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Xiaohan Xu - Top 30 Publications

Ablation of MCM10 using CRISPR/Cas9 restrains the growth and migration of esophageal squamous cell carcinoma cells through inhibition of Akt signaling.

Minichromosome maintenance 10 (MCM10) is deregulated in several malignancies including cervical cancer and urothelial carcinoma. However, the expression and biologic role of MCM10 in esophageal squamous cell carcinoma (ESCC) is still unknown.

Acute myeloid leukemia presenting as erythema nodosum: A case report.

Erythema nodosum (EN), a type of septal panniculitis, could be a rare nonspecific cutaneous presentation of acute myeloid leukemia (AML).

Sjögren's syndrome initially presented as thrombotic thrombocytopenic purpura in a male patient: a case report and literature review.

Thrombotic thrombocytopenic purpura (TTP) is a potentially lethal multisystem disorder which could be caused by autoimmune diseases. However, the concomitant occurrence of TTP and Sjögren's syndrome (SS) is an extremely uncommon scenario, especially in male patients. A 56-year-old Chinese male was admitted for the appearance of diffuse ecchymosis. Then he gradually developed transient slurred speech, progressive confusion, agitation, extremity weakness, and fever. Laboratory investigations suggested anemia, thrombocytopenia, significantly increased lactic dehydrogenase, schistocytes in peripheral blood smear, and a disintegrin-like metalloproteinase with thrombospondin motif type 1 member 13 (ADAMTS13) activity deficiency with high inhibitor titers. TTP was thus diagnosed. The patient also had positive anti-nuclear antibody, anti-SSA, and anti-SSB; however, anti-double stranded DNA (dsDNA) was negative. These drove us to perform ocular and dental sicca evaluation and the finial diagnosis was TTP secondary to SS. Plasma exchange and corticosteroid therapy were effective to control TTP. Cyclophosphamide was subsequently added when the platelet count was stable. The total duration of corticosteroid and cyclophosphamide was 8 and 6 months, respectively. The patient recovered without relapse at 1-year follow-up. To our knowledge, this was the first case of SS initially presented as TTP in a male patient. The case also elucidated the importance of autoantibody screen in the workup of TTP and the benefits of adjunctive immunosuppressive therapy in relapse prevention.

Sample size considerations for paired experimental design with incomplete observations of continuous outcomes.

Paired experimental design is widely used in clinical and health behavioral studies, where each study unit contributes a pair of observations. Investigators often encounter incomplete observations of paired outcomes in the data collected. Some study units contribute complete pairs of observations, while the others contribute either pre- or post-intervention observations. Statistical inference for paired experimental design with incomplete observations of continuous outcomes has been extensively studied in literature. However, sample size method for such study design is sparsely available. We derive a closed-form sample size formula based on the generalized estimating equation approach by treating the incomplete observations as missing data in a linear model. The proposed method properly accounts for the impact of mixed structure of observed data: a combination of paired and unpaired outcomes. The sample size formula is flexible to accommodate different missing patterns, magnitude of missingness, and correlation parameter values. We demonstrate that under complete observations, the proposed generalized estimating equation sample size estimate is the same as that based on the paired t-test. In the presence of missing data, the proposed method would lead to a more accurate sample size estimate comparing with the crude adjustment. Simulation studies are conducted to evaluate the finite-sample performance of the generalized estimating equation sample size formula. A real application example is presented for illustration.

An analytical reconstruction model of the spread-out Bragg peak using laser-accelerated proton beams.

With the development of laser technology, laser-driven proton acceleration provides a new method for proton tumor therapy. However, it has not been applied in practice because of the wide and decreasing energy spectrum of laser-accelerated proton beams. In this paper, we propose an analytical model to reconstruct the spread-out Bragg peak (SOBP) using laser-accelerated proton beams. Firstly, we present a modified weighting formula for protons of different energies. Secondly, a theoretical model for the reconstruction of SOBPs with laser-accelerated proton beams has been built. It can quickly calculate the number of laser shots needed for each energy interval of the laser-accelerated protons. Finally, we show the 2D reconstruction results of SOBPs for laser-accelerated proton beams and the ideal situation. The final results show that our analytical model can give an SOBP reconstruction scheme that can be used for actual tumor therapy.

Endotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation.

