Qiao X

References (5)

Title : SNHG20\/miR-140-5p\/NDRG3 axis contributes to 5-fluorouracil resistance in gastric cancer - Yu_2019_Oncol.Lett_18_1337
Author(s) : Yu J , Shen J , Qiao X , Cao L , Yang Z , Ye H , Xi C , Zhou Q , Wang P , Gong Z
Ref : Oncol Lett , 18 :1337 , 2019
Abstract : 5-fluorouracil (5-FU)-based chemotherapy is the first line treatment for advanced gastric cancer. However, the effectiveness of 5-FU is limited by drug resistance. The N-myc downstream-regulated gene, family member 3 (NDRG3) is a member of the NDRG family and has been implicated in numerous types of cancer. However, the role of NDRG3 in gastric cancer remains unclear. In the present study, NDRG3 mRNA expression in gastric cancer and adjacent normal tissues was analyzed using the Gene Expression Profiling Interactive Analysis web tool. NDRG3 expression was silenced using short hairpin RNAs to examine the effect of NDRG3 on the growth of gastric cancer cells. Potential regulators of NDRG3 were identified using the TargetScan and MicroRNA tools and verified by a luciferase assay and reverse transcription-quantitative PCR analysis. The current study demonstrated that NDRG3 was upregulated in gastric cancer specimens and promoted cell proliferation in gastric cancer cell lines. Furthermore, the present study revealed that the small nucleolar RNA host gene 20 (SNHG20)/microRNA (miR)-140-5p signaling pathway may regulate the expression of NDRG3. SNHG20 was revealed to be involved in mediating resistance to 5-FU in gastric cancer cell lines via NDRG3. In conclusion, the results of the present study suggest that the SNHG20/miR-140-5p/NDRG3 axis may be involved in mediating resistance to 5-FU in gastric cancer.
ESTHER : Yu_2019_Oncol.Lett_18_1337
PubMedSearch : Yu_2019_Oncol.Lett_18_1337
PubMedID: 31423195
Gene_locus related to this paper: human-NDRG3

Title : Long noncoding RNA ABHD11-AS1 predicts the prognosis of pancreatic cancer patients and serves as a promoter by activating the PI3K-AKT pathway - Qiao_2018_Eur.Rev.Med.Pharmacol.Sci_22_8630
Author(s) : Qiao X , Lv SX , Qiao Y , Li QP , Ye B , Wang CC , Miao L
Ref : Eur Rev Med Pharmacol Sci , 22 :8630 , 2018
Abstract : OBJECTIVE: Accumulating evidence showed aberrant expressions of long non-coding RNAs (lncRNAs) strongly correlated to the development of cancers, including pancreatic cancer (PC). Whether lncRNA ABHD11-AS1 (ABHD11-AS1) is involved in PC remains to be elucidated. Thus, we aimed to evaluate the effects of ABHD11-AS1 on PC and the underlying molecular mechanism. PATIENTS AND METHODS: RT-PCR was used to detect the expression level of ABHD11-AS1 in both PC tissue and cell lines. Then, the correlation of ABHD11-AS1 expression with clinicopathological features and prognosis was studied. Cell proliferation, apoptosis, migration and invasion abilities were detected by MTT, flow cytometry, and transwell assays. We further investigated the effect of abnormal ABHD11-AS1 expression through the PI3K/AKT and EMT pathway by Western blot assays in treated PC cells. RESULTS: We found that the expression of ABHD11-AS1 was significantly increased in both PC tissues and cell lines. The clinical analysis revealed that a high level of ABHD11-AS1 expression was correlated with distant metastasis, TNM stage, and tumor differentiation. The Kaplan-Meier analysis showed that high ABHD11-AS1 expression levels predicted poorer survival. Moreover, univariate and multivariate analyses confirmed that the expression of ABHD11-AS1 was an independent and significant factor associated with poor overall survival rates. Loss-of-function experiments showed that the knockdown of ABHD11-AS1 suppressed PC cell proliferation, migration, invasion, and EMT in vitro. Mechanistically, the knockdown of ABHD11-AS1 decreased phospho(p) AKT and phospho(p) PI3K expression, but did not affect the AKT and PI3K expression in PC cells CONCLUSIONS: This study suggested that ABHD11-AS1 may potentially function as a valuable prognostic biomarker and a therapeutic target for PC patients.
ESTHER : Qiao_2018_Eur.Rev.Med.Pharmacol.Sci_22_8630
PubMedSearch : Qiao_2018_Eur.Rev.Med.Pharmacol.Sci_22_8630
PubMedID: 30575903
Gene_locus related to this paper: human-ABHD11

