BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its ro...BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.展开更多
OBJECTIVE: To investigate whether the decrease in expression of interleukin-2 (IL-2) after trauma is associated with changes in DNA binding activity of nuclear factor of activated T cells (NFAT) and activator protein-...OBJECTIVE: To investigate whether the decrease in expression of interleukin-2 (IL-2) after trauma is associated with changes in DNA binding activity of nuclear factor of activated T cells (NFAT) and activator protein-1 (AP-1). METHODS: Mice with closed impact injury with fracture in both hind limbs were adopted as the trauma model. Spleen lymphocytes were isolated from traumatized mice and stimulated with Con-A. Culture supernatants were assayed for IL-2 activity, and total RNA was extracted from spleen lymphocytes and assayed for IL-2 mRNA. DNA binding activity of NFAT and AP-1 were measured by electrophoretic mobility shift assay (EMSA). The expression of c-Fos, c-Jun and JunB proteins was determined by the Western blot analysis. RESULTS: DNA binding activity of NFAT and AP-1 gradually decreased to a minimum of 41% and 49%, respectively, of the control on the 4th day after injury, which was closely followed by the decline in IL-2 activity and IL-2 mRNA. A decrease in the expression of c-Fos on the 1st and 4th day after trauma had no significant effect on c-Jun expression; the increase in expression of JunB was only on the 1st day after injury. CONCLUSION: Decreased IL-2 expression is, at least in part, due to a decline in the activation of NFAT and AP-1 in traumatized mice. The decline in DNA binding activity of NFAT and AP-1 is partly due to a trauma-induced block in the expression of c-Fos.展开更多
PROTEIN kinase C (PKC) is a serine/thronine kinase, which plays a major role in cell sig-nalling, growth control and tumorigenesis. PKC is encoded by a multigene family, which havebeen identified as consisting of at l...PROTEIN kinase C (PKC) is a serine/thronine kinase, which plays a major role in cell sig-nalling, growth control and tumorigenesis. PKC is encoded by a multigene family, which havebeen identified as consisting of at least 12 members in mammalian tissues. PKC isoforms differin their biochemical properties, tissue-specific expression and intracellular localization. Thedifferences imply that the individual PKC isoforms have a distinct physiological function. Inorder to study the role of specific PKC subtype in cell proliferation and transformation, weconstructed the human embryonic lung cell (2BS) model stably overexpressing PKC_α andfound that the overexpression of PKC_α promoted the growth rate and caused the transform-展开更多
目的研究内蒙古地区蒙古族人群白细胞介素15受体α亚单位(interleukin-15 receptorαsubunits,IL-15Rα)及Runt相关转录因子2(recombinant Runt related transcription factor 2,RUNX2)基因多态性与后纵韧带骨化(ossification of poster...目的研究内蒙古地区蒙古族人群白细胞介素15受体α亚单位(interleukin-15 receptorαsubunits,IL-15Rα)及Runt相关转录因子2(recombinant Runt related transcription factor 2,RUNX2)基因多态性与后纵韧带骨化(ossification of posterior longitudinal ligament,OPLL)的关系。方法采用基因测序法选择2014年1月至2019年12月就诊于我院的蒙古族OPLL患者以及同期健康体检的蒙族人群为研究对象,110例内蒙古地区蒙古族后纵韧带骨化患者和118例健康蒙古族人群进行IL-15Rα基因及RUNX2基因多态性的检测。110例内蒙古地区蒙古族后纵韧带骨化患者,其中男75例,女35例;年龄38~78岁,平均(53.0±12.8)岁。118例健康蒙古族人群,其中男65例,女53例;年龄45~68岁,平均(58.0±11.2)岁。两组IL-15Rα基因及RUNX2基因进行比较,筛选出有意义基因。结果两组采用χ^(2)检验对rs1321075位点基因型、等位基因频率进行比较,AC、CC型差异有统计学意义(P<0.05),OR值(95%CI)分别为0.584(0.343,0.997)、1.978(1.166,3.353),等位基因C的OR值(95%CI)为0.588(0.386,0.895);对rs16873379位点基因型、等位基因频率进行比较,CT、TT型差异有统计学意义(P<0.05),OR值(95%CI)分别为2.756(1.595,4.760)、0.266(0.153,0.461),等位基因C的OR值(95%CI)为2.514(1.678,3.768);对rs2296139位点基因型、等位基因频率进行比较,AA基因型差异有统计学意义(P<0.05),OR值(95%CI)为0.416(0.218,0.797);其他位点基因型、等位基因频率进行比较,差异无统计学意义(P>0.05)。结论RUNX2基因及IL-15Rα基因中rs1321075位点和rs2296139位点多态性在内蒙古地区蒙古族后纵韧带骨化人群中可能发挥作用。展开更多
Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats....Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats. Recent findings regarding stroke pathophysiology have recognized that anti-inflammation is an important target for the treatment of ischemic stroke. The cholinergic anti-inflammatory pathway is a highly robust neural-immune mechanism for inflammation control. This study was to investigate whether activating the cholinergic anti-inflammatory pathway can be involved in the mechanism of inhibiting the inflammatory response during puerarin-induced cerebral ischemia/reperfusion in rats. Results showed that puerarin pretreatment （intravenous injection） re- duced the ischemic infarct volume, improved neurological deficit after cerebral ischemia/reperfusion and decreased the levels of interleukin-1β, interleukin-6 and tumor necrosis factor-a in brain tissue. Pretreatment with puerarin （intravenous injection） attenuated the inflammatory response in rats, which was accompanied by janus-activated kinase 2 （JAK2） and signal transducers and activators of transcription 3 （STAT3） activation and nuclear factor kappa B （NF-KB） inhibition. These observa- tions were inhibited by the alpha7 nicotinic acetylcholine receptor （a7nAchR） antagonist a-bungarotoxin （a-BGT）. In addition, puerarin pretreatment increased the expression of a7nAchR mRNA in ischemic cerebral tissue. These data demonstrate that puerarin pretreatment strongly protects the brain against cerebral ischemia/reperfusion injury and inhibits the inflammatory re- sponse. Our results also indicated that the anti-inflammatory effect of puerarin may partly be medi- ated through the activation of the cholinergic anti-inflammatory pathway.展开更多
文摘BACKGROUND A series of long non-coding RNAs(lncRNAs)have been reported to play a crucial role in cancer biology.Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies.However,its role in hepatocellular carcinoma(HCC)has not been fully deciphered.AIM To decipher the role of CDKN2B-AS1 in the progression of HCC.METHODS CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction.The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method,EdU method,and flow cytometry,respectively.RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1(E2F1).Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z(GNAZ).E2F1 and GNAZ were detected by western blot in HCC cells.RESULTS In HCC tissues,CDKN2B-AS1 was upregulated.Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells,and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis.CDKN2B-AS1 could interact with E2F1.Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region.Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells.CONCLUSION CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.
文摘OBJECTIVE: To investigate whether the decrease in expression of interleukin-2 (IL-2) after trauma is associated with changes in DNA binding activity of nuclear factor of activated T cells (NFAT) and activator protein-1 (AP-1). METHODS: Mice with closed impact injury with fracture in both hind limbs were adopted as the trauma model. Spleen lymphocytes were isolated from traumatized mice and stimulated with Con-A. Culture supernatants were assayed for IL-2 activity, and total RNA was extracted from spleen lymphocytes and assayed for IL-2 mRNA. DNA binding activity of NFAT and AP-1 were measured by electrophoretic mobility shift assay (EMSA). The expression of c-Fos, c-Jun and JunB proteins was determined by the Western blot analysis. RESULTS: DNA binding activity of NFAT and AP-1 gradually decreased to a minimum of 41% and 49%, respectively, of the control on the 4th day after injury, which was closely followed by the decline in IL-2 activity and IL-2 mRNA. A decrease in the expression of c-Fos on the 1st and 4th day after trauma had no significant effect on c-Jun expression; the increase in expression of JunB was only on the 1st day after injury. CONCLUSION: Decreased IL-2 expression is, at least in part, due to a decline in the activation of NFAT and AP-1 in traumatized mice. The decline in DNA binding activity of NFAT and AP-1 is partly due to a trauma-induced block in the expression of c-Fos.