Although the neutrophil recruitment cascade during inflammation has been well described, the molecular players that halt neutrophil chemotaxis remain unclear. In this study, we found that lipopolysaccharide (LPS) was a potent stop signal for chemotactic neutrophil migration. Treatment with an antagonist of the ATP receptor (P2X1) in primary human neutrophils or knockout of the P2X1 receptor in neutrophil-like differentiated HL-60 (dHL-60) cells recovered neutrophil chemotaxis. Further observations showed that LPS-induced ATP release through connexin 43 (Cx43) hemichannels was responsible for the activation of the P2X1 receptor and the subsequent calcium influx. Increased intracellular calcium stopped neutrophil chemotaxis by activating myosin light chain (MLC) through the myosin light chain kinase (MLCK)-dependent pathway. Taken together, these data identify a previously unknown function of LPS-induced autocrine ATP signaling in inhibiting neutrophil chemotaxis by enhancing MLC phosphorylation, which provides important evidence that stoppage of neutrophil chemotaxis at infectious foci plays a key role in the defense against invading pathogens.

Pharmacological inhibition of porcupine induces regression of experimental skin fibrosis by targeting Wnt signalling.

Wnt signalling has been implicated in activating a fibrogenic programme in fibroblasts in systemic sclerosis (SSc). Porcupine is an O-acyltransferase required for secretion of Wnt proteins in mammals. Here, we aimed to evaluate the antifibrotic effects of pharmacological inhibition of porcupine in preclinical models of SSc.

Feasibility and efficacy of simultaneous off-pump coronary artery bypass grafting and esophagectomy in elderly patients.

To analyze the outcomes of off-pump coronary artery bypass grafting (OPCABG) and esophagectomy simultaneously for patients with coronary artery disease (CAD) and coexisting esophageal cancer.

Adenosine effectively restores endotoxin-induced inhibition of human neutrophil chemotaxis via A1 receptor-p38 pathway.

Neutrophil chemotaxis plays an essential role in recruiting neutrophils to sites of inflammation. Neutrophil chemotaxis is suppressed both after exposure to lipopolysaccharide (LPS) in vitro and during clinical and experimental endotoxemia, leading to serious consequences. Adenosine (ADO) is a potent anti-inflammatory agent that acts on a variety of neutrophil functions. However, its effects on human neutrophil chemotaxis during infection have been less well characterized. In the present study, we investigated the effect of ADO and its receptor-specific antagonist and agonist on neutrophil chemotaxis in an in vitro LPS-stimulated model. The results showed that increasing the concentration of ADO effectively restored the LPS-inhibited neutrophil chemotaxis to IL-8. A similar phenomenon occurred after intervention with a selective A1 receptor agonist but not with a selective antagonist. Pre-treatment with cAMP antagonist failed to restore LPS-inhibited chemotaxis. Furthermore, protein array and western blot analysis showed that the activation of A1 receptor significantly decreased LPS-induced p38 MAPK phosphorylation. However, the surface expression of the A1 receptor in LPS-stimulated neutrophils was not significantly changed. Taken together, these data indicated that ADO restored the LPS-inhibited chemotaxis via the A1 receptor, which downregulated the phosphorylation level of p38 MAPK, making this a promising new therapeutic strategy for infectious diseases.

Elevated mercury bound to serum proteins in methylmercury poisoned rats after selenium treatment.

Methylmercury is a toxic pollutant and is generated by microbial methylation of elemental or inorganic mercury in the environment. Previous study found decreased hepatic MDA levels and urinary mercury levels in methylmercury poisoned rats after sodium selenite treatment. This study further found increased mercury levels in serum samples from methylmercury poisoned rats after selenium treatment. By using size exclusion chromatography coupled to inductively coupled plasma mass spectrometry, three Hg- binding protein fractions and two Se-binding protein fractions were identified with the molecular weight of approximately 21, 40, and 75 kDa and of 40 and 75 kDa, respectively. Elevated mercury level in the 75 kDa protein fraction was found binding with both Hg and Se, which may explain the decreased urinary Hg excretion in MeHg poisoned rats after Se treatment. MALDI-TOF-MS analysis of the serum found that the 75 kDa protein fractions were albumin binding with both Hg and Se and the 21 kDa fraction was Hg- binding metallothionein.

