Differential diagnosis of benign and lung adenocarcinoma presenting as larger solid nodules and masses based on multiscale CT radiomics.

PURPOSE: To develop a better radiomic model for the differential diagnosis of benign and lung adenocarcinoma lesions presenting as larger solid nodules and masses based on multiscale computed tomography (CT) radiomics. MATERIALS AND METHODS: This retrospective study enrolled 205 patients with solid nodules and masses from Center 1 between January 2010 and February 2022 and Center 2 between January 2019 and February 2022. After applying the inclusion and exclusion criteria, we retrospectively enrolled 165 patients from two centers and assigned them to the training dataset (n = 115) or the test dataset (n = 50). Radiomics features were extracted from volumes of interest on CT images. A gradient boosting decision tree (GBDT) was used for data dimensionality reduction to perform the final feature selection. Four models were developed using clinical data, conventional imaging features and radiomics features, namely, the clinical and image model (CIM), the plain CT radiomics model (PRM), the enhanced CT radiomics model (ERM) and the combined model (CM). Model performance was evaluated to determine the best model for identifying benign and lung adenocarcinoma presenting as larger solid nodules and masses. RESULTS: In the training dataset, the areas under the curve (AUCs) for the CIM, PRM, ERM, and CM were 0.718, 0.806, 0.819, and 0.917, respectively. The differential diagnostic capability of the ERM was better than that of the PRM and the CIM. The CM was optimal. Intermediate and junior radiologists and respiratory physicians achieved improved obviously diagnostic results with the radiomics model. The senior radiologists showed slight improved diagnostic results after using the radiomics model. CONCLUSION: Radiomics may have the potential to be used as a noninvasive tool for the differential diagnosis of benign and lung adenocarcinoma lesions presenting as larger solid nodules and masses.

Apoptotic metabolites ameliorate bone aging phenotypes via TCOF1/FLVCR1-mediated mitochondrial homeostasis.

Over 50 billion cells undergo apoptosis each day in an adult human to maintain tissue homeostasis by eliminating damaged or unwanted cells. Apoptotic deficiency can lead to age-related diseases with reduced apoptotic metabolites. However, whether apoptotic metabolism regulates aging is unclear. Here, we show that aging mice and apoptosis-deficient MRL/lpr (B6.MRL-Faslpr/J) mice exhibit decreased apoptotic levels along with increased aging phenotypes in the skeletal bones, which can be rescued by the treatment with apoptosis inducer staurosporine (STS) and stem cell-derived apoptotic vesicles (apoVs). Moreover, embryonic stem cells (ESC)-apoVs can significantly reduce senescent hallmarks and mtDNA leakage to rejuvenate aging bone marrow mesenchymal stem cells (MSCs) and ameliorate senile osteoporosis when compared to MSC-apoVs. Mechanistically, ESC-apoVs use TCOF1 to upregulate mitochondrial protein transcription, resulting in FLVCR1-mediated mitochondrial functional homeostasis. Taken together, this study reveals a previously unknown role of apoptotic metabolites in ameliorating bone aging phenotypes and the unique role of TCOF1/FLVCR1 in maintaining mitochondrial homeostasis.

Investigating the molecular mechanism of vitexin targeting CDK1 to inhibit colon cancer cell proliferation via GEO chip data mining, computer simulation, and biological activity verification.

