Jie Xiao

Third Xiangya Hospital

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Di Wu

Beijing Xuanwu Traditional Chinese Medicine Hospital

Huanmiao Liu

Third Xiangya Hospital

Jie Peng

Chinese Academy of Medical Sciences & Peking Union Medical College

Xiaoping Ji

Qilu Hospital of Shandong University

Yan Jia

Tongji University

Jianxin Jiang

Daping Hospital

Yilin Huang

Xiangya Hospital Central South University

Chao Yu

Affiliated Hospital of Guizhou Medical University

Feng Peng

First Affiliated Hospital of Fujian Medical University

Junjie Ding

University of Oxford

Cooperative Institutions

Central South University

Sun Yat-sen University

Third Xiangya Hospital

Chinese Academy of Medical Sciences & Peking Union Medical College

Fudan University

Qilu Hospital of Shandong University

The First Affiliated Hospital, Sun Yat-sen University

Shandong University

Huazhong University of Science and Technology

Chinese Academy of Sciences

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Bioengineered Magnetoferritin Nanoprobes for Single-Dose Nuclear-Magnetic Resonance Tumor Imaging

ACS Nano (2016)

Yanzhao Zhao Minmin Liang Xiao Li Kelong Fan Jie Xiao

Despite all the advances in multimodal imaging, it remains a significant challenge to acquire both magnetic resonance and nuclear imaging in a single dose because of the enormous difference in sensitivity. Indeed, nuclear imaging is almost 106-fold more sensitive than magnetic resonance imaging (MRI); thus, repeated injections are generally required to obtain sufficient MR signals after nuclear imaging. Here, we show that strategically engineered magnetoferritin nanoprobes can image tumors with high sensitivity and specificity using SPECT and MRI in living mice after a single intravenous injection. The magnetoferritin nanoprobes composed of 125I radionuclide-conjugated human H-ferritin iron nanocages (125I-M-HFn) internalize robustly into cancer cells via a novel tumor-specific HFn-TfR1 pathway. In particular, the endocytic recycling characteristic of TfR1 transporters solves the nuclear signal blocking issue caused by the high dose nanoprobes injected for MRI, thus enabling simultaneous functional and morphological tumor imaging without reliance on multi-injections.

Nanocages

10.1021/acsnano.5b07408

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Citations (92)

Therapeutic influence on circulating and monocyte-derived dendritic cells in laryngeal squamous cell carcinoma patients

Acta Oto-Laryngologica (2008)

Jie Xiao Xin Pan Zheng Lv Feng Lei Xu Da Yu Liu

Surgical resection of laryngeal squamous cell carcinoma (LSCC) could be associated with improved circulating myeloid dendritic cell (mDC) number and monocyte-derived dentritic cell (MoDC) function. Although adjunctive radiotherapy after surgery did not effect the normalization of mDC number, it may have an impact on MoDC function.To investigate the effects of surgery and adjunctive radiotherapy on both circulating dendritic cells (DCs) and MoDCs of LSCC patients.Forty-six patients with LSCC and 15 age-matched healthy control subjects were enrolled in this study. Blood samples were taken before, during, and after conventional treatment from both patients who underwent surgery only (n=18) and those who had adjunctive radiotherapy after tumor removal (n=28). Three-color flow cytometry was used for determination of circulating DC subsets. Moreover, MoDCs were generated utilizing granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), then the phenotype of MoDCs was measured by flow cytometry and the ability to stimulate autologous T cells was tested in a mixed leukocyte reaction (MLR).The preoperative mDC counts, MoDC surface molecular expression and stimulatory capacity were impaired in patients in comparison with controls. The number of mDCs and the expression of CD80, CD83, and HLA-DR on MoDCs were significantly increased as compared with those pretreatment in patients who underwent surgery only and in those who had surgery followed by adjunctive radiotherapy. However, the recovery of CD86 expression and allostimulatory activity was only observed in patients who underwent surgery alone.