Tatarinan O, a lignin-like compound from the roots of Acorus tatarinowii Schott inhibits osteoclast differentiation through suppressing the expression of c-Fos and NFATc1.

Osteoclasts (OC) are large multinucleated cells derived from monocyte/macrophage precursors. Suppressing osteoclastogenesis is considered as an effective therapeutic approach to erosive bone disease. The root of Acorus tatarinowii Schott, a well-known traditional Chinese medicine was used to treat rheumatosis and other inflammatory disease. However, the effects of tatarinan O (TO), one of the lignin-like compounds isolated from the roots of Acorus tatarinowii Schott during bone development are still unclear. In the present study, we explored the effect of TO on RANKL-induced osteoclastogenesis in vitro. TO was found to suppress osteoclast differentiation from RANKL-stimulated mouse bone marrow macrophages (BMMs) without significant cytotoxicity. TO also dose-dependently suppressed bone resorption activity of mature osteoclasts. Additionally, TO apparently inhibited the expression of osteoclastic marker genes, such as MMP-9, Cts K and TRAP. Furthermore, our results showed that TO decreased RANKL-induced expression of c-Fos and NFATc1 without influencing NF-κB activation and MAPK phosphorylation. Hence, for the first time we revealed that TO dose-dependently inhibited osteoclastogenesis from RANKL-stimulated mouse BMMs via decreasing the expression of NFATc1 and c-Fos.

Puerarin reduces apoptosis in rat hippocampal neurons culturea in high glucose medium by modulating the p38 mitogen activated protein kinase and c-Jun N-terminal kinase signaling pathways.

To investigate the neuroprotective etfect of puerarin on rat hippocampal neurons cultured in high glucose medium, and to examine the role of the p38 mitogen activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways in this effect.

Interactions between endothelial cells and smooth muscle cells of blood vessels in sepsis.

Vascular endothelial cells (EC) and smooth muscle cells (SMC) are target and effecter cells of inflammation, and they play an important role in inflammatory responses. The abnormal structure and function of EC and SMC play a significant role in microcirculation disturbance in septic shock and multiple organ dysfunction. This review was meant to discuss the changes in structure and function of EC and SMC and their bidirectional regulation. The cellular linkage of EC and SMC is essential for the interactions between them, and it contributes to the course of sepsis. Paracrine and autocrine as produced by EC and SMC constitute a network for mutual adjustment. Replication of the interaction between EC and SMC facilitates the potential to support hemodynamics, tissue perfusion and cellular metabolism, thereby lower the mortality rate of sepsis. However, the detailed and specific mechanisms remain to be disclosed.

Suppressive effect of exogenous carbon monoxide on abnormal platelet exocytosis and its molecular mechanism in sepsis.

To investigate the suppressive effect of exogenous carbon monoxide (CO) on abnormal platelet exocytosis and its possible molecular mechanism.

Air particulate matter and cardiovascular disease: the epidemiological, biomedical and clinical evidence.

Air pollution is now becoming an independent risk factor for cardiovascular morbidity and mortality. Numerous epidemiological, biomedical and clinical studies indicate that ambient particulate matter (PM) in air pollution is strongly associated with increased cardiovascular disease such as myocardial infarction (MI), cardiac arrhythmias, ischemic stroke, vascular dysfunction, hypertension and atherosclerosis. The molecular mechanisms for PM-caused cardiovascular disease include directly toxicity to cardiovascular system or indirectly injury by inducing systemic inflammation and oxidative stress in peripheral circulation. Here, we review the linking between PM exposure and the occurrence of cardiovascular disease and discussed the possible underlying mechanisms for the observed PM induced increases in cardiovascular morbidity and mortality.

Effects of exogenous carbon monoxide-releasing molecule 2 intervention in vitro on formation of human neutrophil extracellular traps stimulated by endotoxin/lipopolysaccharide and its mechanism.

To explore the effects of exogenous carbon monoxide-releasing molecule 2 (CORM-2) on formation of human neutrophil extracellular traps (NETs) stimulated by endotoxin/lipopolysaccharide (LPS) and its relevant mechanism.

Prophylactic abdominal aorta balloon occlusion during caesarean section: a retrospective case series.

The management of patients with morbidly adherent placenta has been described using vascular balloon catheters placed in the iliac arteries, but rarely in the aorta. This case series presents our experience with prophylactic lower abdominal aorta balloon occlusion in 45 women.