The objective of this study is to explore the antiproliferative activity of the traditional Chinese medicine monomer vitexin on colon cancer HCT-116 cells and its underlying mechanism. The in vitro antiproliferative activity of vitexin on colon cancer HCT-116 cells was evaluated using the CCK-8 assay. Potential drug targets for colon cancer were identified through GEO chip data mining, and molecular docking using Schrödinger software was conducted. Molecular dynamics simulations were employed to deeply analyze the interaction between candidate compounds and target proteins. Flow cytometry was employed to examine the cell cycle. The impact of vitexin on the expression of CDK1/cyclinB proteins in HCT-116 cells was assessed through Western blot analysis, immunofluorescence, and CDK inhibition assay. Vitexin exhibited inhibitory effects on colon cancer HCT-116 cells, with a half inhibitory concentration (IC50) value of 203.27 ± 9.85 µmol/L. The analysis of differential gene expression in GEO and TCGA datasets, along with the GENECARD dataset of related disease genes, identified 91 disease targets, including "CDK1." Vitexin induced cell cycle arrest in the G2/M phase of HCT-116 cells. Molecular docking revealed a strong interaction between Vitexin and CDK1 (Docking score - 9.497), with molecular dynamics simulations confirming the stability of the Vitexin-CDK1 complex and comparable inhibitory effects to Flavopiridol. Vitexin can inhibit the expression of CDK1/cyclin B proteins in HCT-116 cells, with an IC50 of 58.06 ± 3.07 µmol/L. Vitexin may inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.

Experimental Study on Oil-Gas Interaction Mechanism during Offshore Heavy Oil Gas Injection.

Offshore heavy oil injection gas extraction is a highly scrutinized area in today's petroleum industry. However, the interaction mechanisms between oil and gas are not clear. To elucidate these mechanisms, an indoor experimental setup was established for research purposes. The effects of different types of gases on heavy oil expansion, mass transfer mechanisms between gas and heavy oil, the influence of gas injection on heavy oil phase behavior, and the testing of minimum miscibility pressures are investigated in this study. The results indicate that CO2 yields the best reduction in the heavy oil viscosity. Both forward and backward multiple contact mass transfer processes demonstrate nonmiscible multiple contact dynamic displacement mechanisms involving CO2 dissolution and condensation, as well as C1 extraction and coextraction. Nonmiscible multiple contact dynamic displacement of natural gas primarily involves limited dissolution and condensation of light hydrocarbon components and intermediate hydrocarbon components, with an extremely weak extraction effect. The minimum miscibility pressures are in the order of CO2 < natural gas < N2. This research provides important experimental evidence and theoretical guidance for further improving offshore heavy oil injection gas technology and practice.

Nucleic acid aptamer-based electrochemical sensor for the detection of serum P-tau231 and the instant screening test of Alzheimer's disease.

The instant screening of patients with a tendency towards developing Alzheimer's disease (AD) is significant for providing preventive measures and treatment. However, the current imaging-based technology cannot meet the requirements in the early stage. Developing biosensor-based liquid biopsy technology could be overcoming this bottleneck problem. Herein, we developed a simple, low-cost, and sensitive electrochemical aptamer biosensor for detecting phosphorylated tau protein threonine 231 (P-tau231), the earliest and one of the most efficacious abnormally elevated biomarkers of AD. Gold nanoparticles (AuNPs) were electrochemically synthesized on a glassy carbon electrode as the transducer, exhibiting excellent conductivity, and were applied to amplify the electrochemical signal. A nucleic acid aptamer was designed as the receptor to capture the P-tau231 protein, specifically through the formation of an aptamer-antigen complex. The proposed biosensor showed excellent sensitivity in detecting P-tau 231, with a broad linear detection range from 10 to 107 pg/mL and a limit of detection (LOD) of 2.31 pg/mL. The recoveries of the biosensor in human serum ranged from 97.59 to 103.26%, demonstrating that the biosensor could be used in complex practical samples. In addition, the results showed that the developed biosensor has good repeatability, reproducibility, and stability, which provides a novel method for the early screening of AD.

Near-infrared imaging for visualizing the synergistic relationship between autophagy and NFS1 protein during multidrug resistance using an ICT-TICT integrated platform.

