Suitable Isolation Side Chains: A Simple Strategy for Simultaneously Improving the Phototherapy Efficacy and Biodegradation Capacities of Conjugated Polymer Nanoparticles.

Utilizing one molecule to realize combinational photodynamic and photothermal therapy upon single-wavelength laser excitation, which relies on a multifunctional phototherapy agent, is one of the most cutting-edge research directions in tumor therapy owing to the high efficacy achieved over a short course of treatment. Herein, a simple strategy of "suitable isolation side chains" is proposed to collectively improve the fluorescence intensity, reactive oxygen species production, photothermal conversion efficiency, and biodegradation capacity. Both in vitro and in vivo results reveal the practical value and huge potential of the designed biodegradable conjugated polymer PTD-C16 with suitable isolation side chains in fluorescence image-guided combinational photodynamic and photothermal therapy. These improvements are achieved through manipulation of aggregated states by only side chain modification without changing any conjugated structure, providing new insight into the design of biodegradable high-performance phototherapy agents.

Multifunctional agents based on 3-dicycanovinylindan-1-one acceptor: Molecular design and phototheranostic application.

Phototherapy, including photodynamic therapy (PDT) and photothermal therapy (PTT), has garnered considerable attention in recent years, owing to its precise spatiotemporal accuracy with minimal side effects. Recent research reveals that the combination of PDT and PTT exhibits a remarkable anti-tumor efficacy compared to PDT or PTT alone, which has put forward the new requirements of multifunctional phototherapy agents with both high photosensitization and photothermal conversion efficiencies. Among the newly developed multifunctional agents, the ones with one or two 3-dicycanovinylindan-1-one (IC) moieties as the acceptors attract much more attention, due to their long-wavelength excitation and emission, as well as high phototherapy efficacies. Therefore, in this review, the latest advancement of multifunctional agents based on IC acceptor is summarized. Especially, we focus on the structure-property relationships of the agents, as well as their biomedical application in anti-tumor therapy or image-guided therapy. Our perspective on the further future development of this field is also discussed to conclude.

[Predictive Value of Complete Blood Count and Inflammation Marker on Risk of Recurrence in Children with Henoch-Schönlein Purpura].

OBJECTIVE: To investigate the predictive value of complete blood count (CBC) and inflammation marker on the recurrence risk in children with Henoch-Schönlein purpura (HSP). METHODS: One hundred and thirty-three children with HSP admitted to Cangzhou Central Hospital from February 2017 to March 2019 were enrolled. The clinical data of the children were collected, at the time of admission CBC and C-reactive protein (CRP) were detected. After discharge, the children were followed up for 1 year, the clinical data of children with and without recurrence were compared, and multivariate logistic regression was used to analyze the risk factors affecting HSP recurrence. Receiver operating characteristic (ROC) curve should be drawn and the predictive value of CBC and CRP on HSP recurrence should be analyzed. RESULTS: In the follow-up of 133 children, 8 cases were lost and 39 cases recurred, with a recurrence rate of 31.20% (39/125). The age, skin rash duration, proportion of renal damage at the initial onset, percentage of neutrophils, percentage of lymphocytes, platelet count (PLT), mean platelet volume (MPV) and neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), MPV/PLT ratio (MPR), and CRP level of patients with recurrence were statistically different from those without recurrence (P <0.05). Multivariate logistic regression analysis showed that long skin rash duration, renal damage at the initial onset, increased PLR, high PLT, increased MPV and elevated CRP level were independent risk factors for recurrence in children with HSP (P <0.05). The ROC curve analysis showed that the area under the curve (AUC) of the combination of the four blood and inflammation marker (PLT, MPV, PLR and CPR) in the early prediction of HSP recurrence was 0.898, which was higher than the initial renal damage (AUC=0.687) and persistent skin rash time (AUC=0.708), with a sensitivity of 84.62% and a specificity of 83.72%. CONCLUSION: Observation of CBC and CPR can predict the risk of HSP recurrence early and guide early clinical intervention.

ANGPTL2 promotes VEGF-A synthesis in human lung cancer and facilitates lymphangiogenesis.