The Protective Effects of HJB-1, a Derivative of 17-Hydroxy-Jolkinolide B, on LPS-Induced Acute Distress Respiratory Syndrome Mice.

Acute respiratory distress syndrome (ARDS),which is inflammatory disorder of the lung, which is caused by pneumonia, aspiration of gastric contents, trauma and sepsis, results in widespread lung inflammation and increased pulmonary vascular permeability. Its pathogenesis is complicated and the mortality is high. Thus, there is a tremendous need for new therapies. We have reported that HJB-1, a 17-hydroxy-jolkinolide B derivative, exhibited strong anti-inflammatory effects in vitro. In this study, we investigated its impacts on LPS-induced ARDS mice. We found that HJB-1 significantly alleviated LPS-induced pulmonary histological alterations, inflammatory cells infiltration, lung edema, as well as the generation of inflammatory cytokines TNF-α, IL-1β and IL-6 in BALF. In addition, HJB-1 markedly suppressed LPS-induced IκB-α degradation, nuclear accumulation of NF-κB p65 subunit and MAPK phosphorylation. These results suggested that HJB-1 improved LPS-induced ARDS by suppressing LPS-induced NF-κB and MAPK activation.

Inositol-Requiring Enzyme 1-Dependent Activation of AMPK Promotes Brucella abortus Intracellular Growth.

AMP-activated protein kinase (AMPK) is a serine/threonine kinase that is well conserved during evolution. AMPK activation inhibits production of reactive oxygen species (ROS) in cells via suppression of NADPH oxidase. However, the role of AMPK during the process of Brucella infection remains unknown. Our data demonstrate that B. abortus infection induces AMPK activation in HeLa cells in a time-dependent manner. The known AMPK kinases LKB1, CAMKKβ, and TAK1 are not required for the activation of AMPK by B. abortus infection. Instead, this activation is dependent on the RNase activity of inositol-requiring enzyme 1 (IRE1). Moreover, we also found that B. abortus infection-induced IRE1-dependent activation of AMPK promotes B. abortus intracellular growth with peritoneal macrophages via suppression of NADPH-derived ROS production.

Comparative metalloproteomic approaches for the investigation proteins involved in the toxicity of inorganic and organic forms of mercury in rice (Oryza sativa L.) roots.

The toxicity mechanisms of rice roots under inorganic mercury (IHg) or methylmercury (MeHg) stress were investigated using metalloproteomic approaches. Rice seedlings were cultivated in nutrient solutions with IHg or MeHg for three weeks. Proteins were extracted from the roots and separated by two-dimensional electrophoresis (2-DE). Differentially expressed proteins were analyzed using ESI-MS/MS and identified by PMF. 26 and 29 protein spots were differentially expressed in the IHg- and MeHg-exposed roots, respectively. The proteins responsive to Hg exposure are involved in antioxidative defense, sulfur and glutathione metabolism, carbohydrate and energy metabolism, programmed cell death, and pathogen defense. Chitinase and salt stress-induced proteins exhibited a greater differentially expression in response to MeHg stress compared to IHg stress. Hg-binding proteins were detected by the combined use of 1-DE, SRXRF, and ESI-MS/MS. The results showed that Hg was bound to proteins of 15-25 kDa in rice roots under Hg stress. The Hg contents in the band under IHg stress were remarkably higher than those under MeHg. Hg binds to proteins, which leads to irreversible damage of root growth. Rice roots changed the related protein expression levels in response to Hg stress. These results may provide new insights into the mechanism of toxicity of IHg and MeHg in rice.

Demethylation of methylmercury in growing rice plants: An evidence of self-detoxification.

Mercury (Hg) is a global pollutant that poses a serious threat to human and the environment. Rice was found as an important source for human exposure to Hg in some areas. In this study, the transportation and transformation of IHg and MeHg in rice plants exposed to IHg or MeHg were investigated. The IHg and MeHg concentrations in rice roots and shoots collected every five days were analyzed by HPLC-ICP-MS and SR-XANES. When exposed to MeHg, the percent of IHg in rice roots and shoots increased while MeHg decreased significantly, suggesting prominent demethylation of MeHg occurred. However no notable MeHg was found in both roots and shoots of rice plant when exposed to IHg. SR-XANES analysis further confirmed the demethylation of MeHg with rice. This study provides a new finding that demethylation of MeHg could occur in growing rice, which may be a self-defense process of rice plant.