Drug resistance is a major challenge for cancer treatment, and its identification is crucial for medical research. However, since drug resistance is a multi-faceted phenomenon, it is important to simultaneously evaluate multiple target fluctuations. Recently developed fluorescence-based probes that can simultaneously respond to multiple targets offer many advantages for real-time and in situ monitoring of cellular metabolism, including ease of operation, rapid reporting, and their non-invasive nature. As such we developed a dual-response platform (Vis-H2S) with integrated ICT-TICT to image H2S and viscosity in mitochondria, which could simultaneously track fluctuations in cysteine desulfurase (NFS1 protein and H2S inducer) and autophagy during chemotherapy-induced multidrug resistance. This platform could monitor multiple endogenous metabolites and the synergistic relationship between autophagy and NFS1 protein during multidrug resistance induced by chemotherapy. The results indicated that chemotherapeutic drugs simultaneously up-regulate the levels of NFS1 protein and autophagy. It was also found that the NFS1 protein was linked with autophagy, which eventually led to multidrug resistance. As such, this platform could serve as an effective tool for the in-depth exploration of drug resistance mechanisms.

Decreased NMIIA heavy chain phosphorylation at S1943 promotes mitoxantrone resistance by upregulating BCRP and N-cadherin expression in breast cancer cells.

Mitoxantrone (MX) is an effective treatment for breast cancer; however, high efflux of MX that is accomplished by breast cancer resistance protein (BCRP) leads to acquired multidrug resistance (MDR), reducing MX's therapeutic efficacy in breast cancer. Non-muscle myosin IIA (NMIIA) and its heavy phosphorylation at S1943 have been revealed to play key roles in tumor metastasis and progression, including in breast cancer; however, their molecular function in BCRP-mediated MDR in breast cancer remains unknown. In this study, we revealed that the expression of NMIIA heavy chain phosphorylation at S1943 was downregulated in BCRP-overexpressing breast cancer MCF-7/MX cells, and stable expression of NMIIA-S1943A mutant increased BCRP expression and promoted the resistance of MCF-7/MX cells to MX. Meanwhile, NMIIA S1943 phosphorylation induced by epidermal growth factor (EGF) was accompanied by the downregulation of BCRP in MCF-7/MX cells. Furthermore, stable expression of NMIIA-S1943A in MCF-7/MX cells resulted in upregulation of N-cadherin and the accumulation of ß-catenin on the cell surface, which inhibited the nucleus translocation of ß-catenin and Wnt/ß-catenin-based proliferative signaling. EGF stimulation of MCF-7/MX cells showed the downregulation of N-cadherin and ß-catenin. Our results suggest that decreased NMIIA heavy phosphorylation at S1943 increases BCRP expression and promotes MX resistance in breast cancer cells via upregulating N-cadherin expression.

Impaired cerebral microvascular endothelial cells integrity due to elevated dopamine in myasthenic model.

Myasthenia gravis is an autoimmune disease characterized by pathogenic antibodies that target structures of the neuromuscular junction. However, some patients also experience autonomic dysfunction, anxiety, depression, and other neurological symptoms, suggesting the complex nature of the neurological manifestations. With the aim of explaining the symptoms related to the central nervous system, we utilized a rat model to investigate the impact of dopamine signaling in the central nervous and peripheral circulation. We adopted several screening methods, including western blot, quantitative PCR, mass spectrum technique, immunohistochemistry, immunofluorescence staining, and flow cytometry. In this study, we observed increased and activated dopamine signaling in both the central nervous system and peripheral circulation of myasthenia gravis rats. Furthermore, changes in the expression of two key molecules, Claudin5 and CD31, in endothelial cells of the blood-brain barrier were also examined in these rats. We also confirmed that dopamine incubation reduced the expression of ZO1, Claudin5, and CD31 in endothelial cells by inhibiting the Wnt/ß-catenin signaling pathway. Overall, this study provides novel evidence suggesting that pathologically elevated dopamine in both the central nervous and peripheral circulation of myasthenia gravis rats impair brain-blood barrier integrity by inhibiting junction protein expression in brain microvascular endothelial cells through the Wnt/ß-catenin pathway.

