Design of Ca-type todorokite catalysts with highly active for the selective reduction of NOx by NH3 at low temperatures.

Ca-type todorokite catalysts were designed and prepared by a simple redox method and applied to the selective reduction of NOx by NH3 (NH3-SCR) for the first time. Compared with the Na-type manjiroite prepared by the same method, the todorokite catalysts with different Mn/Ca ratios showed greatly improved catalytic activity for NOx reduction. Among them, Mn8Ca4 catalyst exhibited the best NH3-SCR performance, achieving 90% NOx conversion within temperature range of 70-275°C and having a high sulphur resistance. Compared to the Na-type manjiroite sample, Ca-type todorokite catalysts possessed an increased size of tunnel, resulting in a larger specific surface area. As increased the amounts of Ca doping, the Na content in Ca-type todorokite catalysts significantly decreased, providing larger amounts of Brønsted acid sites for NH3 adsorption to produce NH4+. The NH4+ species were highly active for reaction with NO + O2, playing a determining role in NH3-SCR process at low temperatures. Meanwhile, larger amounts of surface adsorbed oxygen contained over the Ca-doping samples than that over Na-type manjiroite, promoting the oxidation of NO and fast SCR processes. Over the Ca-type todorokite catalysts, furthermore, nitrates produced during the flow of NO + O2, were more active for reaction with NH3 than that over Na-type manjiroite, benefiting the occurrence of NH3-SCR process. This study provides novel insights into the design of NH3-SCR catalysts with high performance.

Secretome of EMSCs neutralizes LPS­induced acute lung injury via aerosol administration.

Ectodermal mesenchymal stem cells (EMSCs) are cells harvested from the stem cell niche (nasal mucosa) with high therapeutic potential. To the best of our knowledge, however, the anti­inflammatory properties of these neural crest­derived EMSCs have been rarely reported. The present study aimed to explore the effects of aerosolized EMSC­Secretome (EMSC­Sec) and clarify underlying mechanisms in treating acute lung injury (ALI). EMSCs were isolated by adherent method and identified by immunofluorescence staining. EMSC­Sec was collected and evaluated using western blotting, BCA and ELISA tests. Then, mouse lung epithelial cells (MLE­12) were used to mimic inflammatory stimulation with lipopolysaccharide (LPS). After developing an ALI model through intraperitoneal injection of LPS, mice were treated with an EMSC­Sec spray. The lung in each group underwent an observation and measurement to preliminarily assess the extent of damage. H&E staining, immunohistochemical staining, immunofluorescence and western­blotting were utilized to further access the impacts of EMSC­Sec. The results showed that EMSC­Sec had great anti­inflammatory potential and was highly successful in vitro and in vivo. EMSC­Sec mitigated LPS­induced ALI with low inflammatory cell inflation and mild damage. EMSC­Sec could regulate inflammation via the NF­κB(p50/p65)/NLRP3 pathway. Overall, the present study demonstrated that EMSC­Sec regulated inflammation, hoping to provide a novel strategy for ALI treatment.

Triggering pyroptosis enhances the antitumor efficacy of PARP inhibitors in prostate cancer.

PURPOSE: PARP inhibitors have revolutionized the treatment landscape for advanced prostate cancer (PCa) patients who harboring mutations in homologous recombination repair (HRR) genes. However, the molecular mechanisms underlying PARP inhibitors function beyond DNA damage repair pathways remain elusive, and identifying novel predictive targets that favorably respond to PARP inhibitors in PCa is an active area of research. METHODS: The expression of GSDME in PCa cell lines and human PCa samples was determined by western blotting. Targeted bisulfite sequencing, gene enrichment analysis (GSEA), clone formation, construction of the stably transfected cell lines, lactate dehydrogenase (LDH) assay, western blotting as well as a mouse model of subcutaneous xenografts were used to investigate the role of GSDME in PCa. The combinational therapeutic effect of olaparib and decitabine was determined using both in vitro and in vivo experiments. RESULTS: We have found low expression of GSDME in PCa. Interestingly, we demonstrated that GSDME activity is robustly induced in olaparib-treated cells undergoing pyroptosis, and that high methylation of the GSDME promoter dampens its activity in PCa cells. Intriguingly, genetically overexpressing GSDME does not inhibit tumor cell proliferation but instead confers sensitivity to olaparib. Furthermore, pharmacological treatment with the combination of olaparib and decitabine synergistically induces GSDME expression and cleavage through caspase-3 activation, thus promoting pyroptosis and enhancing anti-tumor response, ultimately resulting in tumor remission. CONCLUSION: Our findings highlight a novel therapeutic strategy for enhancing the long-term response to olaparib beyond HRR-deficient tumors in PCa, underscoring the critical role of GSDME in regulating tumorigenesis.

