Biomedical subjects

Qiong Zhou

Publications and source records attributed to Qiong Zhou.

At least 19 recordsLinked to original sources

PubMed2006

Apigenin inhibits tumor angiogenesis through decreasing HIF-1alpha and VEGF expression.

Apigenin is a non-toxic dietary flavonoid with anti-tumor properties. We recently showed that apigenin-inhibited hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) expression in human ovarian cancer cells under normoxic condition. However, the effect of apigenin in angiogenesis remains to be elucidated. Angiogenesis is the formation of new blood vessels and is required for tumor growth and metastasis. In this study, we showed that apigenin-inhibited expression of HIF-1 and VEGF in different cancer cells under both normoxic and hypoxic conditions. We demonstrated that apigenin significantly inhibited tumor angiogenesis in vivo, by using both the chicken chorioallantoic membrane and Matrigel plug assays. The inhibition of tumor angiogenesis was associated with the decrease of HIF-1 and VEGF in tumor tissues. Taken together, our results show that apigenin suppresses tumor angiogenesis through HIF-1 and VEGF expression.

Animals↗

PubMed2006

Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells.

Insulin-like growth factor 1 receptor (IGF-1R) activation is required for prostate cell proliferation. Prostate cancer is one of the most commonly diagnosed malignant tumors in Western countries. Overexpression of IGF-1R in prostate cancer is associated with tumor growth. These suggest that IGF-1R inhibitory agents may be of preventive and/or therapeutic value. With evidence accumulating for a chemopreventive role of flavonoids, the effects of luteolin, a bioactive flavonoid, on IGF-1R signaling in prostate cancer cells were examined. Luteolin inhibited insulin-like growth factor 1 (IGF-1) induced activation of IGF-1R and AKT in prostate cancer PC-3 and DU145 cells. Inhibition of AKT by luteolin resulted in decreased phosphorylation of its downstream targets, including p70S6K1, GSK-3beta and FKHR/FKHRL1. Luteolin also inhibited the IGF-1-induced activation of EGFR and MAPK/ERK signaling. Luteolin inhibited expression of cyclin D1 and increased expression of p21. As a result, luteolin suppressed proliferation and induced apoptosis of prostate cancer cells. Knockdown of IGF-1R by siRNA led to inhibition of proliferation of prostate cancer cells. Results of in vivo tumor growth assay indicated that luteolin inhibited PC-3 tumor growth. Immunoblotting of the extracts of tumor tissues showed that luteolin inhibited IGF-1R/AKT signaling. Our results provide a new insight into the mechanisms that luteolin is against cancer cells.

Animals↗

PubMed2006

Transactivation of epidermal growth factor receptor by insulin-like growth factor 1 requires basal hydrogen peroxide.

Insulin-like growth factor (IGF-1) plays an important role in prostate cancer development. Recent studies suggest that IGF-1 has mitogenic action through epidermal growth factor receptor (EGFR). However, the mechanism remains largely unknown. Here, we demonstrated in prostate cancer DU145 cells that IGF-1 induced EGFR transactivation, leading to ERK activation. Matrix metalloproteinase-mediated shedding of heparin-binding EGF is involved in this process. Antioxidants and catalase inhibited IGF-1-stimulated EGFR phosphorylation, indicating that H(2)O(2) is required for EGFR activation. However, exogenous H(2)O(2) did not activate EGFR or IGF-1R in DU145 cells. IGF-1 did not induced production of H(2)O(2) in DU145 cells. Our results suggest that transactivation of EGFR by IGF-1 requires basal intracellular H(2)O(2) in DU145 cells.

Cell Line, Tumor↗

PubMed2006

Reactive oxygen species regulate epidermal growth factor-induced vascular endothelial growth factor and hypoxia-inducible factor-1alpha expression through activation of AKT and P70S6K1 in human ovarian cancer cells.