Sleep fragmentation reduces explorative behaviors and impairs motor coordination in male mice.

Sleep fragmentation (SF), which refers to discontinuous and fragmented sleep, induces cognitive impairment and anxiety-like behavior in mice. However, whether SF can affect motor capability in healthy young wild-type mice and the underlying mechanisms remain unknown. We performed seven days of sleep fragmentation (SF 7d) interventions in young wild-type male mice. While SF mice experienced regular sleep disruption between Zeitgeber time (ZT) 0-12, control mice were allowed to have natural sleep (NS) cycles. Homecage analysis and conventional behavioral tests were conducted to assess the behavioral alterations in behavioral patterns in general and motor-related behaviors. Sleep structures and the power spectrum of electroencephalograms (EEGs) were compared between SF 7d and NS groups. Neuronal activation was measured using c-Fos immunostaining and quantified in multiple brain regions. SF of 7 days significantly decreased bouts of rearing and sniffing and the duration of rearing and impaired motor coordination. An increase in the total sleep time and a decrease in wakefulness between ZT12-24 was found in SF 7d mice. In SF 7d mice, EEG beta1 power was increased in rapid eye movement (REM) sleep while theta power was decreased during wakefulness. SF 7d resulted in significant suppression in c-Fos (+) cell counts in the motor cortex and hippocampus but an increase in c-Fos (+) cell counts in the substantia nigra pars compacta (SNc). In summary, SF 7d suppressed explorative behaviors and impaired motor coordination as compared to NS. EEG power and altered neuronal activity detected by c-Fos staining might contribute to the behavioral changes.

DZ2002 alleviates corneal angiogenesis and inflammation in rodent models of dry eye disease via regulating STAT3-PI3K-Akt-NF-κB pathway.

Dry eye disease (DED) is a prevalent ocular disorder with a multifactorial etiology. The pre-angiogenic and pre-inflammatory milieu of the ocular surface plays a critical role in its pathogenesis. DZ2002 is a reversible type III S-adenosyl-L-homocysteine hydrolase (SAHH) inhibitor, which has shown excellent anti-inflammatory and immunosuppressive activities in vivo and in vitro. In this study, we evaluated the therapeutic potential of DZ2002 in rodent models of DED. SCOP-induced dry eye models were established in female rats and mice, while BAC-induced dry eye model was established in female rats. DZ2002 was administered as eye drops (0.25%, 1%) four times daily (20 µL per eye) for 7 or 14 consecutive days. We showed that topical application of DZ2002 concentration-dependently reduced corneal neovascularization and corneal opacity, as well as alleviated conjunctival irritation in both DED models. Furthermore, we observed that DZ2002 treatment decreased the expression of genes associated with angiogenesis and the levels of inflammation in the cornea and conjunctiva. Moreover, DZ2002 treatment in the BAC-induced DED model abolished the activation of the STAT3-PI3K-Akt-NF-κB pathways in corneal tissues. We also found that DZ2002 significantly inhibited the proliferation, migration, and tube formation of human umbilical endothelial cells (HUVECs) while downregulating the activation of the STAT3-PI3K-Akt-NF-κB pathway. These results suggest that DZ2002 exerts a therapeutic effect on corneal angiogenesis in DED, potentially by preventing the upregulation of the STAT3-PI3K-Akt-NF-κB pathways. Collectively, DZ2002 is a promising candidate for ophthalmic therapy, particularly in treating DED.

PER2 regulates odontoblastic differentiation of dental papilla cells in vitro via intracellular ATP content and reactive oxygen species levels.