Klotho-beta attenuates Rab8a-mediated exosome regulation and promotes prostate cancer progression.

Tumor-secreted exosomes have a wide range of effects on the growth, metastasis, and drug resistance of cancer cells. However, whether and how the molecular mechanisms that regulate the secretion of exosomes could affect tumor progression remains poorly understood. Klotho beta (KLB) has been reported dysregulated in prostate cancer, but its function remains unknown. Herein, we first determined that KLB was upregulated in prostate cancer and its expression level was positively correlated with prostate cancer malignant phenotype both in vitro and in vivo. Intriguingly, KLB overexpression could impair the release of exosomes and cause the intracellular accumulation of multivesicular bodies (MVBs) in prostate cancer cells. Mechanistically, KLB attenuated exosomes secretion through a Rab8a-dependent pathway. Rab8a was downregulated in KLB overexpressing cells whereas overexpression of Rab8a could rescue the impaired release of exosomes and attenuate the KLB-induced malignant phenotype of prostate cancer both in vitro and in vivo. Taken together, this study has unveiled the tumor-promoting role of KLB mediated by its regulation on exosomes secretion through a Rab8a-dependent mechanism. These findings could be exploited to develop novel theranostic targets for prostate cancer.

NDFIP1 limits cellular TAZ accumulation via exosomal sorting to inhibit NSCLC proliferation.

NDFIP1 has been previously reported as a tumor suppressor in multiple solid tumors, but the function of NDFIP1 in NSCLC and the underlying mechanism are still unknown. Besides, the WW domain containing proteins can be recognized by NDFIP1, resulted in the loading of the target proteins into exosomes. However, whether WW domain-containing transcription regulator 1 (WWTR1, also known as TAZ) can be packaged into exosomes by NDFIP1 and if so, whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any extent. Here, we first found that NDFIP1 was low expressed in NSCLC samples and cell lines, which is associated with shorter OS. Then, we confirmed the interaction between TAZ and NDFIP1, and the existence of TAZ in exosomes, which requires NDFIP1. Critically, knockout of NDFIP1 led to TAZ accumulation with no change in its mRNA level and degradation rate. And the cellular TAZ level could be altered by exosome secretion. Furthermore, NDFIP1 inhibited proliferation in vitro and in vivo, and silencing TAZ eliminated the increase of proliferation caused by NDFIP1 knockout. Moreover, TAZ was negatively correlated with NDFIP1 in subcutaneous xenograft model and clinical samples, and the serum exosomal TAZ level was lower in NSCLC patients. In summary, our data uncover a new tumor suppressor, NDFIP1 in NSCLC, and a new exosome-related regulatory mechanism of TAZ.

Reciprocal FGF19-GLI2 signaling induces epithelial-to-mesenchymal transition to promote lung squamous cell carcinoma metastasis.

PURPOSE: Metastatic lung squamous cell carcinoma (LUSC) is one of the most common causes of cancer death worldwide. As yet, however, the molecular mechanism underlying LUSC metastasis remains elusive. In this study, we report a novel mechanism involving signaling interactions between FGF19 and GLI2 that could drive the progression of LUSC. METHODS: The expression of FGF19 in human LUSC samples was assessed by immunohistochemistry. The concentration of FGF19 in serum samples was assessed by ELISA. RNA sequencing, scratch wound-healing, trans-well, GO analysis, GSEA, luciferase reporter, Western blotting, immunofluorescence and immunohistochemistry assays, as well as an animal model were used to investigate the molecular mechanism underlying FGF19 driven LUSC progression. The therapeutic effect of a GLI2 inhibitor was determined using both in vitro cellular and in vivo animal experiments. RESULTS: We found that FGF19, a member of the fibroblast growth factor family, plays a crucial role in the invasion and metastasis of LUSC, and identified GLI2 as an important downstream effector of FGF19 involved in metastasis. Surprisingly, we found that FGF19 and GLI2 could reciprocally induce the expression of each other, and form a positive feedback loop to promote LUSC cell invasion and metastasis. These findings were corroborated by an association between a poor prognosis of LUSC patients and FGF19/GLI2 co-expression. In addition, we found that the GLI inhibitor GANT61 could effectively reduce FGF19-mediated LUSC invasion and metastasis. CONCLUSION: Our data suggest that FGF19 may serve as a novel biomarker for predicting metastatic LUSC. Intervening with the FGF19-GLI2 feedback loop may be a strategy for the treatment of FGF19-driven LUSC metastasis.

