the data in the studies could not be integrated and further analysed, preliminary results showed that maximum mouth opening and pain in patients improved significantly. The therapeutic effect of combining three exercise methods was best and was related to patient compliance. CONCLUSION: Exercise therapy positively affects postoperative rehabilitation in patients with temporomandibular joint ID. It is proposed that targeted, comprehensive studies be conducted to provide a basis for designing more sophisticated exercise therapy regimens and further confirm its curative effect.

Sequence-Guided Redesign of an Omega-Transaminase from Bacillus megaterium for the Asymmetric Synthesis of Chiral Amines.

ω-Transaminases (ω-TAs) are attractive biocatalysts asymmetrically catalyzing ketones to chiral amines. However, poor non-native catalytic activity and substrate promiscuity severely hamper its wide application in industrial production. Protein engineering efforts have generally focused on reshaping the substrate-binding pockets of ω-TAs. However, hotspots around the substrate tunnel as well as distant sites outside the pockets may also affect its activity. In this study, the ω-TA from Bacillus megaterium (BmeTA) was selected for engineering. The tunnel mutation Y164F synergy with distant mutation A245T which was acquired through a multiple sequence alignment showed improved soluble expression, a 3.7-fold higher specific activity and a 19.9-fold longer half-life at 45 °C. Molecule Dynamics simulation explains the mechanism of improved catalytic activity, enhanced thermostability and improved soluble expression of BmeTAY164F/A245T(2 M). Finally, the resting cells of 2 M were used for biocatalytic processes. 450 mM of S-methoxyisopropylamine (S-MOIPA) was obtained with an ee value of 97.3 % and a conversion rate of 90 %, laying the foundation for its industrial production. Mutant 2 M was also found to be more advantageous in catalyzing the transamination of various ketones. These results demonstrated that sites that are far away from the active center also play an important role in the redesign of ω-TAs.

Integrated analyses reveal the diagnostic and predictive values of COL5A2 and association with immune environment in Crohn's disease.

The pathogenesis of Crohn's disease (CD) involves abnormal immune cell infiltration and dysregulated immune response. Therefore, thorough research on immune cell abnormalities in CD is crucial for improved treatment of this disease. Single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data of CD were obtained from the Gene Expression Omnibus (GEO) database. Cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT), weighted gene co-expression network analysis (WGCNA), protein-protein interaction (PPI) networks evaluated the proportion of immune infiltrating cells, constructed co-expression network and identified key genes, respectively. Based on the dataset (GSE134809), 15 cell clusters were defined and labeled as different cell types. Among the 11 modules, the yellow module had the closest relationship with plasma cells (cluster 5). Confirmed using RNA sequencing and IHC assay, the expression of COL5A2 in CD samples was higher than that in control samples. Furthermore, the COL5A2 protein expression remarkably decreased in the group of patients who responded to anti-tumor necrosis factor (TNF) treatments, compared to the non-response group. The comprehensive analyses described here provided novel insight into the landscape of CD-associated immune environment. In addition, COL5A2 were identified as potential diagnostic indicators for CD, as well as promising predictive markers for CD patients.

Synergistic Engineering of CoO/MnO Heterostructures Integrated with Nitrogen-Doped Carbon Nanofibers for Lithium-Ion Batteries.

The integration of heterostructures within electrode materials is pivotal for enhancing electron and Li-ion diffusion kinetics. In this study, we synthesized CoO/MnO heterostructures to enhance the electrochemical performance of MnO using a straightforward electrostatic spinning technique followed by a meticulously controlled carbonization process, which results in embedding heterostructured CoO/MnO nanoparticles within porous nitrogen-doped carbon nanofibers (CoO/MnO/NC). As confirmed by density functional theory calculations and experimental results, CoO/MnO heterostructures play a significant role in promoting Li+ ion and charge transfer, improving electronic conductivity, and reducing the adsorption energy. The accelerated electron and Li-ion diffusion kinetics, coupled with the porous nitrogen-doped carbon nanofiber structure, contribute to the exceptional electrochemical performance of the CoO/MnO/NC electrode. Specifically, the as-prepared CoO/MnO/NC exhibits a high reversible specific capacity of 936 mA h g-1 at 0.1 A g-1 after 200 cycles and an excellent high-rate capacity of 560 mA h g-1 at 5 A g-1, positioning it as a competitive anode material for lithium-ion batteries. This study underscores the critical role of electronic and Li-ion regulation facilitated by heterostructures, offering a promising pathway for designing transition metal oxide-based anode materials with high performances for lithium-ion batteries.

