Association Between SARS-CoV-2 Infection and Acute Ischemic Colitis.

Purpose: Ischemic colitis appears to be a rare but serious complication of COVID-19. About 33.3% hospitalized COVID-19 patients who underwent endoscopy showed features resembling ischemic colitis. The aim of this prospective study was to describe the symptoms, treatment, and outcomes of these patients, particularly their colonoscopy and histologic findings. Patients and methods: We conducted a prospective study on ischemic bowel disease associated with COVID-19 across four centers from December 2022 to January 2023. All cases were identified through a comprehensive search of electronic medical records for procedure-related data. The initial diagnosis of ischemic bowel disease was confirmed using colonoscopy and biopsy findings. After the patients were discharged, a 12-month follow-up was conducted through regular phone interviews to assess their clinical outcomes. Results: Overall, the study included 3 male patients and 9 female patients (age range, 33-76 years). Abdominal pain and hematochezia always occurred within 2 weeks after COVID-19 infection (average 5.5 days). Gastrointestinal manifestations did not parallel the severity of COVID-19 infection. The descending colon was the most susceptible segment, which was involved in 10 patients (83.33%). Colonoscopy revealed diffuse redness, edema, bleeding, erosion, and ulceration of the intestinal mucosa, similar to the findings of ischemic colitis, and biopsy revealed crypt atrophy, reduction, and interstitial bleeding. All patients were self-limited without converting to chronic changes in the next 12 months. Conclusion: SARS-CoV-2 infection may induce transient acute colon ischemia within 2 weeks, accompanied by severe clinical symptoms such as acute abdominal pain and hematochezia, which are self-limiting and do not lead to chronic symptoms.

Association of Short Sleep Duration and Obstructive Sleep Apnea with Central Obesity: A Retrospective Study Utilizing Anthropometric Measures.

Background: Central obesity, as measured by examination instruments, has been shown to be associated with both OSA and short sleep duration. However, objective measurement tools like CT, MRI, and DXA are expensive, cause radiation exposure, and have limited availability, especially in resource-limited settings. Thus, this study aimed to demonstrate the relevance of Body Mass Index (BMI) and Waist-to-Height Ratio (WHtR) as surrogate indicators of visceral obesity in the assessment of OSA and short sleep duration. We also intend to evaluate whether WHtR, in combination with BMI, can be a suitable surrogate marker for visceral adiposity. Methods: We recruited 333 adults with complete polysomnographic (PSG) records retrospectively. Logistic regression helped to assess the association of BMI and WHtR as surrogates for central adiposity with OSA and short sleep duration. Moreover, ROC curve analysis was conducted to evaluate the predictive ability of BMI and WHtR. Results: Following the relevant adjustments, logistic regression analysis results showed that the combination of WHtR and BMI acting as central obesity surrogates was significantly associated with OSA and short sleep duration (p<0.05). According to univariate regression analysis, sleep latency and wake after sleep onset were independent predictors of the risk of central obesity in patients with short sleep duration and OSA. Additionally, ROC curve analysis demonstrated that the combination of BMI and WHtR provided a better assessment of central adiposity in patients with OSA and short sleep duration, compared to each measure alone. Conclusion: BMI and WHtR are significantly associated with OSA and short sleep duration, and might serve as a potential surrogate marker for central obesity. Sleep latency and wake after sleep onset can independently predict the risk of central obesity in patients with short sleep time and OSA. Thus, larger prospective studies are needed to verify our findings.

Influence of the internet celebrity' attributes of the host on the loyalty of users on live platforms.

Since 2019, live e-commerce has experienced significant growth, effectively driving consumption, with various e-commerce platforms, video platforms, enterprises, and businesses venturing into the live e-commerce sector. However, this development has brought forth several issues, one of which prominently pertains to the lack of customer loyalty. Hosts play a crucial role in live e-commerce. To investigate the impact of internet celebrity attributes on platform user loyalty, this study employed a survey questionnaire distributed on internet websites, collecting 200 valid samples. A research model based on the ABC attitude model was constructed, with customer satisfaction and customer trust as mediating variables. The findings indicate that the internet celebrity attributes of network popularity and interactivity positively influence customer loyalty through the mediation of customer satisfaction and customer trust. On the other hand, the host's purpose as an internet celebrity attribute does not directly or indirectly affect customer loyalty. The primary reason for this discrepancy is that the host failed to establish trust and employ suitable methods to attain the goal of selling and promoting products. Consequently, platforms and businesses can enhance the network popularity of hosts through communication media, while fostering their literacy and professional skills. Moreover, strengthening communication and interaction between hosts and customers serves as a foundation for nurturing enduring and positive relationships.