Exosomal PD-L1 predicts response with immunotherapy in NSCLC patients.

Immune Check-Point Inhibitors (ICIs) have shown remarkable promise in treating tumors, including non-small cell lung cancer (NSCLC). Nevertheless, the treatment response rate is low. Studies have found that the high expression of exosomal PD-L1 is one of the reasons for the low treatment response. Therefore, this study focused on the relationship between the exosomal PD-L1 and the clinical response to immunotherapy in NSCLC patients to evaluate whether it could be used as a biomarker to predict the efficacy of ICIs. In this study, clinical information and blood samples of 149 NSCLC patients receiving ICIs were collected. The expression level of exosomal PD-L1 was detected by enzyme-linked immunosorbent assay method, and the relationship between exosomal PD-L1 and the efficacy of ICIs was explored. Overall, our study found that the expression level of exosomal PD-L1 was lower at pre-treatment, or the max fold increasing change higher at 3-6 weeks had a higher disease control rate and longer progression-free survival. It revealed that the exosomal PD-L1 was associated with the treatment response of patients using ICIs and provided a new tool for the evaluation of clinical efficacy of lung cancer immunotherapy.

FGF19 Is Coamplified With CCND1 to Promote Proliferation in Lung Squamous Cell Carcinoma and Their Combined Inhibition Shows Improved Efficacy.

Lung squamous cell carcinoma (LUSC) remains as a major cause of cancer-associated mortality with few therapeutic options. Continued research on new driver genes is particularly important. FGF19, a fibroblast growth factor, is frequently observed as amplified in human LUSC, which is also associated with multiple genomic gains and losses. However, the importance of these associated changes is largely unknown. In this study, we aimed to clarify a novel mechanism that link neighboring oncogene co-amplification in the development of LUSC. We found that FGF19 was co-amplified and co-expressed with its neighboring gene CCND1 in a subset of LUSC patients and associated with poor prognosis. Moreover, FGF19 combined with CCND1 promoted the cell cycle progression of LUSC cells. Mechanistically, FGF19 also enhanced CCND1 expression by activating FGFR4-ERK1/2 signaling and strengthening CCND1-induced phosphorylation and inactivation of retinoblastoma (RB). In a murine model of lung orthotopic cancer, knockdown of CCND1 was found to prolong survival by attenuating FGF19-induced cell proliferation. Furthermore, the combination treatment of the FGFR4 inhibitor BLU9931 and the CDK4/6 inhibitor palbociclib potentiated the growth inhibition and arrested cells in G1 phase. In vivo, co-targeting FGFR4 and CDK4/6 also showed marked inhibition of tumor growth than single agent treatment. These findings further elucidate the oncogenic role of FGF19 in LUSC and provide insights into how the co-amplification of neighboring genes synergistically function to promote cancer growth, and combined inhibition against both FGF19 and CCND1 is more effective.

Coating metal-organic frameworks on plasmonic Ag/AgCl nanowire for boosting visible light photodegradation of organic pollutants.

Photoactive metal-organic frameworks, MIL-100(Fe), with controllable thickness are coated on plasmonic Ag/AgCl nanowire, for boosting visible light photodegradation of rhodamine B and tetracycline hydrochloride. The morphology and composition of the obtained nano-heterostructure were investigated in detail by SEM imaging, TEM imaging, XRD patterns, FT-IR spectra, N2 adsorption-desorption curves and TGA patterns. Photoelectric performance test suggested that a Z-scheme photocatalysis system for efficient transfer of photogenerated charge carriers was established between MIL-100(Fe) and plasmonic Ag/AgCl nanowire.

Knockdown of CDK5 down-regulates PD-L1 via the ubiquitination-proteasome pathway and improves antitumor immunity in lung adenocarcinoma.