Lung cancer is an extremely common cancer and metastatic lung cancer has a greatly low survival rate. Lymphangiogenesis is essential for the development and metastasis of lung cancer. The adipokine angiopoietin-like protein 2 (ANGPTL2) regulates tumor progression and metastasis, although the functions of ANGPTL2 in lung cancer are unknown. Analysis of data from TCGA genomics program, the GEPIA web server and the Oncomine database revealed that higher levels of ANGPTL2 expression were correlated with progressive disease and lymph node metastasis. ANGPTL2 enhanced VEGF-A-dependent lymphatic endothelial cell (LEC) tube formation and migration. Integrin α5ß1, p38 and nuclear factor (NF)-κB signaling mediated ANGPTL2-regulated lymphangiogenesis. Importantly, overexpression ANGPTL2 facilitated tumor growth and lymphangiogenesis in vivo. Thus, ANGPTL2 is a promising therapeutic object for treating lung cancer.

Theranostic Nanoprobes with Aggregation-Induced NIR-II Emission: from Molecular Design to Biomedical Application.

The development of fluorophores with other powerful features has received much attention for the diagnosis and treatment of diseases. Nanoprobes (NPs) with aggregation-induced emission (AIE) have demonstrated superior performance in deeper penetration depth with better resolution, higher signal-to-noise ratio, and lower side effects in the second near-infrared window (NIR-II, 1000-1700 nm) than in any other range. Herein, the latest advances in NIR-II AIE NPs in cancer theranostics are summarized. In particular, we focus on the design of multifunctional AIE agents with both strong NIR-II emission and effective photothermal conversion or reactive oxygen species (ROS) production, as well as their translational biomedical applications, including imaging diagnosis, image-guided surgery, and image-guided phototherapy, etc. At the end of this review, the opportunities and challenges of this field are also discussed.

Genetic Associations of Visfatin Polymorphisms with EGFR Status and Clinicopathologic Characteristics in Lung Adenocarcinoma.

Lung adenocarcinoma (LUAD) is the most common histologic type of lung cancer. Mutations of the epidermal growth factor receptor (EGFR) gene are among the most common genetic alterations in LUAD and are the targets of EGFR tyrosine kinase inhibitors. The enzyme visfatin is involved in the generation of the oxidized form of nicotinamide adenine dinucleotide (NAD+) and regulation of intracellular adenosine triphosphate (ATP), critical processes in cancer cell survival and growth. This study explored the relationship between visfatin single nucleotide polymorphisms (SNPs) with EGFR status and the clinicopathologic development of LUAD in a cohort of 277 Taiwanese men and women with LUAD. Allelic discrimination of four visfatin SNPs rs11977021, rs61330082, rs2110385 and rs4730153 was determined using a TaqMan Allelic Discrimination assay. We observed higher prevalence rates of advanced (T3/T4) tumors and distant metastases in EGFR wild-type patients carrying the rs11977021 CT + TT and rs61330082 GA + AA genotypes, respectively, compared with patients carrying the CC and GG genotypes. EGFR wild-type patients carrying the rs11977021 CT + TT genotypes were also more likely to develop severe (stage III/IV) malignancy compared with patients carrying the CC genotype. An analysis that included all patients found that the association persisted between the rs11977021 CT + TT and rs61330082 GA + AA genotypes and the development of T3/T4 tumors compared with patients carrying the rs11977021 CC and rs61330082 GG genotypes. In conclusion, these data indicate that visfatin SNPs may help to predict tumor staging in LUAD, especially in patients with EGFR wild-type status.

Cigarette smoke-promoted increases in osteopontin expression attract mesenchymal stem cell recruitment and facilitate lung cancer metastasis.

INTRODUCTION: Cigarette smoking is the main risk factor for lung cancer. MSCs in the TME promoting tumor angiogenesis, growth, and metastasis. SIBLING proteins enable cancer cells to extend, invade and metastasize. OBJECTIVES: Cigarette smoke promotes the progression and metastasis of lung cancer, although how this occurs is poorly understood. We evaluated the impact of whether cigarette smoking motivates SIBLING protein expression and is involved in MSC-mediated lung tumor metastasis. METHODS: We investigated the expression of OPN in the Gene Expression Omnibus (GEO) databases and confirmed the results by immunohistochemistry (IHC), qPCR and Western blotting (WB) of lung cancer cells and tissues. The effect of OPN on the recruitment and adhesion of mesenchymal stem cells (MSCs) to lung cancer cells and lung cancers metastasis was investigated by Transwell, adhesion assays. A series of in vitro and in vivo experiments were conducted to demonstrate the mechanisms by which OPN modulates recruitment and adhesion of MSCs to lung cancer cells and lung cancer metastasis. RESULTS: Cigarette smoke extract (CSE) and benzo[α]pyrene (B[α]P) increased levels of OPN expression and facilitated the recruitment and adhesion of MSCs to lung cancer cells via JAK2/STAT3 signaling. We also observed that OPN promotes tumor-associated MSC (TA-MSC) formation through the OPN receptor (integrins αvß1, αvß3, αvß5 or CD44), inducing lung cancer cell migration and invasion. In an orthotopic mouse model of lung cancer, increases in OPN expression promoted by cigarette smoke upregulated MSC recruitment and facilitated lung cancer metastasis. Knockdown of OPN expression inhibited cigarette smoke-induced lung cancer metastasis in vivo. CONCLUSION: Cigarette smoke increases OPN expression through the JAK2/STAT3 signaling pathway to attract MSC cell recruitment and promote lung cancer metastasis. Our findings offer important insights into how lung cancer metastasis develops in smokers.