Enhancing Target Tracking: A Novel Grid-Based Beetle Antennae Search Algorithm and Confusion-Aware Detection.

Unmanned aerial vehicle target tracking is a complex task that encounters challenges in scenarios involving limited computing resources, real-time requirements, and target confusion. This research builds on previous work and addresses challenges by proposing a grid-based beetle antennae search algorithm and designing a lightweight multi-target detection and positioning method, which integrates interference-sensing mechanisms and depth information. First, the grid-based beetle antennae search algorithm's rapid convergence advantage is combined with a secondary search and rollback mechanism, enhancing its search efficiency and ability to escape local extreme areas. Then, the You Only Look Once (version 8) model is employed for target detection, while corner detection, feature point extraction, and dictionary matching introduce a confusion-aware mechanism. This mechanism effectively distinguishes potentially confusing targets within the field of view, enhancing the system's robustness. Finally, the depth-based localization of the target is performed. To verify the performance of the proposed approach, a series of experiments were conducted on the grid-based beetle antennae search algorithm. Comparisons with four mainstream intelligent search algorithms are provided, with the results showing that the grid-based beetle antennae search algorithm excels in the number of iterations to convergence, path length, and convergence speed. When the algorithm faces non-local extreme-value-area environments, the speed is increased by more than 89%. In comparison with previous work, the algorithm speed is increased by more than 233%. Performance tests on the confusion-aware mechanism by using a self-made interference dataset demonstrate the model's high discriminative ability. The results also indicate that the model meets the real-time requirements.

EFHD1 promotes osteosarcoma proliferation and drug resistance by inhibiting the opening of the mitochondrial membrane permeability transition pore (mPTP) by binding to ANT3.

Chemoresistance is the main obstacle in the clinical treatment of osteosarcoma (OS). In this study, we investigated the role of EF-hand domain-containing protein 1 (EFHD1) in OS chemotherapy resistance. We found that the expression of EFHD1 was highly correlated with the clinical outcome after chemotherapy. We overexpressed EFHD1 in 143B cells and found that it increased their resistance to cell death after drug treatment. Conversely, knockdown of EFHD1 in 143BR cells (a cisplatin-less-sensitive OS cell line derived from 143B cells) increased their sensitivity to treatment. Mechanistically, EFHD1 bound to adenine nucleotide translocase-3 (ANT3) and inhibited its conformational change, thereby inhibiting the opening of the mitochondrial membrane permeability transition pore (mPTP). This effect could maintain mitochondrial function, thereby favoring OS cell survival. The ANT3 conformational inhibitor carboxyatractyloside (CATR), which can promote mPTP opening, enhanced the chemosensitivity of EFHD1-overexpressing cells when combined with cisplatin. The ANT3 conformational inhibitor bongkrekic acid (BKA), which can inhibit mPTP opening, restored the resistance of EFHD1 knockdown cells. In conclusion, our results suggest that EFHD1-ANT3-mPTP might be a promising target for OS therapy in the future.

Synthesis of 1-Benzyl-2,4-diarylimidazole through I2/CuI-Catalyzed Cyclization of Benzylamine and Hydrazone.

In this paper, we report an innovative method for synthesizing 1-benzyl-2,4-diarylimidazole utilizing 1-phenylethanone-2-(2-pyridinyl) hydrazine and benzylamine, catalyzed by an I2/CuI system. This approach represents a significant departure from traditional methods for synthesizing polysubstituted imidazoles; it employs the I2/CuI catalyst to replace rare metal catalysts, thereby achieving high yields of substitution products (≤85%). This method for the generation of 1,2,4-triimidazole derivatives is characterized by its exceptional chemical selectivity and extensive substrate compatibility.

Erratum: ATF6 aggravates angiogenesis-osteogenesis coupling during ankylosing spondylitis by mediating FGF2 expression in chondrocytes.

[This corrects the article DOI: 10.1016/j.isci.2021.102791.].

Enhancer-mediated FOXO3 expression promotes MSC adipogenic differentiation by activating autophagy.