Although immunotherapy (anti-PD-1/PD-L1 antibodies) has been approved for clinical treatment of lung cancer, only a small proportion of patients respond to monotherapy. Hence, understanding the regulatory mechanism of PD-L1 is particularly important to identify optimal combinations. In this study, we found that inhibition of CDK5 induced by shRNA or CDK5 inhibitor leads to reduced expression of PD-L1 protein in human lung adenocarcinoma cells, while the mRNA level is not substantially altered. The PD-L1 protein degradation is mediated by E3 ligase TRIM21 via ubiquitination-proteasome pathway. Subsequently, we studied the function of CDK5/PD-L1 axis in LUAD. In vitro, the absence of CDK5 in mouse Lewis lung cancer cell (LLC) has no effect on cell proliferation. However, the attenuation of CDK5 or combined with anti-PD-L1 greatly suppresses tumor growth in LLC implanted mouse models in vivo. Disruption of CDK5 elicits a higher level of CD3+, CD4+ and CD8+ T cells in spleens and lower PD-1 expression in CD4+ and CD8+ T cells. Our findings highlight a role for CDK5 in promoting antitumor immunity, which provide a potential therapeutic target for combined immunotherapy in LUAD.

Targeted inhibition of SIRT6 via engineered exosomes impairs tumorigenesis and metastasis in prostate cancer.

The treatment for metastatic castration-resistant prostate cancer patients remains a great challenge in the clinic and continuously demands discoveries of new targets and therapies. Here, we assess the function and therapeutic value of SIRT6 in metastatic castration-resistant prostate cancer. Methods: The expression of SIRT6 was examined in prostate cancer tissue microarray by immunohistochemistry staining. The functions of SIRT6 and underlying mechanisms were elucidated by in vitro and in vivo experiments. We also developed an efficient method to silence SIRT6 by aptamer-modified exosomes carrying small interfering RNA and tested the therapeutic effect in the xenograft mice models. Results: SIRT6 expression is positively correlated with prostate cancer progression. Loss of SIRT6 significantly suppressed proliferation and metastasis of prostate cancer cell lines both in vitro and in vivo. SIRT6-driven prostate cancer displays activation of multiple cancer-related signaling pathways, especially the Notch pathway. Silencing SIRT6 by siRNA delivered through engineered exosomes inhibited tumor growth and metastasis. Conclusions: SIRT6 is identified as a driver and therapeutic target for metastatic prostate cancer in our findings, and inhibition of SIRT6 by engineered exosomes can serve as a promising therapeutic tool for clinical application.

Photocatalytic Performance of the MOF-Coating Layer on SPR-Excited Ag Nanowires.

The photoactive metal-organic frameworks (MOFs) were controllably coated on the surface plasmon resonance-excited Ag nanowires in a layer manner to adjust the photocatalytic activity. The influence of the thickness of the MOF coating layer on the photocatalytic activity was investigated. A thicker MOF coating layer not only facilitated the photogenerated electron-hole separation efficiency but also provided a larger Brunauer-Emmett-Teller surface area, thus enhancing the photocatalytic activity. This work provided a new way to adjust the photocatalytic activity of the photoactive MOF.

Sirt3 Protects Against Ischemic Stroke Injury by Regulating HIF-1α/VEGF Signaling and Blood-Brain Barrier Integrity.

Sirtuin 3 (Sirt3) is a member of the Sirtuin family proteins and known to regulate multiple physiological processes such as metabolism and aging. As stroke is an aging-related disease, in this work, we attempt to examine the role and potential mechanism of Sirt3 in regulating ischemic stroke by using a permanent middle cerebral artery occlusion (pMCAO) model in wild type (WT) and Sirt3 knockout (KO) mice, coupled with oxygen glucose deprivation (OGD) experiments in cultured primary astrocytes. Sirt3 deficiency aggravated neuronal cell apoptosis and neurological deficits after brain ischemia. In addition, Sirt3 KO mice showed more severe blood-brain barrier (BBB) disruption and inflammatory responses compared with WT group in the acute phase. Furthermore, specific overexpression of Sirt3 in astrocytes by injecting glial fibrillary acidic protein (GFAP)::Sirt3 virus in ischemic region showed protective effect against stroke-induced damage. Mechanistically, Sirt3 could regulate vascular endothelial growth factor (VEGF) expression by inhibiting hypoxia inducible factor-1α (HIF-1α) signaling after ischemia (OGD). Our results have shown that Sirt3 plays a protective role in ischemic stroke via regulating HIF-1α/VEGF signaling in astrocytes, and reversal of the Sirt3 expression at the acute phase could be a worthy direction for stroke therapy.

Progressive Increasing of Pt Nanoparticles with Multiple-Layered Manner inside Metal-Organic Frameworks for Enhanced Catalytic Activity.