The epidermal growth factor (EGF) and EGF receptor (EGFR) family are often overexpressed in various human cancers including ovarian cancer. While it is generally believed that reactive oxygen species (ROS) are involved in the intracellular signaling events, the role of ROS in EGF-induced angiogenesis and carcinogenesis remains to be elucidated. The present study investigated the role of ROS in the regulation of AKT, p70S6K1, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor 1 (HIF-1) in ovarian cancer cells. In this study, OVCAR-3 cells were treated with EGF and catalase, an H2O2 scavenger. EGF treatment increases H2O2 production, leading to activation of the AKT/p70S6K1 pathway, resulting in increased VEGF expression at the transcriptional level. The inhibition of H(2)O(2) production by catalase abolished EGF-induced AKT and p70S6K1 activation, and VEGF expression through HIF-1alpha expression. Forced expression of p70S6K1 and HIF-1alpha reversed catalase- and rapamycin-inhibited VEGF transcriptional activation. We also showed that rapamycin, p70S6K1 inhibitor and catalase overexpression inhibited tumor angiogenesis. This study demonstrates a novel mechanism of EGF-induced VEGF and HIF-1alpha expression through production of H2O2 and activation of AKT and p70S6K1 in human ovarian cancer cells. This study also indicates that p70S6K1 and H2O2 are important in tumor angiogenesis. The results of the study could have an important implication in ovarian cancer therapy.

Animals↗

PubMed2006

Reactive oxygen species regulate insulin-induced VEGF and HIF-1alpha expression through the activation of p70S6K1 in human prostate cancer cells.

Vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1 (HIF-1) are important regulators of angiogenesis. HIF-1 is composed of HIF-1alpha and HIF-1beta subunits, and regulates VEGF expression at transcriptional level. In this study, we demonstrated that insulin induced H2O2 production and p70S6K1 activation in PC-3 prostate cancer cells. The inhibition of H2O2 production by catalase abolished insulin-induced p70S6K1 activation. H2O2 production is also required for insulin-induced VEGF and HIF-1alpha expression in the cells. Over-expression of p70S6K1 or HIF-1alpha reversed catalase- and rapamycin-inhibited VEGF transcriptional activation. These results suggest that insulin induced HIF-1alpha and VEGF expression through H2O2 production and p70S6K1 activation in prostate cancer cells. In addition, we found that inhibition of p70S6K1 by rapamycin decreased prostate tumor angiogenesis, suggesting that p70S6K1 plays an important role in tumor angiogenesis. These results provide some useful information for prostate cancer therapy in the future.

Animals↗

PubMed2006

[Detection of expression of p53, p16, and cyclooxygenase 2 in pancreatic cancer by tissue microarray and correlation among these three genes].

OBJECTIVE: To detect the expression of tumor suppressor protein p53, cyclin-dependent kinase inhibitor p16, and cyclooxygenase 2 (COX-2) in pancreatic cancer by tissue microarray and investigate the correlation among these three genes. METHODS: 104 specimens of tissues, including pancreatic cancer tissue, non-cancer tissues not more than 1.5 cm from the cancer, and normal tissues, underwent microarray examination and immunohistochemistry to detect the expression of p53, p16, and COX-2. The correlation among these 3 genes was analyzed. RESULTS: p53, p16, and COX-2 were all significantly highly expressed in the cancerous tissues in comparison with other tissues. P53 and p16 were both significantly correlated with COX-2 (both P < 0.05), however, there was not a correlation between p53 and p16 (P > 0.05). There was a reciprocal relationship between p53 and COX-2 (P < 0.05, OR = 19.686) influencing the pathogenesis of pancreatic cancer. CONCLUSION: Tissue microarray technique is effective method to detect multiple gene protein expression. Pathogenesis of pancreatic cancer is associated with p53, p16, and COX-2.

Adolescent↗

PubMed2006

Expression of p53, p16 and COX-2 in pancreatic cancer with tissue microarray.