BACKGROUND: Mesenchymal stem cells (MSCs) are pluripotent stem cells capable of differentiating into osteocytes, adipocytes and chondrocytes. However, in osteoporosis, the balance of differentiation is tipped toward adipogenesis and the key mechanism is controversial. Researches have shown that, as upstream regulatory elements of gene expression, enhancers ar involved in the expression of identity genes. In this study, we identified enhancers-mediated gene FOXO3 promoting MSC adipogenic differentiation by activating autophagy. METHODS: We integrated data of RNA sequencing (RNA-seq), chromatin immunoprecipitation sequencing (ChIP-seq) and ATAC-sequencing (ATAC-seq) to find the identity gene FOXO3. The expression of FOXO3 protein, adipogenic transcription factors and the substrate of autophagy were measured by western blotting. The Oil Red O (ORO) staining was used to visualize the adipogenesis of MSCs. Immunohistochemistry was used to visualize the FOXO3 expression in adipocytes in bone marrow. Immunofluorescence was used to detect the expression of PPARγ and LC3B. RESULTS: During adipogenesis, enhancers redistribute to genes associated with adipogenic differentiation, among which we identified the pivotal identity gene FOXO3. FOXO3 could promote the expression of the adipogenic transcription factors PPARγ, CEBPα, and CEBPß during adipogenic differentiation, while PPARγ, CEBPα, and CEBPß could in turn bind to FOXO3 and continue to promote FOXO3 expression to form a positive feedback loop. Consistently elevated FOXO3 expression promotes autophagy by activating the PI3K-AKT pathway which mediates adipogenic differentiation. CONCLUSIONS: Pivotal identity gene FOXO3 promotes autophagy by activating PI3K-AKT pathway, which provokes adipogenic differentiation of MSCs. Enhancer-regulated adipogenic identity gene FOXO3 could be an attractive treatment for osteoporosis.

Low expression of ZFP36L1 in osteosarcoma promotes lung metastasis by inhibiting the SDC4-TGF-ß signaling feedback loop.

ZFP36L1, which is a negative regulator of gene transcripts, has been proven to regulate the progression of several carcinomas. However, its role in sarcoma remains unknown. Here, by using data analyses and in vivo experiments, we found that ZFP36L1 inhibited the lung metastasis of osteosarcoma (OS). Knockdown of ZFP36L1 promoted OS cell migration by activating TGF-ß signaling and increasing SDC4 expression. Intriguingly, we observed a positive feedback loop between SDC4 and TGF-ß signaling. SDC4 protected TGFBR3 from matrix metalloproteinase (MMP)-mediated cleavage and therefore relieved the inhibition of TGF-ß signaling by soluble TGFBR3, while TGF-ß signaling positively regulated SDC4 transcription. We also proved that ZFP36L1 regulated SDC4 mRNA decay through adenylate-uridylate (AU)-rich elements (AREs) in its 3'UTR. Furthermore, treatment with SB431542 (a TGF-ß receptor kinase inhibitor) and MK2 inhibitor III (a MAPKAPK2 inhibitor that increases the ability of ZFP36L1 to degrade mRNA) dramatically inhibited OS lung metastasis, suggesting a promising therapeutic approach for the treatment of OS lung metastasis.

Research on programmatic multi-attribute decision-making problem: An example of bridge pile foundation project in karst area.

The selection of construction plans for adverse geological conditions frequently encountered during the construction of bridge pile foundations will have a significant impact on the project's progress, quality, and cost. There is a need for the optimization of multi-attribute decision-making methods, considering the subjectivity in in weight allocation and the practical implementation obstacles. In this study, an evaluation framework for pile foundation construction schemes in karst areas was established. The directed graph and Bellman-Ford algorithm are employed to improve the Analytic Network Process (ANP) in the systematic structure, thereby calculating the subjective weights of various indicators. Simultaneously, based on the concept of dynamic weighting, a multiple linear regression is introduced for analyzing the weights of similar projects, resulting in the derivation of universal weights for the primary indicators within the evaluation system. The combination weights are subsequently determined through the weighted average of the two types of weights. Finally, the comprehensive scores of alternative schemes are computed using the grey-fuzzy evaluation method to enable decision-making in scheme selection. Cloud model, ELECTRE-II, and VIKOR methodologies were utilized for the comparison of results. Combining with a case study of a bridge project in karst development area in southern China, the findings indicate that the improved ANP method possesses practical applicability and yields effective computational results. The introduction of universal weights serves to ameliorate the inherent subjectivity in weight allocation. The pile foundation quality achieved using the optimal construction plan is classified as Class I, which prove the feasibility of the model.

