Expression and clinical significance of FPARγ and β-catenin in breast cancer

Objective To study the expression of peroxisome proliferator-activated receptor γ (PPARγ) and β-catenin in breast cancer, and their correlations with clinicopathological parameters and prognosis. Methods Tissue samples obtained from 70 patients with breast cancer and 20 patients with breast benign mass were immunohistochemically examined for the expression of PPARγ and p-catenin. Results Overexpression rate of PPARγ protein was 34. 3% in breast cancer, significantly lower than that in breast benign mass. Abnormal expression rate of β-catenin in breast cancer was 67. 1%. A significant negative-correlation was found between the expression of PPARγ and β-catenin (r=-0. 398,P<0.05 ). PPARγ expression was inversely associated with histologic grade, tumor size, axillary lymph node metastasis,TNM stage and Ki-67 expression (P<0. 05), while positively correlated with ER status and overall survival rate (P<0. 05). Abnormal β-catenin expression was positively associated with histologic grade, axillary lymph node metastasis and TNM stage (P<0. 05), while inversely correlated with overall survival rate (P<0.05). Conclusion PPARγ and β-catenin are correlated with development of breast carcinoma,suggesting that detection of PPARγ and β-catenin may be of value in evaluating the biological behaviors and the prognosis of breast cancer.     

乳腺癌中过氧化物酶体增殖激活受体γ和β-连环蛋白表达及临床意义

目的 探讨过氧化物酶体增殖激活受体γ(PPARγ)和β-连环蛋白(β-catenin)在乳腺癌组织中的表达、相关性及与乳腺癌临床和预后的关系.方法 采用免疫组织化学法检测70例乳腺癌组织和20例乳腺良性肿瘤中PPARγ和β-catenin的表达,并进行临床分析.结果 乳腺癌PPARγ高表达率为34.3%(24/70),明显低于乳腺良性肿瘤;β-catenin在乳腺癌中异常表达率为67.1%(47/70),PPARγ和β-catenin蛋白表达呈显著负相关(r=-0.398,P<0.05).PPARγ蛋白表达水平与乳腺癌组织学分级、TNM分期、淋巴结转移、肿瘤大小及Ki-67表达负相关(P<0.05),与雌激素受体(ER)状态及总体生存率正相关(P<0.05);β-catenin蛋白异常表达与乳腺癌组织学分级、TNM分期、淋巴结转移正相关(P<0.05),与总体生存率负相关(P<0.05).结论 PPARγ和β-catenin表达与乳腺癌发展有关,检测PPARγ和β-catenin表达对判断乳腺癌生物学行为和预后具有参考价值.     

Expressions and significances of Nek2 and β-catenin in breast invasive ductal carcinoma

Objective To investigate the expression and significance of NIMA related kinases 2 ( Nek2) and β-catenin (β-cat) in breast invasive ductal carcinoma (IDC) and concomitant ductal carcinoma in situ (DCIS). The roles of Nek2 and β-acat in the development and progression of breast cancer were explored. Methods The protein expression of Nek2 and β-cat in the tissues from 186 patients with IDC, 75 concomitant DCIS, 80 normal tissue adjacent to carcinoma and 40 fibroadenoma of breast was detected by using immunohistochemistry. Their relationship between clinicopathologic parameters was analyzed. Results There were correlations between the Nek2 expression in cytoplasm and grade(x2=8. 756;P<0.05) as well as tumor size (x2=6. 518;P<0.05) in IDC. The positive expression of Nek2 in nuclei was 32/186 and 15/75 in IDC and DCIS, respectively. There were correlations between the β-cat expression on the cytomembrane and grade (x2=45.493;P<0. 01) , TNM stage (x2=9. 510;P<0. 01), node status (Z=-2.035;P<0. 05) and estrogen receptor (ER) status (Z=-3. 004;P<0. 01). The β-cat expression on the cytoplasm was related with TNM stage (x2=8. 194;P<0. 05). The expression of Nek2 and β-cat had no correlation with clinicopathologic parameters in concomitant DCIS (P>0. 05), the Nek2 expression in cytoplasm had a correlation with the β-cat expression in cytoplasm (r=0. 226,P<0.05) in concomitant DCIS, and the same relationship could also be seen in IDC (r=0. 368,P<0.01). There was significant difference in the β-cat expression on the cytomembrane between IDC and concomitant DCIS (Z=-3. 804,P<0. 01). In the normal tissue adjacent to carcinoma and fibroadenoma, the Nek2 expression in cytoplasm and nuclei Was low or negative;the β-cat expression on the cytomembrane was high but that Was low in cytoplasm.Conclusion Centrosome regulatory factor Nek2 and β-cat can support a new way to explore the mechanisms of breast tumorigrenesis.And they may become a new antitumor drug target in the future.     