Development and validation of a nomogram to predict recurrence in children with Henoch-Schönlein purpura.

BACKGROUND: To screen risk factors for the recurrence in children with Henoch-Schönlein Purpura (HSP) and to develop and validate a nomogram for recurrence in children with HSP. METHODS: During September 2019 and September 2021, 212 children with HSP were selected in this study. The children were divided into two sets in a proportion of 7:3 using R language, with the first group as the training sets and the second as the internal validation sets. The related variables were analyzed by univariate and multivariate logistic regression analyses, and a nomogram for predicting the recurrence in HSP children was established. The nomogram was evaluated by ROC curve, calibration curve and decision curve, and 1000 times bootstrap resampling method was used to verify the model internally. RESULTS: Univariate and multivariate regression analyses identified respiratory infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine as risk factors for the recurrence in children with HSP. Those risk factors were used to construct a predictive nomogram. The calibration curves revealed excellent accuracy of the predictive nomogram model, internally and externally. CONCLUSIONS: We constructed and validated a clinical nomogram to predict the recurrence in children with HSP. We confirmed that respiratory tract infection, without preventive medication and diet restriction, age, allergen positive and abnormal urine routine were independent recurrence risk factors. This nomogram had a good performance in clinical decision-making.

Platelet membrane-cloaked selenium/ginsenoside Rb1 nanosystem as biomimetic reactor for atherosclerosis therapy.

Cardiovascular disease remains the dominant contributor to human mortality, and the main etiology of which is atherosclerosis (AS). Enhancing the targeted ability of nanosystem and improving plaque stability are critical challenges for the current management of AS. Herein, we leverage the marked role of platelets in AS to construct a biomimetic nanodrug delivery system (PM@Se/Rb1 NPs), which prepared by cloaking platelet membrane (PM) around Selenium (Se) and ginsenoside Rb1 nanoparticles (Se/Rb1 NPs) core. The core endows the delivery system antioxidant, lipid metabolism and anti-inflammatory effects for AS effective treatment. Moreover, PM-coated nanoparticles reserve platelets' inherent biological elements to deliver drugs to plaques. We further explored the potential effect of PM@Se/Rb1 NPs' combination with the clinical anticoagulant drug warfarin (War) to treat AS and elucidated the possible drug interaction mechanism. As a result, the PM@Se/Rb1 NPs are not only capable of improving inflammatory behaviors such as inhibitory adhesion ability and anti-angiogenesis therapeutic effect in vitro, but also administer efficiently localizing to atherosclerotic plaque explaining by aortic samples from established ApoE-/- mice. Therefore, this study provided a theoretical basis of biomimetic nanodrug in the treatment of AS as well as an effective reference for the combined application of nanodrug and clinical drugs.

lncRNA-NEAT1 Sponges miR-128 to Promote Inflammatory Reaction and Phenotypic Transformation of Airway Smooth Muscle Cells.