CD80

CD86

Adjunctive treatment

Monocyte

10.1080/00016480802020459

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miR-7a/b attenuates post-myocardial infarction remodeling and protects H9c2 cardiomyoblast against hypoxia-induced apoptosis involving Sp1 and PARP-1

Scientific Reports (2016)

Rui Li Hai-Hua Geng Jie Xiao Xiaoteng Qin Fu Wang

Abstract miRs (microRNAs, miRNAs) intricately regulate physiological and pathological processes. Although miR-7a/b protects against cardiomyocyte injury in ischemia/reperfusion injury, the function of miR-7a/b in myocardial infarction (MI)-induced cardiac remodeling remains unclear. Here, we sought to investigate the function of miR-7a/b in post-MI remodeling in a mouse model and to determine the underlying mechanisms involved. miR-7a/b overexpression improved cardiac function, attenuated cardiac remodeling and reduced fibrosis and apoptosis, whereas miR-7a/b silencing caused the opposite effects. Furthermore, miR-7a/b overexpression suppressed specific protein 1 (Sp1) and poly (ADP-ribose) polymerase (PARP-1) expression both in vivo and in vitro and a luciferase reporter activity assay showed that miR-7a/b could directly bind to Sp1. Mithramycin, an inhibitor of the DNA binding activity of Sp1, effectively repressed PARP-1 and caspase-3, whereas knocking down miR-7a/b partially counteracted these beneficial effects. Additionally, an immunoprecipitation assay indicated that hypoxia triggered activation of the binding activity of Sp1 to the promoters of PARP-1 and caspase-3, which is abrogated by miR-7a/b. In summary, these findings identified miR-7a/b as protectors of cardiac remodeling and hypoxia-induced injury in H9c2 cardiomyoblasts involving Sp1 and PARP-1.

Hypoxia

10.1038/srep29082

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Citations (69)

Silencing the Girdin gene enhances radio-sensitivity of hepatocellular carcinoma via suppression of glycolytic metabolism

Journal of Experimental & Clinical Cancer Research (2017)

Yu Li Yifan Sun Jingjing Li Yan Wang Yuxing Zhu

Radiotherapy has been used increasingly to treat primary hepatocellular carcinoma. Clinically, the main cause of radiotherapy failure is cellular radioresistance, conferred via glycolytic metabolism. Our previous study demonstrated that Girdin is upregulated in primary hepatocellular carcinoma and promotes the invasion and metastasis of tumor cells. However, whether Girdin underlies the radio-sensitivity of hepatocellular carcinoma remains unclear. A short hairpin RNA (shRNA) was used to silence CCDC88A (encoding Girdin), and real-time PCR was performed to determine CCDC88A mRNA expression. Then, cell proliferation, colony formation, flow cytometric, scratch, and transwell assays were to examine the influence of Girdin silencing on cellular radiosensitivity. Glycolysis assays were conducted to exam cell glycolysis process. Western blotting was performed to explore the signaling pathway downstream of Girdin. Finally, animal experiments were performed to demonstrate the effect of CCDC88A silencing on the radiosensitivity of hepatoma in vivo. shRNA-induced Girdin silencing suppressed glycolysis and enhanced the radio-sensitivity of hepatic cell lines, HepG2 and Huh-7. Furthermore, silencing of Girdin inhibited the PI3K/AKT/HIF-1α signaling pathway, which is a central regulator of glycolysis. Girdin can regulate glycolysis in hepatocellular carcinoma cells through the PI3K/AKT/HIF-1α signaling pathway, which decreases the sensitivity of tumor cells to radiotherapy.