Single-layered, double-layered, and triple-layered Pt nanoparticles with a well-defined arrangement were encapsulated inside metal-organic frameworks (MOFs) to investigate the catalytic performance influenced by the progressive increasing of Pt nanoparticles inside MOFs; the results show that the catalytic activity of the Pt-MOF hybrid catalysts increases progressively with the progressive increasing of the Pt nanoparticles inside MOFs. Progressive increasing of Pt nanoparticles with a multiple-layered manner inside MOFs provides a new route for designing well-organized hybrid catalysts of noble metal nanoparticles and MOFs with enhanced catalytic activity.

Inserting Pt Nanoparticles at the Designated Location inside Metal-Organic Frameworks for Promoted Catalytic Performance.

Metal-organic frameworks (MOFs)-supported noble metal nanoparticles (NMNPs) catalysts attract increasing attention due to their high durability and efficiency in catalytic reactions. In this work, Pt nanoparticles are inserted at the designated location inside MIL-100(Fe) to investigate the location-effect of NMNPs inside MOFs on the catalytic reaction. The comparison test on the reduction of p-nitrophenol suggests that the location of the Pt nanoparticles inside MIL-100(Fe) largely influences the catalytic performance and the Pt nanoparticles inside MIL-100(Fe) locate closer to the outer surface of the MIL-100(Fe), providing higher catalytic efficiency. Possible reasons are concluded as the location of the Pt nanoparticles inside MIL-100(Fe) dominates the reactants transport pathway and the loading amount of Pt nanoparticles.

Controlling crystal growth of MIL-100(Fe) on Ag nanowire surface for optimizing catalytic performance.

Ag/MIL-100(Fe) core/sheath nanowire with controllable thickness of the MIL-100(Fe) sheath was prepared by controlling the crystal growth of MIL-100(Fe) on the Ag nanowire surface. The evolution of the MIL-100(Fe) sheath monitored by transmission electron microscopy (TEM), scanning electron microscopy (SEM), powder X-ray diffraction (XRD), thermogravimetric analyses (TGA), X-ray photoelectron spectroscopy (XPS), fourier transform infrared spectroscopy (FT-IR), and N2 adsorption-desorption analysis indicates that the thickness of the MIL-100(Fe) sheath increases with the increasing number of crystal growth cycles of MIL-100(Fe) on the Ag nanowire surface. Catalytic reaction over Ag/MIL-100(Fe) core/sheath nanowire suggests that the thickness of the MIL-100(Fe) sheath largely influences the catalytic performance and it is quite important to control the crystal growth of MIL-100(Fe) on the Ag nanowire surface for optimizing catalytic performance.

Primary experience of small bowel polypectomy with balloon-assisted enteroscopy in young pediatric Peutz-Jeghers syndrome patients.

For Peutz-Jeghers syndrome (PJS) patients, small bowel polyps develop and result in symptoms at an early age. Balloon-assisted enteroscopy (BAE) is verified as a safe and efficient choice to evaluate and remove small intestinal polyps in adult PJS. But the safety of BAE, especially BAE-facilitated polypectomy for young pediatrics, is little known. This prospective study focused on the effectiveness and safety of BAE-facilitated polypectomy in small bowel for young pediatric PJS. PJS patients (aged 0-14 years old) with BAE (including both single-balloon and double-balloon enteroscopies) were included from 1 September 2012 to 30 April 2018. The demographic data, medical history, and details of BAE were recorded. BAE-related complications and symptom relief after BAE were evaluated and compared between the PJS patients aged 5-10 years old (the younger pediatric group) and those aged 11-14 years old (the older pediatric group). A total of 41 pediatric PJS patients (5-14 years old) subjected to 82 BAEs were included. BAE-facilitated polypectomy was performed for 33 children (80.5%), and 242 polyps in small bowel were removed. For 10 (24.4%) patients, one or more giant polyps (maximum diameter larger than 5 cm) were removed. For eight patients, no polypectomy was done as no polyps were observed (six subjects) or not suitable for BAE-facilitated polypectomy (two subjects) because of high risk of perforation. The complication rates of BAE and BAE-facilitated polypectomy were 1.2% (1/82) and 1.8% (1/55), and the symptom relief rate was 70.8% (17/24). Compared with the older pediatric group, the younger pediatric group showed no increased BAE complication rate (0.0% vs. 5.0%, p = 0.488) and a comparable rate of symptom relief after BAE therapy (80.8% vs. 55.6%, p = 0.356).Conclusion: BAE-facilitated polypectomy in young pediatric PJS is safe and effective.What is known:• Small bowel evaluation and prophetic polypectomy are important for pediatric PJS patients to avoid polyp-related intussusception, obstruction, and bleeding.• BAE polypectomy was a recommended intervention for removing small bowel polyps in adult PJS patients.What is new:• BAE-facilitated small bowel polypectomy is safe and effective for young pediatric PJS, even for those aged less than 10 years old.