OBJECTIVE: Pediatric asthma is still a health threat to the children. Long noncoding RNA-NEAT1 (lncRNA-NEAT1) was reported to be positively correlated with the severity of asthma. We aimed to study the effects and mechanism of lncRNA-NEAT1on inflammatory reaction and phenotypic transformation of airway smooth muscle cells (ASMCs) in the bronchial asthma. METHOD: The degree of lncRNA-NEAT1 and miR-128 mRNA in children with bronchial asthma and healthy individuals was tested by qRT-PCR. After the inflammatory reaction and phenotypic transformation of PDGF-BB-induced ASMCs, the expression of lncRNA-NEAT1 or miR-128 in the AMSC was disturbed in the AMSC. Subsequently, the expression of lncRNA-NEAT1 and miR-128 was detected by the way of qRT-PCR, and western blot was applied to measure the expression of MMP-2, MMP-9, α-SMA, calponin, NF-κB, and so on in the cells. The content of TNF-α, IL-1ß, IL-6, and IL-8 in the cell culture supernatant was checked by ELISA. MTT, Transwell, and flow cytometry were used to detect cell proliferation, migration, and apoptosis. Further, the targeting relations between lncRNA-NEAT1 and miR-128 were evaluated by the dual-luciferase reporter assay. RESULT: In the sputum of children with bronchial asthma, lncRNA-NEAT1 was significantly upregulated while miR-128 was rapidly downregulated. Besides, lncRNA-NEAT1 and miR-128 were competitively combined and, for their expression, negatively correlated. CONCLUSION: lncRNA-NEAT1 sponges miR-128 to boost PDGF-BB-induced inflammatory reaction and phenotypic transformation of ASMCs to aggravate the occurrence and development of childhood bronchial asthma.

Driving factors of carbon emissions in China's municipalities: a LMDI approach.

China, as the world's largest carbon dioxide emitter, is bound to assume the important responsibility of energy conservation and emission reduction. To this end, each city, led by representative municipalities, must enhance efforts in carbon emission reduction to jointly realize China's low-carbon transition. Taking four representative municipalities, namely, Beijing, Tianjin, Shanghai, and Chongqing as the case cities, this paper establishes a decomposition analysis for the driving factors of carbon emissions by applying the LMDI method covering data from 2007 to 2017. Kaya identity is used to decompose the effects into eight driving factors: GDP effect, industrial structure effect, energy intensity effect, overall energy structure effect, population effect, urbanization effect, per capita energy consumption effect, urban and rural energy structure effect. The results show that at the municipality level, the driving factors that contribute to carbon emissions are the GDP growth effect and the population effect, with the former still being the most important factor in the municipalities with faster economic growth; and industrial structure effect is the most important factor that inhibits carbon emissions, followed by energy structure effect. This paper considers the driving factors of both the production side and the residential consumption side from the city level. The research reveals the main driving factors that effect the carbon emissions of megacities in developing countries, and highlights the leading role of megacities in terms of carbon emission reduction in China and even the world. The paper thereby puts forward policy implications for China's economic policies.

Visible-Light-Promoted Diboron-Mediated Transfer Hydrogenation of Azobenzenes to Hydrazobenzenes.

A visible-light-promoted transfer hydrogenation of azobenzenes has been developed. In the presence of B2pin2 and upon visible-light irradiation, the reactions proceeded smoothly in methanol at ambient temperature. The azobenzenes with diverse functional groups have been reduced to the corresponding hydrazobenzenes with a yield of up to 96%. Preliminary mechanistic studies indicated that the hydrogen atom comes from the solvent and the transformation is achieved through a radical pathway.

Melatonin interrupts osteoclast functioning and suppresses tumor-secreted RANKL expression: implications for bone metastases.

Cancer-related bone erosion occurs frequently in bone metastasis and is associated with severe complications such as chronic bone pain, fractures, and lower survival rates. In recognition of the fact that the darkness hormone melatonin is capable of regulating bone homeostasis, we explored its therapeutic potential in bone metastasis. We found that melatonin directly reduces osteoclast differentiation, bone resorption activity and promotes apoptosis of mature osteoclasts. We also observed that melatonin inhibits RANKL production in lung and prostate cancer cells by downregulating the p38 MAPK pathway, which in turn prevents cancer-associated osteoclast differentiation. In lung and prostate bone metastasis models, twice-weekly melatonin treatment markedly reduced tumor volumes and numbers of osteolytic lesions. Melatonin also substantially lowered the numbers of TRAP-positive osteoclasts in tibia bone marrow and RANKL expression in tumor tissue. These findings show promise for melatonin in the treatment of bone metastases.

ATG5 regulates mesenchymal stem cells differentiation and mediates chemosensitivity in acute myeloid leukemia.