Background: Dental papilla cells (DPCs) are one of the key stem cells for tooth development, eventually forming dentin and pulp. Previous studies have reported that PER2 is expressed in a 24-hour oscillatory pattern in DPCs in vitro. In vivo, PER2 is highly expressed in odontoblasts (which are differentiated from DPCs). However, whether PER2 modulates the odontogenic differentiation of DPCs is uncertain. This research was to identify the function of PER2 in the odontogenic differentiation of DPCs and preliminarily explore its mechanisms. Methods: We monitored the expression of PER2 in DPCs differentiated in vivo. We used PER2 overexpression and knockdown studies to assess the role of PER2 in DPC differentiation and performed intracellular ATP content and reactive oxygen species (ROS) assays to further investigate the mechanism. Results: PER2 expression was considerably elevated throughout the odontoblastic differentiation of DPCs in vivo. Overexpressing Per2 boosted levels of odontogenic differentiation markers, such as dentin sialophosphoprotein (Dspp), dentin matrix protein 1 (Dmp1), and alkaline phosphatase (Alp), and enhanced mineralized nodule formation in DPCs. Conversely, the downregulation of Per2 inhibited the differentiation of DPCs. Additionally, downregulating Per2 further affected intracellular ATP content and ROS levels during DPC differentiation. Conclusion: Overall, we demonstrated that PER2 positively regulates the odontogenic differentiation of DPCs, and the mechanism may be related to mitochondrial function as shown by intracellular ATP content and ROS levels.

Influences of Adenoid Hypertrophy on Children's Maxillofacial Development.

This study aims to investigate the association between adenoid hypertrophy and facial development. A total of 388 children aged 1-13 years old who had undergone head MRI in Foshan Maternal and Child Health Hospital were collected, including 196 hypertrophic cases and 192 normal cases. The maxillofacial soft tissue indicators were measured and compared. The A/N ratio and adenoid thickness consistently increased with age in the hypertrophic group and the A/N ratio reached a maximum value three years earlier than the normal group. The pharyngeal airway space, vallecula of epiglottis to anterior plane distance of the third/fourth cervical vertebrae, angle of convexity, total angle of convexity, and the nasolabial angle in the hypertrophy group were smaller than those in the control group (p < 0.05). The thickness of adenoids, palate height, palate length, and tongue length in the hypertrophy group exceeded that of the control group (p < 0.05). To conclude, adenoid hypertrophy was associated with craniofacial features such as a convex facial profile, a narrowed nasopharyngeal airway, an elongated and heightened palate, a lengthened tongue or a lower tongue position. These findings emphasize the importance of early intervention for children with adenoid hypertrophy to mitigate potential adverse effects on maxillofacial development.

Targeting GPR65 alleviates hepatic inflammation and fibrosis by suppressing the JNK and NF-κB pathways.

BACKGROUND: G-protein coupled receptors (GPCRs) are recognized as attractive targets for drug therapy. However, it remains poorly understood how GPCRs, except for a few chemokine receptors, regulate the progression of liver fibrosis. Here, we aimed to reveal the role of GPR65, a proton-sensing receptor, in liver fibrosis and to elucidate the underlying mechanism. METHODS: The expression level of GPR65 was evaluated in both human and mouse fibrotic livers. Furthermore, Gpr65-deficient mice were treated with either bile duct ligation (BDL) for 21 d or carbon tetrachloride (CCl4) for 8 weeks to investigate the role of GPR65 in liver fibrosis. A combination of experimental approaches, including Western blotting, quantitative real-time reverse transcription­polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA), confocal microscopy and rescue studies, were used to explore the underlying mechanisms of GPR65's action in liver fibrosis. Additionally, the therapeutic potential of GPR65 inhibitor in the development of liver fibrosis was investigated. RESULTS: We found that hepatic macrophages (HMs)-enriched GPR65 was upregulated in both human and mouse fibrotic livers. Moreover, knockout of Gpr65 significantly alleviated BDL- and CCl4-induced liver inflammation, injury and fibrosis in vivo, and mouse bone marrow transplantation (BMT) experiments further demonstrated that the protective effect of Gpr65 knockout is primarily mediated by bone marrow-derived macrophages (BMMs). Additionally, in vitro data demonstrated that Gpr65 silencing and GPR65 antagonist inhibited, while GPR65 overexpression and application of GPR65 endogenous and exogenous agonists enhanced the expression and release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and transforming growth factor-ß (TGF-ß), all of which subsequently promoted the activation of hepatic stellate cells (HSCs) and the damage of hepatocytes (HCs). Mechanistically, GPR65 overexpression, the acidic pH and GPR65 exogenous agonist induced up-regulation of TNF-α and IL-6 via the Gαq-Ca2+-JNK/NF-κB pathways, while promoted the expression of TGF-ß through the Gαq-Ca2+-MLK3-MKK7-JNK pathway. Notably, pharmacological GPR65 inhibition retarded the development of inflammation, HCs injury and fibrosis in vivo. CONCLUSIONS: GPR65 is a major regulator that modulates the progression of liver fibrosis. Thus, targeting GPR65 could be an effective therapeutic strategy for the prevention of liver fibrosis.