A pathological joint-liver axis mediated by matrikine-activated CD4+ T cells.

The knee joint has long been considered a closed system. The pathological effects of joint diseases on distant organs have not been investigated. Herein, our clinical data showed that post-traumatic joint damage, combined with joint bleeding (hemarthrosis), exhibits a worse liver function compared with healthy control. With mouse model, hemarthrosis induces both cartilage degeneration and remote liver damage. Next, we found that hemarthrosis induces the upregulation in ratio and differentiation towards Th17 cells of CD4+ T cells in peripheral blood and spleen. Deletion of CD4+ T cells reverses hemarthrosis-induced liver damage. Degeneration of cartilage matrix induced by hemarthrosis upregulates serological type II collagen (COL II), which activates CD4+ T cells. Systemic application of a COL II antibody blocks the activation. Furthermore, bulk RNAseq and single-cell qPCR analysis revealed that the cartilage Akt pathway is inhibited by blood treatment. Intra-articular application of Akt activator blocks the cartilage degeneration and thus protects against the liver impairment in mouse and pig models. Taken together, our study revealed a pathological joint-liver axis mediated by matrikine-activated CD4+ T cells, which refreshes the organ-crosstalk axis and provides a new treatment target for hemarthrosis-related disease. Intra-articular bleeding induces cartilage degradation through down-reulation of cartilage Akt pathway. During this process, the soluble COL II released from the damaged cartilage can activate peripheral CD4+ T cells, differention into Th17 cells and secretion of IL-17, which consequently induces liver impairment. Intra-articular application of sc79 (inhibitor of Akt pathway) can prevent the cartilage damage as well as its peripheral influences.

Efficient and selective external activator-free cobalt catalyst for hydroboration of terminal alkynes enabled by BiPyPhos.

Herein, a robust catalyst system, composed of a bipyridine-based diphosphine ligand (BiPyPhos) and a cobalt precursor Co(acac)2, is successfully developed and applied in the hydroboration of terminal alkynes, exclusively affording various versatile ß-E-vinylboronates in high yields at room temperature.

Exploring the Anticancer Properties of Sakuranin Flavanone in Human Oropharyngeal Squamous Carcinoma Cells by Studying Its Effects on Caspase-driven Apoptosis, Mitochondrial Membrane Potential (MMP) Loss, Cell Migratory and Invasiveness and m-TOR/PI3K/AKT Signalling Pathway.

Sakuranin is a flavanone which is a class of flavonoids found abundantly in Prunus species. Flavonoids have been long known for their anticancer properties against a range of human cancers. However, there are no previous reports on the anticancer effects of sakuranin flavanone molecule. This study was designed to study the anticancer effects of sakuranin against human oropharyngeal carcinoma cells along with investigating its effects on caspase-mediated apoptosis, mitochondrial membrane potential (MMP) loss, cell migration and invasion and m-TOR/PI3K/AKT signalling pathway. MTT assay was used to study effects on cell viability. The apoptotic studies were carried out through AO/EB staining, annexin V/FITC staining, comet assay and western blotting assay. Transwell chambers assay was used to study effects on cell migration and invasion. Flow cytometry was used to study effects of Sakuranin on mitochondrial membrane potential loss (MMP). Finally, western blotting was used to investigate m-TOR/PI3K/AKT signalling pathway. Results indicated that Sakuranin led to potent cell proliferation inhibition in a dose-dependent manner. Sakuranin also induced apoptotic cell death as indicated by fluorescence microscopy and annexin V/FITC staining assays. The apoptotic induction was mediated via activation of caspase-3, caspase-9, and Bax while as it led to downregulation of Bcl-2. Sakuranin also caused inhibition of cell migration and cell invasion along with causing significant decrease in MMP. Sakuranin also caused inhibition of expressions of proteins related with m-TOR/PI3K/AKT signalling pathway. In conclusion, the current findings clearly indicate anticancer effects of Sakuranin flavanone in human oropharyngeal cancer cells and are mediated via caspase activated apoptosis, inhibition of cell migration and invasion, loss of mitochondrial membrane potential and targeting m-TOR/PI3K/AKT signalling pathway.