Autophagy is related to the development of several tumors including acute myeloid leukemia (AML). Inhibition of autophagy in AML cells can make them more susceptible to chemotherapy. However, the influence of autophagy in mesenchymal stem cells (MSCs) remains inconclusive. In the present study, we demonstrated that the expression of ATG5 and autophagy were elevated in MSCs derived from AML patients (AML-MSCs) compared to healthy donors (HD-MSCs). After inhibiting autophagy by 3-Methyladenine (3 MA) or silencing ATG5, the differentiation potential of AML-MSCs was decreased, the fraction of G0/G1 phase was increased while that of G2 phase was reduced, and the expression of CXCL12 was reduced in AML-MSCs. After co-culture of NB4 and THP1 with MSCs pretreated with 3 MA or ATG5 knockdown respectively, the sensitivity of AML cell lines to daunorubicin and doxorubicin was improved in a dose- and time-dependent manner compared to controls. The increased sensitivity of AML cells to genotoxic agents was related to ERK1/2 and AKT pathway. These results suggested ATG5 mediated potential differentiation capacities and cell cycle distribution of AML-MSCs, and targeting autophagy, especially ATG5 in AML-MSCs could improve the chemosensitivity of AML.

Upregulation of AKR1C1 in mesenchymal stromal cells promotes the survival of acute myeloid leukaemia cells.

The leukaemic bone marrow microenvironment, comprising abnormal mesenchymal stromal cells (MSCs), is responsible for the poor prognosis of acute myeloid leukaemia (AML). Therefore, it is essential to determine the mechanisms underlying the supportive role of MSCs in the survival of leukaemia cells. Through in silico analyses, we identified a total of 271 aberrantly expressed genes in the MSCs derived from acute myeloid leukemia (AML) patients that were associated with adipogenic differentiation, of which aldo-keto reductase 1C1 (AKR1C1) was significantly upregulated in the AML-MSCs. Knockdown of AKR1C1 in the MSCs suppressed adipogenesis and promoted osteogenesis, and inhibited the growth of co-cultured AML cell lines compared to the situation in wild- type AML-derived MSCs. Introduction of recombinant human AKR1C1 in the MSCs partially alleviated the effects of AKR1C1 knockdown. In addition, the absence of AKR1C1 reduced secretion of cytokines such as MCP-1, IL-6 and G-CSF from the MSCs, along with inactivation of STAT3 and ERK1/2 in the co-cultured AML cells. AKR1C1 is an essential factor driving the adipogenic differentiation of leukaemic MSCs and mediates its pro-survival effects on AML cells by promoting cytokine secretion and activating the downstream pathways in the AML cells.

Effects of Epstein-Barr virus infection on liver function in children.

OBJECTIVE: In order to analyze the effect of Epstein-Barr (EB) virus infection on the liver function of children, the age and season of children susceptible to EB virus were analyzed in this study. METHODS: In this study, 118 children with EB infection from Cangzhou Central Hospital were selected as the subjects, and 10 children with normal liver function were selected as the control group. Compared with normal children, the changes of blood cells, immune cells and indicators related to liver function in patients with EB virus infection were compared, and the expression of EB virus -DNA in patients' peripheral blood was analyzed. Immunohistochemistry was used to analyze the location and changes of CD4+T lymphocytes, CD8+T lymphocytes, and granzyme B cells in the liver of the patients. And changes in liver tissue were studied by in situ hybridization. RESULTS: It was found that children in early childhood (1-3 years old) were the most susceptible group, and summer and autumn were the most susceptible seasons. Compared with normal children, the number of red blood cells and white blood cells in patients infected with EB virus increased, while the number of platelets decreased, but the difference was not significant. The liver function indexes of Alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), total bilirubin (TBIL), and lactate dehydrogenase (LDH) increased after infection. The content of CD4+T lymphocytes decreased, while that of CD8+T lymphocytes increased. The level of immune factor IgG increased significantly (P<0.01), granzyme B cells were positive compared to that of normal humans, and positive lymphocytes containing EBER appeared. CONCLUSION: Therefore, EB virus may affect liver function by acting CD8+T lymphocytes in children.

[Bioinformatics Analysis and Verification of Aging-Related Genes of Bone Marrow Mesenchymal Stem Cells in Patients with Acute Myeloid Leukemia].