Efficient cross-protection against serotype 4/8a fowl adenoviruses (FAdVs): recombinant FAdV-4 with FAdV-8a Fiber.

IMPORTANCE: Epidemiological data reveal that FAdV-4 and FAdV-8a are the dominant serotypes of FAdVs in the poultry industry in China. Although three commercial inactivated vaccines against FAdV-4 have been licensed in China, the bivalent vaccine against both FAdV-4 and FAdV-8a is not available. Here, we used CRISPR-Cas9 and Cre-LoxP system to generate a recombinant virus FAdV4-F/8a-rF2 expressing the Fiber of FAdV-8a. Notably, FAdV4-F/8a-rF2 was highly attenuated and could provide efficient protection against both FAdV-4 and FAdV-8a in the chicken infection model, highlighting the applaudable application of FAdV4-F/8a-rF2 as a novel live-attenuated bivalent vaccine against the diseases caused by the infection of FAdV-4 and FAdV-8a.

SIRPA enhances osteosarcoma metastasis by stabilizing SP1 and promoting SLC7A3-mediated arginine uptake.

The function of signal regulatory protein alpha (SIRPA) has been well studied in macrophages and dendritic cells, but relatively less in tumors. Notably, SIRPA is upregulated in osteosarcoma tissues, particularly in metastatic tissues, and is associated with unfavorable clinical outcomes. Knockdown of SIRPA impaired OS cell migration by decreasing specificity protein 1 (SP1) stability and arginine uptake. Importantly, SIRPA phosphorylated SP1 at threonine 278 (Thr278) through extracellular signal-regulated kinase (ERK) activation to protect SP1 from proteasomal degradation. In addition, SP1 increased solute carrier family 7 member 3 (SLC7A3) expression by binding to the SLC7A3 promoter and increased the capability of arginine uptake, thereby facilitating OS cell migration. More interestingly, arginine promoted the stability of SP1 in an ERK-independent manner and thus formed the "SP1 stabilization circle". Combined treatment with the anti-SIRPA antibody and arginase, which blocked the circle, impaired tumor metastasis in mice bearing xenografts formed from SIRPA-overexpressing cells. In summary, our study demonstrates that the upregulation of SIRPA promotes OS metastasis via the "SP1 stabilization circle" and SLC7A3-mediated arginine uptake, which might serve as a target for OS treatment.

Immunomodulatory zinc-based materials for tissue regeneration.

Zinc(Zn)-based materials have contributed greatly to the rapid advancements in tissue engineering. The qualities they possess that make them so beneficial include their excellent biodegradability, biocompatibility, anti-bacterial activity, among and several others. Biomedical materials that act as a foreign body, will inevitably cause host immune response when introduced to the human body. As the osteoimmunology develops, the immunomodulatory characteristics of biomaterials have become an appealing concept to improve implant-tissue interaction and tissue restoration. Recently, Zn-based materials have also displayed immunomodulatory functions, especially macrophage polarization states. It can promote the transformation of M1 macrophages into M2 macrophages to enhance the tissue regeneration and reconstruction. This review covers mainly Zn-based materials and their characteristics, including metallic Zn alloys and Zn ceramics. We highlight the current advancements in the type of immune responses, as well as the mechanisms, that are induced by Zn-based biomaterials, most importantly the regulation of innate immunity and the mechanism of promoting tissue regeneration. To this end, we discuss their applications in biomedicine, and conclude with an outlook on future research challenges.

Administration methods of lipid-based nanoparticle delivery systems for cancer treatment.

As nano medications have developed in the recent four decades, nano-delivery systems have been applied in treating various diseases and are especially common in cancer treatment. Nano-delivery systems could target cancer-associated cells, enhance the accuracy and efficacy of treatment, and reduce systemic side effects. Among the many drugs on nano-carriers, the load system of lipid-based nanoparticles has the brightest prospect due to the high level of biocompatibility, biodegradability, loading capability, and immunogenicity. Previous reviews have comprehensively introduced their effects and progress. However, most of them did not provide great attention to practical applications. This article will focus on different intake methods, which decide the biological process of drugs. This suggests that we can modify lipid-based nano-delivery systems according to how they are capable of prolonging the half-life span and magnifying therapy effects in treating cancer. Besides, we put forth the problems that should be further studied in the future and their probable solutions.