文摘PROTEIN kinase C (PKC) is a serine/thronine kinase, which plays a major role in cell sig-nalling, growth control and tumorigenesis. PKC is encoded by a multigene family, which havebeen identified as consisting of at least 12 members in mammalian tissues. PKC isoforms differin their biochemical properties, tissue-specific expression and intracellular localization. Thedifferences imply that the individual PKC isoforms have a distinct physiological function. Inorder to study the role of specific PKC subtype in cell proliferation and transformation, weconstructed the human embryonic lung cell (2BS) model stably overexpressing PKC_α andfound that the overexpression of PKC_α promoted the growth rate and caused the transform-
文摘目的研究内蒙古地区蒙古族人群白细胞介素15受体α亚单位(interleukin-15 receptorαsubunits,IL-15Rα)及Runt相关转录因子2(recombinant Runt related transcription factor 2,RUNX2)基因多态性与后纵韧带骨化(ossification of posterior longitudinal ligament,OPLL)的关系。方法采用基因测序法选择2014年1月至2019年12月就诊于我院的蒙古族OPLL患者以及同期健康体检的蒙族人群为研究对象,110例内蒙古地区蒙古族后纵韧带骨化患者和118例健康蒙古族人群进行IL-15Rα基因及RUNX2基因多态性的检测。110例内蒙古地区蒙古族后纵韧带骨化患者,其中男75例,女35例;年龄38~78岁,平均(53.0±12.8)岁。118例健康蒙古族人群,其中男65例,女53例;年龄45~68岁,平均(58.0±11.2)岁。两组IL-15Rα基因及RUNX2基因进行比较,筛选出有意义基因。结果两组采用χ^(2)检验对rs1321075位点基因型、等位基因频率进行比较,AC、CC型差异有统计学意义(P<0.05),OR值(95%CI)分别为0.584(0.343,0.997)、1.978(1.166,3.353),等位基因C的OR值(95%CI)为0.588(0.386,0.895);对rs16873379位点基因型、等位基因频率进行比较,CT、TT型差异有统计学意义(P<0.05),OR值(95%CI)分别为2.756(1.595,4.760)、0.266(0.153,0.461),等位基因C的OR值(95%CI)为2.514(1.678,3.768);对rs2296139位点基因型、等位基因频率进行比较,AA基因型差异有统计学意义(P<0.05),OR值(95%CI)为0.416(0.218,0.797);其他位点基因型、等位基因频率进行比较,差异无统计学意义(P>0.05)。结论RUNX2基因及IL-15Rα基因中rs1321075位点和rs2296139位点多态性在内蒙古地区蒙古族后纵韧带骨化人群中可能发挥作用。
基金supported by the Young Scientists Foundation of Hubei Provincial Health Department,No.QJX2012-16
文摘Puerarin, a major isoflavonoid derived from the Chinese medical herb radix puerariae （Gegen）, has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebral ischemia model rats. Recent findings regarding stroke pathophysiology have recognized that anti-inflammation is an important target for the treatment of ischemic stroke. The cholinergic anti-inflammatory pathway is a highly robust neural-immune mechanism for inflammation control. This study was to investigate whether activating the cholinergic anti-inflammatory pathway can be involved in the mechanism of inhibiting the inflammatory response during puerarin-induced cerebral ischemia/reperfusion in rats. Results showed that puerarin pretreatment （intravenous injection） re- duced the ischemic infarct volume, improved neurological deficit after cerebral ischemia/reperfusion and decreased the levels of interleukin-1β, interleukin-6 and tumor necrosis factor-a in brain tissue. Pretreatment with puerarin （intravenous injection） attenuated the inflammatory response in rats, which was accompanied by janus-activated kinase 2 （JAK2） and signal transducers and activators of transcription 3 （STAT3） activation and nuclear factor kappa B （NF-KB） inhibition. These observa- tions were inhibited by the alpha7 nicotinic acetylcholine receptor （a7nAchR） antagonist a-bungarotoxin （a-BGT）. In addition, puerarin pretreatment increased the expression of a7nAchR mRNA in ischemic cerebral tissue. These data demonstrate that puerarin pretreatment strongly protects the brain against cerebral ischemia/reperfusion injury and inhibits the inflammatory re- sponse. Our results also indicated that the anti-inflammatory effect of puerarin may partly be medi- ated through the activation of the cholinergic anti-inflammatory pathway.