Title : Gene expression profiling in a mouse model of infantile neuronal ceroid lipofuscinosis reveals upregulation of immediate early genes and mediators of the inflammatory response - Qiao_2007_BMC.Neurosci_8_95
Author(s) : Qiao X , Lu JY , Hofmann SL
Ref : BMC Neurosci , 8 :95 , 2007
Abstract : BACKGROUND: The infantile form of neuronal ceroid lipofuscinosis (also known as infantile Batten disease) is caused by hereditary deficiency of a lysosomal enzyme, palmitoyl-protein thioesterase-1 (PPT1), and is characterized by severe cortical degeneration with blindness and cognitive and motor dysfunction. The PPT1-deficient knockout mouse recapitulates the key features of the disorder, including seizures and death by 7-9 months of age. In the current study, we compared gene expression profiles of whole brain from PPT1 knockout and normal mice at 3, 5 and 8 months of age to identify temporal changes in molecular pathways implicated in disease pathogenesis.
RESULTS: A total of 267 genes were significantly (approximately 2-fold) up- or downregulated over the course of the disease. Immediate early genes (Arc, Cyr61, c-fos, jun-b, btg2, NR4A1) were among the first genes upregulated during the presymptomatic period whereas immune response genes dominated at later time points. Chemokine ligands and protease inhibitors were among the most transcriptionally responsive genes. Neuronal survival factors (IGF-1 and CNTF) and a negative regulator of neuronal apoptosis (DAP kinase-1) were upregulated late in the course of the disease. Few genes were downregulated; these included the alpha2 subunit of the GABA-A receptor, a component of cortical and hippocampal neurons, and Hes5, a transcription factor important in neuronal differentiation. CONCLUSION: A molecular description of gene expression changes occurring in the brain throughout the course of neuronal ceroid lipofuscinosis suggests distinct phases of disease progression, provides clues to potential markers of disease activity, and points to new targets for therapy.
ESTHER : Qiao_2007_BMC.Neurosci_8_95
PubMedSearch : Qiao_2007_BMC.Neurosci_8_95
PubMedID: 18021406
Gene_locus related to this paper: mouse-ppt

Title : Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 plays a critical role in the lipolytic processing of chylomicrons - Beigneux_2007_Cell.Metab_5_279
Author(s) : Beigneux AP , Davies BS , Gin P , Weinstein MM , Farber E , Qiao X , Peale F , Bunting S , Walzem RL , Wong JS , Blaner WS , Ding ZM , Melford K , Wongsiriroj N , Shu X , de Sauvage F , Ryan RO , Fong LG , Bensadoun A , Young SG
Ref : Cell Metab , 5 :279 , 2007
Abstract : The triglycerides in chylomicrons are hydrolyzed by lipoprotein lipase (LpL) along the luminal surface of the capillaries. However, the endothelial cell molecule that facilitates chylomicron processing by LpL has not yet been defined. Here, we show that glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) plays a critical role in the lipolytic processing of chylomicrons. Gpihbp1-deficient mice exhibit a striking accumulation of chylomicrons in the plasma, even on a low-fat diet, resulting in milky plasma and plasma triglyceride levels as high as 5000 mg/dl. Normally, Gpihbp1 is expressed highly in heart and adipose tissue, the same tissues that express high levels of LpL. In these tissues, GPIHBP1 is located on the luminal face of the capillary endothelium. Expression of GPIHBP1 in cultured cells confers the ability to bind both LpL and chylomicrons. These studies strongly suggest that GPIHBP1 is an important platform for the LpL-mediated processing of chylomicrons in capillaries.
ESTHER : Beigneux_2007_Cell.Metab_5_279
PubMedSearch : Beigneux_2007_Cell.Metab_5_279
PubMedID: 17403372

Title : Resistance mechanisms and associated mutations in acetylcholinesteras genes in Sitobion avenae (Fabricius) - Chen_2007_Pestic.Biochem.Physiol_87_189
Author(s) : Chen M , Han Z , Qiao X , Qu M
Ref : Pesticide Biochemistry and Physiology , 87 :189 , 2007
Abstract : Wheat aphid, Sitobion avenae (fabricius), is one of the most important wheat pests and has been reported to be resistant to commonly used insecticides in China. To determine the resistance mechanism, the resistant and susceptible strains were developed in laboratory and comparably studied. A bioassay revealed that the resistant strain showed high resistance to pirimicarb (RR: 161.8), moderate reistance to omethoate (32.5) and monocrotophos (33.5), and low resistance to deltamethrin (6.3) and thiodicarb (5.5). A biochemistry analysis showed that both strains had similar glutathione-S-transferase (GST) activity, but the resistant strain had 3.8-fold higher esterase activity, and its AChE was insensitive to this treatment. The I50 increased by 25.8-, 10.7-, and 10.4-folds for pirimicarb, omethoate, and monocrotophos, respectively, demonstrating that GST had not been involved in the resistance of S. avenae. The enhanced esterase contributed to low level resistance to all the insecticides tested, whereas higher resistance to pirimicarb, omethoate, and monocrotophos mainly depended on AChE insensitivity. However, the AChE of the resistant strain was still sensitive to thiodicarb (1.7-fold). Thus, thiodicarb could be used as substitute for control of the resistant S. avenae in this case. Furthermore, the two different AChE genes cloned from different resistant and susceptible individuals were also compared. Two mutations, L436(336)S in Sa.Ace1 and W516(435)R in Sa.Ace2, were found consistently associated with the insensitivity of AChE. They were thought to be the possible resistance mutations, but further work is needed to confirm this hypothesis.
ESTHER : Chen_2007_Pestic.Biochem.Physiol_87_189
PubMedSearch : Chen_2007_Pestic.Biochem.Physiol_87_189
PubMedID:
Gene_locus related to this paper: sitav-ACHE1 , sitav-ACHE2