Prognosis-related molecular subtyping in head and neck squamous cell carcinoma patients based on glycolytic/cholesterogenic gene data.

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) remains an unmet medical challenge. Metabolic reprogramming is a hallmark of diverse cancers, including HNSCC. METHODS: We investigated the metabolic profile in HNSCC by using The Cancer Genome Atlas (TCGA) (n = 481) and Gene Expression Omnibus (GEO) (n = 97) databases. The metabolic stratification of HNSCC samples was identified by using unsupervised k-means clustering. We analyzed the correlations of the metabolic subtypes in HNSCC with featured genomic alterations and known HNSCC subtypes. We further validated the metabolism-related subtypes based on features of ENO1, PFKFB3, NSDHL and SQLE expression in HNSCC by Immunohistochemistry. In addition, genomic characteristics of tumor metabolism that varied among different cancer types were confirmed. RESULTS: Based on the median expression of coexpressed cholesterogenic and glycolytic genes, HNSCC subtypes were identified, including glycolytic, cholesterogenic, quiescent and mixed subtypes. The quiescent subtype was associated with the longest survival and was distributed in stage I and G1 HNSCC. Mutation analysis of HNSCC genes indicated that TP53 has the highest mutation frequency. The CDKN2A mutation frequency has the most significant differences amongst these four subtypes. There is good overlap between our metabolic subtypes and the HNSCC subtype. CONCLUSION: The four metabolic subtypes were successfully determined in HNSCC. Compared to the quiescent subtype, glycolytic, cholesterogenic and mixed subtypes had significantly worse outcome, which might offer guidelines for developing a novel treatment strategy for HNSCC.

The interaction between obesity and visceral hypersensitivity.

Obesity has been a worldwide problem associated with numerous chronic diseases such as cardiovascular disease, type 2 diabetes, and metabolic disorders. It may also play a role in visceral hypersensitivity, contributing to irritable bowel syndrome. (i) Adipose tissue secretes various inflammatory mediators, causing intestinal hyperpermeability and nerve endings activation. (ii) Obesity and gastrointestinal microbiota could affect each other, and microbial metabolites can increase sensitivity of the colon. (iii) Vitamin D deficiency contributes to both fat accumulation and disruption of the intestinal mucosal barrier. (iv) Brain-gut axis may be another bridge from obesity to visceral hypersensitivity.

CLP36 promotes p53 deficient sarcoma progression through suppression of atrophin-1 interacting protein-4 (AIP-4)-dependent degradation of YAP1.

Background: p53 deficiency is a key causal factor for tumor development and progression. p53 acts in this process through, at least in part, cooperation with YAP1 but the underlying molecular mechanism is incompletely understood. In this paper, we show that CLP36, an actinin-binding cytoskeletal protein, links p53 deficiency to up-regulation of YAP1 expression and sarcoma progression. Methods: Immunohistochemical staining and Western blotting were used to investigate the effect of p53 deficiency on CLP36 expression in sarcoma tissues and cells. Furthermore, molecular, cellular, and genetic knockout and knockdown approaches were employed to investigate the functions of CLP36 in regulation of sarcoma cell behavior in culture and tumor growth in mice. Finally, biochemical approaches were used to investigate the molecular mechanism by which CLP36 regulates the malignant behavior of p53 deficient sarcoma cells. Results: We have found that the expression of CLP36 is up-regulated in response to loss of p53 in sarcoma tissues and cells. Depletion of CLP36 inhibited malignant behavior of p53 deficient sarcoma cells. Furthermore, knockout of CLP36 in mice markedly inhibited p53 deficiency-induced tumorigenesis and improved the survival of the p53 deficient mice. Mechanistically, CLP36 promoted p53 deficiency-induced tumorigenesis through inhibition of E3 ligase atrophin-1 interacting protein-4 (AIP-4)-dependent proteasomal degradation of YAP1 and consequently increase of YAP1 expression. Conclusions: Our results reveal a crucial role of CLP36 in linking p53 deficiency to up-regulation of YAP1 expression and sarcoma progression. Our findings suggest that therapeutic targeting the CLP36/YAP1 signaling axis may provide an effective strategy for alleviation of p53 deficient sarcoma progression.