OBJECTIVE: To screen and verify the differentially expressed genes related with aging of bone marrow mesenchymal stem cells (BM-MSCs) in acute myeloid leukemia (AML) patients by bioinformatics, so as to provide new molecular markers for the research and clinical treatment of AML. METHODS: The gene expression profiling chip related with BM-MSCs in AML patients in our hospital and the gene chip GSE84881 selected from NCBI database GEO were used for data analysis and exploration. The DAVID analysis software was used to perform gene ontology (GO) enrichment analysis and KEGG pathway enrichment analysis. Furthermore, the differentially expressed genes related with aging of BM-MSCs in AML patients were identified. Bone marrow samples were collected and MSCs were amplified in vitro, and RT-PCR was used to verify the differentially expressed genes, which should be further identified with senescence-associated ß-galactosidase staining and MTT cell proliferation assays. RESULTS: A total of 247 differentially expressed genes were screened out by bioinformatics methods, including genes of 132 up-regulated expression and 115 down-regulated expression. Six differentially expressed genes related with aging of BM-MSCs in AML patients were screened out, including the genes of up-regulated expression, COL3A1 (P<0.05), CRYAB (P<0.01), DCN (P<0.05), and the genes of down-regulated expression, including CCL2 (P<0.05), CTSC (P<0.01) and IL6 (P<0.05). These 6 differentially expressed genes were consistent with data from chip assays, and which was significantly correlated with aging of BM-MSCs in AML patients. Meanwhile, the positive rate of senescence-associated ß-galactosidase staining in BM-MSCs of AML patients was significantly different from that of healthy donors (P<0.01). MTT cell proliferation assay showed that BM-MSCs in AML patients had proliferative ability lower than the healthy donors' BM-MSCs. CONCLUSION: The data here suggest novel clues for the clinical research and treatment of BM-MSCs aging in AML patients.

CXCL8 derived from mesenchymal stromal cells supports survival and proliferation of acute myeloid leukemia cells through the PI3K/AKT pathway.

The role of proinflammatory cytokines secreted by the bone marrow mesenchymal stromal cells (BM-MSCs) in the progression of acute myeloid leukemia (AML) is poorly understood. We compared C-X-C motif chemokine ligand (CXCL)8 expression levels in the BM-MSCs of patients with AML and normal control subjects and detected significantly higher levels in the former. Furthermore, CXCL8 was up-regulated in cocultures of BM-MSCs and leukemic cell lines compared with either monoculture. CXCL8 expression was significantly higher in MSCs compared with mononuclear cells in patients with de novo AML. To elucidate the function of paracrine CXCL8 in AML, we blocked CXCL8 binding to the C-X-C motif chemokine receptor (CXCR)2 in the AML cells using SB225002. Inhibition of CXCL8/CXCR2 binding decreased proliferation in the AML cells by inducing cell cycle arrest at the G0/G1 phase and apoptosis via decreased AKT phosphorylation. Blocking the PI3K/AKT signaling pathway by a specific inhibitor induced similar apoptosis induction and lower proliferation, suggesting that the PI3K/AKT signaling pathway was also involved in CXCL8 action. Taken together, our findings demonstrate that BM-MSCs are the main source of CXCL8 in the AML bone marrow microenvironment and promote leukemogenesis via the PI3K/AKT signaling pathway, indicating a novel therapeutic target.-Cheng, J., Li, Y., Liu, S., Jiang, Y., Ma, J., Wan, L., Li, Q., Pang, T. CXCL8 derived from mesenchymal stromal cells supports survival and proliferation of acute myeloid leukemia cells through the PI3K/AKT pathway.

CXCL8 is associated with the recurrence of patients with acute myeloid leukemia and cell proliferation in leukemia cell lines.

Acute myeloid leukemia (AML) blasts release a wide range of chemokines in which CXCL8 has recently been recognized to be important for tumor progression. To find out the function of CXCL8 in AML, we compared blood serum of AML patients and healthy donors and found that the average level of CXCL8 was higher in AML patients. Among patients, higher expression of CXCL8 was also a positive recurrence indicator which illustrated the critical role of CXCL8 in AML. Knocking down of CXCL8 in leukemic cell lines led to significant reduction of proliferation via inducing G0/G1 cell cycle arrest and apoptosis, which was accompanied by the inactivation of ERK1/2. Furthermore, inhibition of ERK1/2 by specific chemical inhibitors reconstructed the CXCL8 knocking down phenomenon. Overall, we demonstrated that expression level of CXCL8 had a positive relationship with recurrence probability in AML. And CXCL8 was strongly implicated in AML cells growth by activating the ERK1/2 signal pathway.