Total ocular surface amniotic membrane transplantation for paraquat-induced ocular surface injury.

To evaluate the therapeutic efficacy of modified amniotic membrane transplantation (MAMT) for paraquat-induced ocular surface injury.

Asiatic Acid Attenuates the Progression of Left Ventricular Hypertrophy and Heart Failure Induced by Pressure Overload by Inhibiting Myocardial Remodeling in Mice.

Cardiac structural remodeling, including cardiomyocyte apoptosis, interstitial fibrosis, and inflammation, appears to be a key event associated with the progression of left ventricular hypertrophy and heart failure. Asiatic acid (AA) is a triterpenoid compound extracted from Centella asiatica that exhibits antiapoptotic, antifibrotic, and anti-inflammatory activities. In the present study, a transverse aortic constriction (TAC) model was created in mice to mimic the progression of hypertrophy (2 weeks post-TAC) and heart failure (4 weeks post-TAC) to investigate whether the potential therapeutic drug AA ameliorates hypertrophy progression and which mechanisms are involved in this amelioration. Our results demonstrated that AA markedly inhibited the process of progression induced by pressure overload. The increases cardiomyocyte apoptosis and interstitial fibrosis, and inflammatory responses were significantly suppressed by AA. Our investigation revealed that this inhibitory effect was mediated by blocking the activation of both mitochondrial and death receptor-dependent apoptotic signaling pathways. Additional experiments demonstrated that AA attenuated fibrosis by blocking both transforming growth factor-β1/Smad and interleukin-6, signaling activation. Consequently, these findings indicated that AA attenuated pathological cardiac structural remodeling and preserved cardiac function via multiple intracellular signaling pathways in response to cardiac stimuli.

Asiatic acid inhibits cardiac hypertrophy by blocking interleukin-1β-activated nuclear factor-κB signaling in vitro and in vivo.

Activated interleukin (IL)-1β signaling pathway is closely associated with pathological cardiac hypertrophy. This study investigated whether asiatic acid (AA) could inhibit IL-1β-related hypertrophic signaling, and thus suppressing the development of cardiac hypertrophy.

Nanomaterial-based approaches for the detection and speciation of mercury.

Mercury is toxic with widespread contamination. Highly sensitive and selective approaches for mercury analysis are desired. Although conventional techniques are accurate and sensitive in the determination of mercury, these procedures are time-consuming, labor-intensive and dependent heavily on expensive instrumentation. In recent years, nanomaterial-based approaches have been proved to be effective alternatives in the detection and speciation of mercury. In this review, the development of different nanomaterial-based approaches was summarized, as well as their utilization for the detection of mercury in environmental and biological samples, such as gold nanomaterials, carbon nanomaterials, quantum dots and so on. Moreover, the speciation of mercury using nanomaterials was also reviewed.

17-Hydroxy-jolkinolide A inhibits osteoclast differentiation through suppressing the activation of NF-κB and MAPKs.

Osteoclasts (OC) are bone-specific multinucleated giant cells (MNCs) derived from the monocyte/macrophage hematopoietic lineage cells. Inhibiting osteoclast formation is considered as an effective therapeutic approach for the treatment of the pathological bone loss. In this study, we investigated effects of 17-hydroxy-jolkinolide A (HJA), an ent-abietane diterpenoid isolated from the dried root of Euphorbia fischeriana, on osteoclastogenesis induced by RANKL. The results showed that HJA significantly inhibited RANKL-induced osteoclast formation from primary bone marrow macrophages (BMMs). HJA also prevented bone resorption by mature osteoclasts in a dose-dependent manner. In addition, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (Cts K) and MMP-9, was significantly inhibited by HJA. Furthermore, HJA also significantly inhibited RANKL-induced activation of NF-κB and phosphorylation of MAPK. Our results indicate that HJA has an inhibitory role in the bone loss by preventing osteoclast formation as well as its bone resorptive activity. Therefore, HJA may be useful as a therapeutic reagent for bone loss-associated diseases.

Platelet granule secretion mechanisms: Are they modified in sepsis?