BACKGROUND: Pancreatic cancer development and progression is driven by the accumulation of genetic changes. In this study we constructed tissue microarray containing specimens from pancreatic cancer, adjacent non-cancer tissue and normal tissue to survey the expression of p53, p16 and cyclooxygenase-2 (COX-2). METHODS: Tissue microarray containing 337 specimens from different stages of pancreatic cancer, adjacent non-cancer tissue and normal tissues was constructed, and the expression of p53, p16 and COX-2 was assayed by immunohistochemistry to consecutive formalin-fixed tissue microarray sections. RESULTS: The expression of p53, p16 and COX-2 was significantly higher in tumorous tissues than in non-tumorous ones. A significant relationship was observed between p53 and COX-2, or p16 and COX-2. But no obvious correlation was seen between p53 and p16 expressions. Logistic regression analysis showed p53 and COX-2 as dependent predictors in pancreatic carcinogenesis, and a reciprocal relationship to neoplastic progression between p53 and COX-2. CONCLUSION: Combination analysis of p53 and COX-2 may be useful in predicting pancreatic carcinogenesis.

Adolescent↗

PubMed2006

[Expression of tissue microarray p53, p16 and cyclooxygenase-2 in gastric cancer].

OBJECTIVE: To constructed tissue microarray containing specimens from gastric cancer and adjacent non-cancer tissue to survey the expression of p53, p16 and cyclooxygenase-2 (COX-2), and to obtain a comprehensive survey on the expression of three proteins in gastric cancer progression and their clinical significance. METHODS: We constructed a tissue microarray containing 50 specimens from gastric cancer and 78 specimens from adjacent non-cancer tissue, and assayed three different proteins (p53, p16 and COX-2) by immunohistochemistry to consecutive formalin-fixed tissue microarray sections. RESULTS: In non-cancer tissue, p53, p16 and COX-2 positive staining were 19%, 15% and 74% respectively. In gastric cancer tissue, p53, p16 and COX-2 positive staining were 50%, 54% and 94% respectively. There were a significant difference between two different tissues (P < 0.05). 52% (66/128) cases were COX-2+/p53-, only 1 case were COX-2-/p53+. There was a significant association between COX-2 and p53 (P < 0.05). COX-2 negative expression tissues were found significantly more often in p53-negative than in p53-positive cases. 52% (67/128) cases were COX-2+/p16-, only 1 case were COX-2-/p16+. A significant correlation was recognized between expression of COX-2 and p16 (P < 0.05). Logistic regression analysis revealed that the risk factors of tumorous histotype were p53, p16 and COX-2 positive expression together, determined by Wald chi2 test (P < 0.05; odds ratio, 18.889). There was reciprocal relationship among p53, p16 and COX-2. CONCLUSION: Combination analysis of p53, p16 and COX-2 may be useful for the prediction of gastric carcinogenesis.

Adult↗

PubMed2005

Apigenin inhibits expression of vascular endothelial growth factor and angiogenesis in human lung cancer cells: implication of chemoprevention of lung cancer.

Apigenin is a natural dietary flavonoid. It has recently been shown to have anticancer effects on prostate and ovarian cancer cells. However, the molecular basis of the effect of apigenin on cancer cells remains to be elucidated. In this study, we found that apigenin inhibited A549 lung cancer cell proliferation and vascular endothelial growth factor (VEGF) transcriptional activation in a dose-dependent manner. In an attempt to understand the mechanism of apigenin-inhibited VEGF expression, we found that apigenin inhibited VEGF transcriptional activation through the hypoxia-inducible factor 1 (HIF-1) binding site and specifically decreased HIF-1alpha but not HIF-1beta subunit expression in the cells. In our efforts to understand the signaling pathway that mediates VEGF transcriptional activation, we found that apigenin inhibited AKT and p70S6K1 activation. When testing the effect of apigenin in vivo, we found that apigenin significantly inhibited tumor growth in nude mice. Apigenin inhibited HIF-1alpha and VEGF expression in the tumor tissues, suggesting an inhibitory effect of apigenin on angiogenesis. To confirm this, we showed that apigenin inhibited angiogenesis in nude mice using the Matrigel assay. HIF-1alpha and VEGF are well known inducers of angiogenesis. Our data suggested that apigenin may inhibit human lung cancer angiogenesis by inhibiting HIF-1alpha and VEGF expression, thus providing a novel explanation for the anticancer action of apigenin.