Radiosensitivity

10.1186/s13046-017-0580-7

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Characterization of miR-218/322-Stxbp1 pathway in the process of insulin secretion

Journal of Molecular Endocrinology (2014)

Hongmei Lang Zhihua Ai Zhiqing You Yong Wan Wei Guo

MicroRNAs (miRNAs) have been implicated in a variety of physiological processes, however, the function of miRNAs in insulin secretion and type 2 diabetes is still unclear. Stxbp1 plays an essential role in exocytosis, and is crucial for insulin secretion. In this study, we focused on the molecular mechanism of Stxbp1 in insulin secretion by identifying its upstream regulators: miR-218 and miR-322. The expression of Stxbp1 was significantly increased in isolated mouse islets exposed to high levels of glucose within 1 h; while two of its predicted upstream miRNAs were found to be downregulated. Further study found that miR-218 and miR-322 directly interact with Stxbp1 by targeting the 3'UTR of its mRNA. MIN6 cells overexpressing the two miRNAs showed a sharp decline in insulin secretion and a decreased sensitivity to glucose; while the inhibition of the two miRNAs promoted insulin secretion. However, islets treated with prolonged high levels of glucose, which is known as glucolipotoxicity, displayed relatively high expression of miR-218 and miR-322, and a reduced level of expression of Stxbp1 accompanied by the blocking of insulin secretion. In summary, this study identified a pathway consisting of miR-218/322 and Stxbp1 in insulin secretion, contributing to a network of β-cell function involving miRNA.

10.1530/jme-14-0305

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Citations (16)

Predictors of mortality in acute pancreatitis complicated with multidrug-resistant Klebsiella pneumoniae infection

BMC Infectious Diseases (2021)

Di Wu Junjie Ding Yan Jia Huanmiao Liu Jie Xiao

Abstract Background Multidrug-resistant (MDR) Klebsiella pneumoniae infections, from pancreatic infections to bloodstream infections, influence the mortality of patients with acute pancreatitis (AP) on the condition of limited antibiotic choices. The aim of this study was to investigate the predictor of mortality among AP patients complicated with MDR- K. pneumoniae infections. Methods Seventy-one AP patients who occurred MDR- K. pneumoniae infections from August 1st, 2016 to August 1st, 2020 were enrolled. MDR- K. pneumoniae was defined as the K. pneumoniae strain non-susceptible to at least one agent in three or more antimicrobial categories. MDR- K. pneumoniae isolates were confirmed by Vitek-2 system. Antibiotic susceptibility test was carried out using a micro broth dilution method. Clinical characteristics and drug-resistance rates were retrospectively reviewed, and the predictors of mortality were evaluated by univariate and multivariate analyses. Results The mortality rate of AP patients complicated with MDR- K. pneumoniae infections reached 46.5% (33 of 71), and pancreas (n = 53) was the most common site of MDR- K pneumoniae strains. The drug resistance rates of MDR- K. pneumoniae were high to 11 of 12 common antibiotics (more than 50.0%) except of tigecycline (23.9%). The predictor independently associated with mortality was septic shock (hazard ratio 2.959, 95% confidence intervals 1.396 – 6.272, P = 0.005). Conclusions More attention should be paid for pancreatic MDR- K. pneumoniae infections among AP patients The predictor for mortality of AP patients complicated with MDR- K. pneumoniae infection is septic shock. Therefore, further clinical investigations should focus on areas against septic shock.

Tigecycline

10.1186/s12879-021-06709-0

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Parecoxib inhibits glioblastoma cell proliferation, migration and invasion by up-regulating miRNA-29c

Biology Open (2016)

Lin-Yong Li Jie Xiao Qiang Liu Kun Xia

Glioblastoma (GBM) is one of the most lethal brain cancers worldwide, and there is an urgent need for development of novel therapeutic approaches. Parecoxib is a well-known cyclooxygenase-2 (COX-2) inhibitor, had already been developed for postoperative analgesia with high efficience and low adverse reaction. Recent study suggested that parecoxib potently enhances immunotherapeutic efficacy of GBM, but its effects on GBM growth, migration and invasion had never been studied before. In the present study, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and, BrdU (5-Bromo-2-deoxyUridine) incorporation assays were used to evaluate the cell proliferation of GBM cells. Wound-healing and Transwell assays were preformed to analyze GBM cell migration and invasion, respectively. The results suggested that parecoxib inhibits cell proliferation, migration and invasion of GBM cells in a dose-dependent manner. RT-qPCR (Quantitative Real-time PCR) analysis demonstrated that miRNA-29c can be significantly induced by parecoxib. Furthermore, our data suggested that miRNA-29c inhibitor can significantly attenuate parecoxib's effect on proliferation, migration and invasion of GBM. In conclusion, the present study suggested that parecoxib inhibits GBM cell proliferation, migration and invasion by up-regulating miRNA-29c.