lncRNA Helf promotes hepatic inflammation and fibrosis by interacting with PTBP1 to facilitate PIK3R5 mRNA stabilization.

BACKGROUND: Hepatic fibrosis is a common consequence of chronic liver diseases without approved antifibrotic therapies. Long noncoding RNAs (lncRNAs) play an important role in various pathophysiological processes. However, the functions of certain lncRNAs involved in mediating the antifibrotic role remain largely unclear. METHODS: The RNA level of lnc-High Expressed in Liver Fibrosis (Helf) was detected in both mouse and human fibrotic livers. Furthermore, lnc-Helf-silenced mice were treated with carbon tetrachloride (CCl4) or bile duct ligation (BDL) to investigate the function of lnc-Helf in liver fibrosis. RESULTS: We found that lnc-Helf has significantly higher expression in human and mouse fibrotic livers as well as M1 polarized hepatic macrophages (HMs) and activated hepatic stellate cells (HSCs). In vivo studies showed that silencing lnc-Helf by AAV8 vector alleviates CCl4- and BDL-induced hepatic inflammation and fibrosis. Furthermore, in vitro experiments revealed that lnc-Helf promotes HSCs activation and proliferation, as well as HMs M1 polarization and proliferation in the absence or presence of cytokine stimulation. Mechanistically, our data illustrated that lnc-Helf interacts with RNA binding protein PTBP1 to promote its interaction with PIK3R5 mRNA, resulting in increased stability and activating the AKT pathway, thus promoting HSCs and HMs activation and proliferation, which augments hepatic inflammation and fibrosis. CONCLUSION: Our results unveil a lnc-Helf/PTBP1/PIK3R5/AKT feedforward, amplifying signaling that exacerbates the process of hepatic inflammation and fibrosis, thus providing a possible therapeutic strategy for hepatic fibrosis.

Invasiveness identification in pure ground-glass nodules: exploring the generalizability of radiomics based on external validation and stress testing.

PURPOSE: This study aimed to apply external validation and stress tests to evaluate the generalizability of radiomics models built using various machine-learning methods for identifying the invasiveness of lung adenocarcinomas manifesting as pure ground-glass nodules (pGGNs). METHODS: This retrospective study enrolled 495 patients (514 pGGNs) confirmed as lung adenocarcinomas by postoperative pathology from three centers. All nodules were included in the primary cohort (randomly divided into training and test cohorts), two external validation cohorts, and two stress test cohorts. Six machine-learning radiomics models were constructed in the training cohort using the optimal features. Performance of radiomics models and clinical models were compared in primary cohort and external validation cohorts. The stress tests included stratified performance evaluation and shifted performance evaluation and contrastive evaluation under three single-condition modification settings. The predictive performance was validated by area under curve (AUC) of receiver operating characteristic (ROC). RESULTS: Of the six radiomics models, the best logistic regression (LR) model was able to maintain high differential diagnostic capability (AUC: 0.849 ± 0.049) and good stability (relative standard deviation, 5.719%), but it showed poorer performance (AUC = 0.835) than the clinical model (AUC = 0.862) in the external validation cohort E1. The stress tests suggested LR model had no significant difference in performance between subgroups after stratification and had good consistency in the predictions before and after the three transformations (Kappa = 0.960, 0.840, and 0.933, respectively; p < 0.05, all). CONCLUSION: The rigorous testing procedure facilitates the selection of high-performance radiomics models with good clinical generalizability.