Animals↗

PubMed2005

[Effect of antisense RNA targeting Polo-like kinase 1 on cell cycle of lung cancer cell line A549].

BACKGROUND & OBJECTIVE: Expression of polo-like kinase 1 (Plk1), which has several functions in mitotic progression, is elevated in lung adenocarcinoma cell line A549. It suggests that over-expression of Plk1 relates to chemotherapy- and radiotherapy-resistance, and poor prognosis of lung cancer patients. This study was to investigate the effect of down-regulation of Plk1 on cell cycle of A549 cells using the technique of antisense RNA. METHODS: Antisense RNA targeting Plk1 (pcDNA3.0-Plk1, pc3.0P) was designed and constructed, and transfected into A549 cells. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to examine expression of Plk1 gene. Cell proliferation was evaluated by BrdU stain; cell cycle changes and apoptosis were examined by flow cytometry; expression of alpha-tubulin was detected by immunofluorescence. RESULTS: mRNA level of Plk1 was significantly lower in pc3.0P-transfected A549 cells than in control cells (P < 0.05). pc3.0P reduced Plk1 mRNA in A549 cells by 46.75% 24 h after transfection, and by 61.84% 48 h after transfection. Protein level of Plk1 was also decreased after transfection. Positive rate of BrdU stain in experimental cells was only 25.59% 48 h after transfection, which was significantly lower than that in control cells (P < 0.05). A549 cells showed a strong G(2)/M arrest and apoptosis 72 h after transfection. alpha-tubulin staining showed absence of microtubule connection,and spindle abnormalities. CONCLUSION: Down-regulation of Plk1 interferes spindle formation, and inhibits cell proliferation, induces cell cycle arrest and apoptosis.

Adenocarcinoma↗

PubMed2005

[Controlling effects of plant extracts and pesticides on Myzus persicae and Lipaphis erysimi populations].

This paper studied the controlling effects of Xanthium sibiricum and Syngonium podophyllum ethanol extracts, mobile oil emulsion and 0.3% azadirachtin EC on Myzus persicae and Lipaphis erysimi populations both in laboratory and in field. The results showed that in laboratory, X. sibiricum extract was the key deterrent to Myzus persicae, while sprayed it with S. podophyllum extract and with petroleum spray oil or 0.3 % azadirachtin EC, the deterrent effect could be improved. As for pterigota Lipaphis erysimi, the extracts of the two plants were the main deterrents, and their interference effect was non-linear. In field, S. podophyllum extract had a stronger deterrent effect when sprayed independently. L. erysimi population could be successfully controlled by the mixtures of plant extracts and insecticides, with an efficiency of 95.7%. The best treatment against M. persicae population was X. sibiricum extract, with an efficiency of 87%, while S. podophyllum extract mixed with 0.3% azadirachtin EC, and X. sibiricum extract mixed with 0.3% azadirachtin EC had an efficiency of >80%.

Animals↗

PubMed2005

[Effects of eutrophication on distribution and population density of Corbicula fluminea and Bellamya sp. in Chaohu Lake].

The investigation on the distribution an d population density of C. fluminea and Bellamya sp. in Chaohu Lake during September 2001 and September 2002 showed that in the west region of the lake where was seriously eutrophic, the density and biomass of C. fluminea were 5.1 ind. x m(-2) and 17.87 g x m(-2) in 2001, and 8.8 ind. x m(-2) and 47.29 g x m(-2) in 2002, while those of Bellamya sp. were 13.3 ind. x m(-2) and 45.45 g x m(-2) in 2001, and 3.8 ind. x m(-2) and 12.56 g x m(-2) in 2002, respectively. In the east region of the lake where was eutrophic, the density and biomass of C. fluminea were 23.8 ind. x m(-2) and 67.86 g x m(-2) in 2001, and 29.2 ind. x m(-2) and 96.18 g x m(-2) in 2002, while those of Bellamya sp. were 10.1 ind. x m(-2) and 32.00 g x m(-2) in 2001, and 9.4 ind. x m(-2) and 31.21 g x m(-2) in 2002, respectively. The density and biomass of C. fluminea and Bellamya sp. were declined with increasing eutrophication. In hypertrophic region, C. fluminea and Bellamya sp. were absent. The density and biomass of the two species were obviously higher in littoral than in pelagic region. The distribution type of C. fluminea was core-model, while that of Bellamya sp. was random. The correlation between the density and biomass of C. fluminea and Bellamya sp. and water depth was not significant (P > 0.05). The biomass of Bellamya sp. was negatively correlated with water TN (P < 0.01), NO3-N (P < 0.05), TP(P < 0.01) and PO4-P (P < 0.05), while that of C. fluminea only had a significantly negative correlation with PO4-P(P < 0.05). Compared with 1981, there was fewer C. fluminea in the lake nowadays. The effects of other environmental factors on the population distribution and growth of C. fluminea and Bellamya sp. were also discussed.