Parecoxib

10.1242/bio.021410

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Citations (19)

Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

Cancer Medicine (2018)

Tao Cai Yu Liu Jie Xiao

Glioblastoma (GBM) is the most common and lethal tumor of the central nervous system with highly infiltrative and resistant to chemotherapy. Temozolomide (TMZ) is widely used as the first-line treatment for the therapy of GBM. However, a considerable percentage inherent or acquired resistance in GBM accounts for many treatment failures of the TMZ chemotherapy. Therefore, a deeper understanding of the molecular characteristics underlying TMZ resistance and the identification of novel therapeutic target is urgent. Here, we show that MALAT1 was significantly upregulated in TMZ-resistant GBM cells. On the other hand, MALAT1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis. We also show that miR-101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT1. Importantly, we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR-101 signaling pathway via directly binding it in GBM cells. In conclusion, our study indicates that knockdown of MALAT1 reverses chemoresistance to TMZ via promoting miR-101 regulatory network in GBM and thus offers a novel prognostic marker and potential target for GBM TMZ-based chemotherapy.

Temozolomide

10.1002/cam4.1384

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Citations (90)

The Effect of siRNA Down-Regulating XIAP On the Apoptosis and Chemo-Sensitivity of K562 Cells in Vitro.

Blood (2009)

Shuangfeng Xie Songmei Yin Dan Li Danian Nie Yiqing Li

XIAP

K562 cells

Inhibitor of apoptosis

10.1182/blood.v114.22.5053.5053

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Citations (2)

Recombinant adenovirus-p53 combined with chemotherapy in treatment of locally advanced cervical cancer (a phase II study).

Journal of Clinical Oncology (2013)

Jian Zhou Fumin Liu Jie Xiao

5525 Background: To evaluate the efficacy and safety of recombinant adenovirus-p53 (rAd-p53) combined with chemotherapy in treatment of locally advanced cervical cancer. Methods: Forty patients with stage IIb2 IV locally advanced cervical cancer were randomly divided into 2 groups: 20 patients receiving gene plus chemotherapy (PCG) and 20 receiving sole chemotherapy (CG). The patients in PCG were given one course of PVB (cisplatin + vincristine + pingyangmycin) and 5 times intratumoral injections of rAd-p53 at a dose of 2 x 10 12 viral particles once per 3 days. The CG patients received a sole course of PVB. The study patients were followed up for at least one year. The VEGF, p53, Bax, and p21 protein expression in pre- and post-treatment tumor tissues were examined by immunohistochemistry. Results: The response was evaluated at 3 months after treatments. The response rates (CR + PR) were 95% and 75% for the PCG and CG patients, respectively. P53 proteins were strongly expressed in the tumor tissues from both groups. There were no significant changes in expression level of the p53 protein in the tumor tissue from pre- and post-treatment. However, the VEGF, Bax, and p21 protein expressions significantly increased in PCG after treatment. The overall one-year survive rates were 90% and 65%, respectively. A mild to medium grade of fever was found in 90% of the PCG patients. No serious of adverse events relative to rAd-p53 were observed. Conclusions: Combined the rAd-p53 gene with chemotherapy is an effective treatment for the patients with advanced cervical cancer. The rAd-p53 gene therapy is a safe treatment.

Pingyangmycin

10.1200/jco.2013.31.15_suppl.5525

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Citations (5)