Sepsis is a progressive systemic inflammatory response syndrome associated with multi-organ dysfunction caused by overwhelming infection. In sepsis, platelet factor 4, β-thromboglobulin, and other inflammatory mediators are secreted from platelet granules to participate in the inflammatory response and increase sepsis-related impairments. Recently, an increasing number of studies showed a critical role of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complexes in the platelet granule secretion. However, whether SNARE complex-regulated platelet granule secretion is involved in the pathophysiology of sepsis is unclear. Thus, in this review, we discussed the recent advances of SNARE complexes and their regulators in platelets as well as the mechanism of SNARE complexes on mediating platelet granule secretion.

The association of perioperative autologous blood transfusion with the early postoperative cognitive dysfunction in aged patients following lumbar surgery.

Intraoperation autologous blood transfusion is an effective method that is used in surgeries with an important blood loss. Several studies suggest that massive blood transfusion is one of the independent risks for postoperative cognitive dysfunction (POCD). Whether the autologous blood is one of the risk factor for POCD or not, we retrospectively examined the incidence of POCD and the probable risk factors in patients undergoing lumbar surgery in our hospital, with the same aged non-POCD patients as controls.

Percutaneous Coronary Intervention Rates and Associated Independent Predictors for Progression of Nontarget Lesions in Patients With Diabetes Mellitus After Drug-Eluting Stent Implantation.

Little is known about clinically driven percutaneous coronary intervention (PCI) rates and predictors for progression of nontarget lesions in diabetic patients who have undergone drug-eluting stent (DES) implantation. We retrospectively analyzed the clinical and angiographic data of 2187 diabetic patients undergoing DES implantation. The cumulative rate of nontarget lesion PCI was 6.3% at 1 year, 14.3% at 2 years, and 19.8% at 3 years. The independent predictors of need for clinically driven PCI in patients with diabetes mellitus after DES implantation included obesity (odds ratio [OR] 2.303, 95% confidence interval [CI] 1.657-3.199, P < .001), low levels of high-density lipoprotein cholesterol (OR 1.412, 95% CI 1.114-1.789, P = .004), statin use (OR 0.669, 95% CI 0.454-0.986, P = .042), insulin use (OR 1.310, 95% CI 1.030-1.665, P = .027), and Synergy Between PCI With Taxus and Cardiac Surgery (SYNTAX) score (OR 1.061, 95% CI 1.045-1.077, P < .001) at baseline PCI. These findings may facilitate prediction of the risk of repeat revascularization and improve repeat revascularization rates in diabetic patients after DES implantation.

Near-infrared light remote-controlled intracellular anti-cancer drug delivery using thermo/pH sensitive nanovehicle.

Stimuli-responsive drug delivery systems have been developed to enhance the tumor-targeting drug transportation and minimize the severe side effects along with the chemotherapy. In this study, a near-infrared (NIR) light triggered drug delivery system was developed based on the amphiphilic chitosan derivative-coated single-wall carbon nanotubes (CNT) encapsulated in the thermo/pH sensitive nanogel (CS/[email protected]). The PEG diacrylate (Mw = 250 Da) was applied in the present work to tune the nanoparticles with the phase transition temperature at ∼ 38 °C, which was an attempt to match the prerequisite for the in vivo applications. Owing to the π-π stacking, hydrophobic interaction and the opportunity of Schiff-base formation between chitosan and doxorubicin (DOX), the nanoparticles possessed a relative high drug loading capacity (∼ 43%). The DOX loaded CS/[email protected] released DOX faster at 40 °C than at 25 °C, meanwhile faster at pH 5.0 in comparison with that at pH 7.4. Moreover, the rapid and repetitive release of DOX was observed when the DOX-loaded CS/[email protected] was irradiated under NIR light. Furthermore, DOX-loaded CS/[email protected] upon NIR irradiation showed significantly greater cytotoxicity in HeLa cells owing to NIR-triggered increase in temperature and enhanced DOX release. Confocal laser scanning microscopy (CLSM) was utilized to demonstrate the enhanced cell uptake of the as prepared nanoparticles and the faster drug release under the NIR irradiation and lower pH. All the results suggest that multifunctional DOX-loaded CS/[email protected] nanocomposite is a promising therapeutic nanocarrier for intracellular drug delivery with great potential for targeted cancer therapy.