Growth assessment of pure ground-glass nodules on CT: comparison of density and size measurement methods.

PURPOSE: To investigate the differences of size and density measurements in assessing pure ground-glass nodules (pGGNs) growth, and compare the growth rates and growth proportions of the two methods during follow-up period. METHODS: Ninety patients with at least 3 consecutive thin-section chest CTs and confirmed 103 pGGNs on baseline CT were enrolled retrospectively. Using the two definitions of size and density to evaluate pGGNs growth with semi-automated segmentation. Then, the two methods were compared to assess differences in pGGNs growth. RESULTS: For the size and density methods to assess nodule growth, 50.5% and 26.2% showed interval growth at the last CT (p < 0.001). Among the 19 nodules that grew in both size and density, the volume doubling time (VDT) of solid component (mean, 317.1; standard deviation, 224.8 days) was shorter than total VDT (median, 942.8; range, 400.1-2315.9 days) (p < 0.001). Of the 27 growth pGGNs assessed by the density method, the growth rates at years 1 and 2 were 25.9% and 63.0%, while the growth rates of 52 growing nodules assessed by size method were 11.5% and 48.1%, respectively. Twenty of 103 (19.4%) nodules were classified into category 4A lesions, and 7 (6.8%) were 4B lesions. CONCLUSION: Compared to size measurements, observed density increases have a higher proportion of early growth and faster growth rates in growing nodules. Clinicians need to pay close attention to the nodules of new solid components and make timely decision management.

Promotive Effect of FBXO32 on the Odontoblastic Differentiation of Human Dental Pulp Stem Cells.

Odontoblastic differentiation of human dental pulp stem cells (hDPSCs) is crucial for the intricate formation and repair processes in dental pulp. Until now, the literature is not able to demonstrate the role of ubiquitination in the odontoblastic differentiation of hDPSCs. This study investigated the role of F-box-only protein 32 (FBXO32), an E3 ligase, in the odontoblastic differentiation of hDPSCs. The mRNA expression profile was obtained from ribonucleic acid sequencing (RNA-Seq) data and analyzed. Immunofluorescence and immunohistochemical staining identify the FBXO32 expression in human dental pulp and hDPSCs. Small-hairpin RNA lentivirus was used for FBXO32 knockdown and overexpression. Odontoblastic differentiation of hDPSCs was determined via alkaline phosphatase activity, Alizarin Red S staining, and mRNA and protein expression levels were detected using real-time quantitative polymerase chain reaction and Western blotting. Furthermore, subcutaneous transplantation in nude mice was performed to evaluate the role of FBXO32 in mineralization in vivo using histological analysis. FBXO32 expression was upregulated in the odontoblast differentiated hDPSCs as evidenced by RNA-Seq data analysis. FBXO32 was detected in hDPSCs and the odontoblast layer of the dental pulp. Increased FBXO32 expression in hDPSCs during odontoblastic differentiation was confirmed. Through lentivirus infection method, FBXO32 downregulation in hDPSCs attenuated odontoblastic differentiation in vitro and in vivo, whereas FBXO32 upregulation promoted the hDPSCs odontoblastic differentiation, without affecting proliferation and migration. This study demonstrated, for the first time, the promotive role of FBXO32 in regulating the odontoblastic differentiation of hDPSCs, thereby providing novel insights into the regulatory mechanisms during odontoblastic differentiation in hDPSCs.