Animals↗

PubMed2004

An immunohistochemical method that distinguishes free from complexed SNAP-25.

Soluble N-ethylmaleimide-sensitive fusion protein (NSF) attachment protein receptor (SNARE) complexes composed of target (t-) SNAREs syntaxin and SNAP-25 and vesicle SNARE synaptobrevin play an essential role in neurosecretion. It is hypothesized that a transient intermediate complex between the t-SNAREs is formed during the assembly of the ternary complex. The existence of the t-SNARE binary complexes in vivo, however, has not been demonstrated. By using an affinity absorption scheme with preformed syntaxin-SNAP-25 complexes, we isolated antibodies capable of distinguishing free SNAP-25 from those associated with syntaxin. By semiquantitative immunohistochemistry, we estimated that, in cultured cerebellar neurons, the majority of SNAP-25 existed as complexes. Compared with the cultured neurons, PC12 cells expressed significantly less syntaxin, and we found that SNAP-25 was primarily in free forms. In contrast, a PC12 line that stably expressed a recombinant syntaxin showed a marked increase in SNAP-25 complexes. By using fluorescence resonance energy transfer (FRET) techniques, we observed FRET between cyan fluorescence protein-syntaxin and yellow fluorescence protein-SNAP-25 fusion proteins expressed in COS-7 and PC12 cells, suggesting a physiological interaction between syntaxin and SNAP-25. Our results demonstrate that, unlike what was previously hypothesized, syntaxin and SNAP-25 exist preferably as stable binary complexes in neurons. These findings offer novel insight into the mechanisms underlying the initiation and regulation of SNARE complex assembly.

Animals↗

PubMed2004

Intercellular adhension molecule-1 in the pathogenesis of heroin-induced acute lung injury in rats.

The expression of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of heroin-induced acute lung injury (ALI) in rats was investigated. The model of ALI was established by intravenous injection of heroin into tail vein in rats. Thirty-six rats were randomly divided into heroin-treated groups (1 h, 2 h, 4 h, 6 h and 24 h) and normal control group. Changes in histopathologic morphology and biological markers of ALI were measured. The expression of ICAM-1 in lung tissue was detected by using immunohistochemistry and RT-PCR. The results showed that the W/D ratio and protein contents in BALF of the heroin-treated groups were significantly higher than that of the, control group (P<0.01). The histopathological changes in the lung tissue were more obvious in heroin-treated groups. The ICAM-1 protein and mRNA expression in the lung tissue of heroin-treated groups were significantly increased as compared with that of the control group (P<0.01), and correlated with the ALI parameters in a time-dependent manner. Increasing of ICAM-1 expression was involved in the formation of heroin-induced lung injury. Furthermore, the level of expression was positively correlated with the severity of lung injury.

Animals↗

PubMed2004

[Repellent effect of volatile oil from whitefly (Syngonium podophyllum) on aphids and its chemical constituents].

The interference effect of volatile oil from whitefly (Syngonium podophyllum) on aptera aphid, guard aphid (Aphis gossypii), mustard aphid (Lipaphis erysimi) and red peach aphid (Myzus persicae) was studied by using four arms olfraetometes. The results showed that the volatile oil had distinct repelling effect. The staying periods of test aphids in test areas were obviously shorter than in control areas, and the selecting frequencies were less than the control, too. The volatile oil did not show repelling effect on red peach aphid at the test concentrations. The components of the volatile oil from S. podophyllum were analysed by GC-MS. 43 constituents were identified.