Encapsulating Pt Nanoparticles through Transforming Fe3O4 into MIL-100(Fe) for Well-Defined Fe3O4@Pt@MIL-100(Fe) Core-Shell Heterostructures with Promoting Catalytic Activity.

Metal-organic framework (MOF)-based magnetic Pt catalyst Fe3O4@Pt@MIL-100(Fe) core-shell heterostructures were prepared through transforming Fe3O4 into MIL-100(Fe) in benzene-1,3,5-tricarboxylic acid solution along with encapsulating the Pt nanoparticles successively adsorbed onto the surface of the Fe3O4 nanosphere and the continuously forming surfaces of the growing MIL-100(Fe) crystals. This method circumvented the obstacles, controlling the formation of metal nanoparticles (MNPs) inside MOFs or regulating growth of MOFs around the MNPs, for preparing an MNP-MOF composite catalyst. The obtained well-defined Fe3O4@Pt@MIL-100(Fe) core-shell heterostructure was shown promoting catalytic activity on the reduction of 4-nitrophenol due to the synergistic effect between the Pt nanoparticles and the MIL-100(Fe) shell and recycling convenience due to the rapid separation of the Fe3O4 core under an external magnetic field.

Sirt3 deficiency impairs neurovascular recovery in ischemic stroke.

AIMS: Sirt3 is one member of the NAD+ -dependent protein deacetylase family and plays crucial roles in diverse aspects of mammalian biological function. Then the role of Sirt3 on ischemia stroke is unknown. METHODS: To examine the effect of Sirt3 on ischemic stroke, we performed transient middle cerebral artery occlusion (tMCAO) in adult male Sirt3 knockout (KO) and wild-type (WT) mice. RESULTS: The level of Sirt3 in infarct region is decreased after ischemic stroke. In addition, we found that Sirt3 KO mice showed worse neurobehavioral outcome compared with WT mice, accompanied by decreased neurogenesis and angiogenesis as shown by the reduction in number of DCX+ /BrdU+ cells, NeuN+ /BrdU+ cells, and CD31+ /BrdU+ cells in the perifocal region during recovery phase after ischemic stroke. Furthermore, Sirt3 deficiency reduced the activation of vascular endothelial growth factor (VEGF), AKT, and extracellular signal-regulated kinases (ERK) signaling pathways. CONCLUSION: Our results indicated that Sirt3 is beneficial to neurovascular and functional recovery following chronic ischemic stroke.

Tubules of plant reoviruses exploit tropomodulin to regulate actin-based tubule motility in insect vector.

Plant reoviruses are known to exploit virion-packaging tubules formed by virus-encoding non-structural proteins for viral spread in insect vectors. Tubules are propelled by actin-based tubule motility (ABTM) to overcome membrane or tissue barriers in insect vectors. To further understand which insect factors mediate ABTM, we utilized yeast two-hybrid and bimolecular fluorescence complementation assays to test interactions between tubule protein Pns10 of rice dwarf virus (RDV), a plant reovirus, and proteins of its insect vector, the leafhopper Nephotettix cincticeps. Tropomodulin (Tmod), vitellogenin, and lipophorin precursor of N. cincticep displayed positive and strong interaction with Pns10, and actin-associated protein Tmod interacted with Pns10 in pull-down assay and the co-immunoprecipitation system. Further, we determined Pns10 tubules associated with Tmod in cultured cells and midgut of N. cincticep. The expression dynamic of Tmod was consistent with that of Pns10 and the fluctuation of RDV accumulation. Knockdown of Tmod inhibited the Pns10 expression and viral accumulation, thus decreasing the viruliferous rates of leafhopper. These results suggested that Tmod was involved in viral spread by directly interacting with Pns10 tubules, finally promoting RDV infection. This study provided direct evidence of plant reoviruses utilizing an actin-associated protein to manipulate ABTM in insect vectors, thus facilitating viral spread.