Environmental Factors Affecting Diversity, Structure, and Temporal Variation of Airborne Fungal Communities in a Research and Teaching Building of Tianjin University, China.

Airborne fungi are widely distributed in the environment and may have adverse effects on human health. A 12-month survey on the diversity and concentration of culturable airborne fungi was carried out in a research and teaching building of Tianjin University. Indoor and outdoor environments were analyzed using an HAS-100B air sampler. A total of 667 fungal strains, belonging to 160 species and 73 genera were isolated and identified based on morphological and molecular analysis. The most abundant fungal genera were Alternaria (38.57%), Cladosporium (21.49%), and Aspergillus (5.34%), while the most frequently appearing species was A. alternata (21%), followed by A. tenuissima (12.4%), and C. cladosporioides (9.3%). The concentration of fungi in different environments ranged from 0 to 150 CFU/m3 and was significantly higher outdoor than indoor. Temperature and sampling month were significant factors influencing the whole building fungal community, while relative humidity and wind speed were highly correlated with fungal composition outdoor. Variations in the relative abundance of major airborne fungal taxa at different heights above-ground could lead to different community structures at different floors. Our results may provide valuable information for air quality monitoring and microbial pollution control in university building environments.

A dual-mode immunosensing strategy for prostate specific antigen detection: Integration of resonance Raman scattering and photoluminescence properties of ZnS:Mn2+ nanoprobes.

Luminescence-based methods are widely used for the detection of prostate specific antigen (PSA), for example during the diagnosis of prostate cancer. However, the accuracy of these methods is sub-optimal. The aim of this study was to develop an accurate and sensitive dual-mode immunosensing technique using a combination of resonance Raman scattering (RRS) and photoluminescence (PL) signals for the detection of PSA. A ZnS:Mn2+ nanoprobe was used as the signal reporter, which exhibits both multi-phonon RRS and PL properties. The RRS signal intensity at 348 cm-1 and the PL signal intensity at 590 nm were used for the quantitative assay of PSA. The reproducibility, selectivity and specificity of this dual-mode immunosensing strategy demonstrated an improvement compared with commercial PSA ELISA kits in the analysis of serum samples. Therefore, the RRS-PL immunosensing technique developed in this study shows potential as a reliable technique to be used in the clinical diagnosis of prostate cancer.

ZIP10 drives osteosarcoma proliferation and chemoresistance through ITGA10-mediated activation of the PI3K/AKT pathway.

BACKGROUND: The zinc transporters Zrt- and Irt-related protein (ZIP/SLC39) are overexpressed in human tumors and correlate with poor prognosis; however, their contributions to carcinogenesis and chemoresistance in osteosarcoma (OS) remain unclear. METHODS: We collected 64 OS patient tissues with (n = 12) or without (n = 52) chemotherapy. The expression levels of ZIP10 were measured by immunohistochemistry and applied to prognostic analysis. ZIP10 was knocked down or overexpressed in OS cell lines to explore its effect on proliferation and chemoresistance. RNA sequencing, quantitative real-time PCR, and western blotting analysis were performed to explore ZIP10-regulated downstream target genes. A xenograft mouse model was established to evaluate the mechanisms by which ZIP10 modulates chemoresistance in OS cells. RESULTS: The expression of ZIP10 was significantly induced by chemotherapy and highly associated with the clinical outcomes of OS. Knockdown of ZIP10 suppressed OS cell proliferation and chemoresistance. In addition, ZIP10 promoted Zn content-induced cAMP-response element binding protein (CREB) phosphorylation and activation, which are required for integrin α10 (ITGA10) transcription and ITGA10-mediated PI3K/AKT pathway activation. Importantly, ITGA10 stimulated PI3K/AKT signaling but not the classical FAK or SRC pathway. Moreover, overexpression of ZIP10 promoted ITGA10 expression and conferred chemoresistance. Treatment with the CREB inhibitor 666-15 or the PI3K/AKT inhibitor GSK690693 impaired tumor chemoresistance in ZIP10-overexpressing cells. Finally, a xenograft mouse model established by subcutaneous injection of 143B cells confirmed that ZIP10 mediates chemotherapy resistance in OS cells via the ZIP10-ITGA10-PI3K/AKT axis. CONCLUSIONS: We demonstrate that ZIP10 drives OS proliferation and chemoresistance through ITGA10-mediated activation of the PI3K/AKT pathway, which might serve as a target for OS treatment.