Animals↗

PubMed2004

Effect of antisense RNA targeting polo-like kinase 1 on cell cycle and proliferation in A549 cells.

BACKGROUND: Expression of polo-like kinase 1 (Plk1) is elevated in lung cancer and has been proposed as having prognostic value and related to resistance to chemotherapy and radiation. In addition, Plk1 has several functions in mitotic progression. In this study, the authors investigated the effect of Plk1 depletion on cell cycle progression and proliferation in A549 cells, a lung cancer cell line. METHODS: A recombinant plasmid containing antisense RNA targeting Plk1 (pcDNA3-Plk1) was transfected into A549 cells. Reverse transcription-polymerase chain reaction and Western blot were used to examine Plk1 gene expression. Cell proliferation was evaluated by direct cell counting and bromodeoxyuridine (BrdU) labelling. Cell cycle and apoptosis were examined by flow cytometry. Expression of alpha-tubulin was detected by immunofluorescence, and the inhibition rate (IR) by chemotherapeutic agents was determined by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyl-tetrazolium bromide assay. RESULTS: After transfection into A549 cells, pcDNA3-Plk1 reduced Plk1 mRNA by 46.75% for 24 hours and by 61.84% for 48 hours. Plk1 protein was significantly decreased simultaneously (P < 0.05). Abnormal morphological changes of cells and growth inhibition were observed in pcDNA3-Plk1 transfected groups. The BrdU labelling index was 25.59% 48 hours after transfection, which was significantly lower than that of the control groups (P < 0.05). Forty-eight hours after transfection, there showed absence of microtubule polymerization and spindle abnormalities in staining for alpha-tubulin. A549 cells showed a strong G2/M arrest and apoptosis 72 hours post transfection. IR of vinorelbine in pcDNA3-Plk1 transfected groups was significantly higher than that of the other groups (P < 0.05, respectively). CONCLUSIONS: Plk1 depletion interferes with spindle formation, induces cell cycle arrest and apoptosis, and consequently inhibits cell proliferation in A549 cells. Moreover, it sensitizes lung cancer cells to chemotherapy.

Apoptosis↗

PubMed2004

[Bioassay on oviposition repellency of non-preferable plant extracts against citrus red mite Panonychus citri].

The oviposition repellency of the alcohol extracts from 50 species of non-preferable plants and azadirachtin against citrus red mite (Panonychus citri) was determined using laboratory bioassays. In choice tests, the extracts from 42 of the 50 plant species and 1% azadirachtin (2000 x) significantly reduced oviposition 1d after treatment. The repellency effect of the extracts from the 42 plant species was better than that of azadirachtin. Mikania micrantha extract had the best result, with an Interference Index of Population Control (IIPC) of 0.087 1 d after treatment, and significantly reduced oviposition for 9 d, while the extracts from Sesbania cannabina, Allium tuberosum, Paederia scandens, Duranta erecta and Dicranopteris pedata also had good effects, with an oviposition repellency of over 70% 1 d after treatment, and significantly reduced oviposition for 4-6 d. The effect became weaker as time went on. None of the extracts showed significant oviposition attraction.

Animals↗

PubMed2003

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3'UTR.

Transfection of cDNA in 3'untranslated region of human nuclear factor for interleukin-6 (NF-IL6 3'UTR) induced tumor suppression in a human hepatoma cell line. cDNA array analysis was used to reveal changes in gene expression profile leading to tumor suppression The results indicate that this suppression was not due to activation of dsRNA-dependent protein kinase, nor to inactivation of oncogenes; rather, all the changes in expression of known genes, induced by NF-IL6 3'UTR cDNA may be ascribed to the suppression of cellular malignancy. Therefore, our results imply that this 3'untranslated region may have played role of a regulator of gene expression profile.

3' Untranslated Regions↗