Expressions and significances of Nek2 and β-catenin in breast invasive ductal carcinoma

Objective To investigate the expression and significance of NIMA related kinases 2 ( Nek2) and β-catenin (β-cat) in breast invasive ductal carcinoma (IDC) and concomitant ductal carcinoma in situ (DCIS). The roles of Nek2 and β-acat in the development and progression of breast cancer were explored. Methods The protein expression of Nek2 and β-cat in the tissues from 186 patients with IDC, 75 concomitant DCIS, 80 normal tissue adjacent to carcinoma and 40 fibroadenoma of breast was detected by using immunohistochemistry. Their relationship between clinicopathologic parameters was analyzed. Results There were correlations between the Nek2 expression in cytoplasm and grade(x2=8. 756;P<0.05) as well as tumor size (x2=6. 518;P<0.05) in IDC. The positive expression of Nek2 in nuclei was 32/186 and 15/75 in IDC and DCIS, respectively. There were correlations between the β-cat expression on the cytomembrane and grade (x2=45.493;P<0. 01) , TNM stage (x2=9. 510;P<0. 01), node status (Z=-2.035;P<0. 05) and estrogen receptor (ER) status (Z=-3. 004;P<0. 01). The β-cat expression on the cytoplasm was related with TNM stage (x2=8. 194;P<0. 05). The expression of Nek2 and β-cat had no correlation with clinicopathologic parameters in concomitant DCIS (P>0. 05), the Nek2 expression in cytoplasm had a correlation with the β-cat expression in cytoplasm (r=0. 226,P<0.05) in concomitant DCIS, and the same relationship could also be seen in IDC (r=0. 368,P<0.01). There was significant difference in the β-cat expression on the cytomembrane between IDC and concomitant DCIS (Z=-3. 804,P<0. 01). In the normal tissue adjacent to carcinoma and fibroadenoma, the Nek2 expression in cytoplasm and nuclei Was low or negative;the β-cat expression on the cytomembrane was high but that Was low in cytoplasm.Conclusion Centrosome regulatory factor Nek2 and β-cat can support a new way to explore the mechanisms of breast tumorigrenesis.And they may become a new antitumor drug target in the future.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

Expression and significance of estrogen receptor α and β in prostate cancer and peri-cancer tissue

Objective To investigate the expression of estrogen receptor (ER) α and β in human prostate cancer (PC), peri-cancer tissue and benign prostatic hyperplasia (BPH) tissue, and to discuss the role of estrogen receptor in prostate cancer. Methods The expression of ERα and ERβ in PC (n=28), peri-cancer tissue (n=28) and BPH (n=29) were detected by immunohistochemistry with En vision method. The ERα and ERβ expression were compared among different tissues by chisquare. The relationship between ER expression and related clinicopathologic features was statistically analyzed by spearman rank collection. Results ERα was localized dominantly in the stromal cell of PC. There were significant differences of the expression of ERα in PC, peri-cancer tissue and BPH tissue (epithelial cell 0%, 14%, 24%, P＜0. 05; stromal cell 57%, 68%, 31%,P＜0. 05). ERβ was localized in both epithelial and stromal cell of PC. There were significant differences of the expression of ERβ in PC, peri-cancer tissue and BPH tissue (epithelial cell 39%, 64%, 29%, P＜0.01; stromal cell 50%, 75%, 79%, P＜0.05). There was a significant difference of the expression of ERβ in different Gleason scores of PC tissue. Conclusions ERα is localized in the stromal cell of PC tissue.ERβ is localized in both epithelial and stromal cell of PC tissue. The ERβ might be related to the tumor differentiation of PC.     

Expression and significance of estrogen receptor α and β in prostate cancer and peri-cancer tissue

Objective To investigate the expression of estrogen receptor (ER) α and β in human prostate cancer (PC), peri-cancer tissue and benign prostatic hyperplasia (BPH) tissue, and to discuss the role of estrogen receptor in prostate cancer. Methods The expression of ERα and ERβ in PC (n=28), peri-cancer tissue (n=28) and BPH (n=29) were detected by immunohistochemistry with En vision method. The ERα and ERβ expression were compared among different tissues by chisquare. The relationship between ER expression and related clinicopathologic features was statistically analyzed by spearman rank collection. Results ERα was localized dominantly in the stromal cell of PC. There were significant differences of the expression of ERα in PC, peri-cancer tissue and BPH tissue (epithelial cell 0%, 14%, 24%, P＜0. 05; stromal cell 57%, 68%, 31%,P＜0. 05). ERβ was localized in both epithelial and stromal cell of PC. There were significant differences of the expression of ERβ in PC, peri-cancer tissue and BPH tissue (epithelial cell 39%, 64%, 29%, P＜0.01; stromal cell 50%, 75%, 79%, P＜0.05). There was a significant difference of the expression of ERβ in different Gleason scores of PC tissue. Conclusions ERα is localized in the stromal cell of PC tissue.ERβ is localized in both epithelial and stromal cell of PC tissue. The ERβ might be related to the tumor differentiation of PC.     

吡格列酮对肥胖小鼠骨髓间充质干细胞分化的影响

目的通过建立饮食诱导的高脂小鼠的模型,观察过氧化物酶体增生物激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)激动剂吡格列酮对肥胖小鼠的骨量变化的影响以及骨髓间充质干细胞(mesenchymal stem cell,MSCs)分化的情况,探讨PPARγ与MSCs分化之间的关系及可能的作用机制。方法建立饮食诱导的肥胖鼠模型,吡格列酮(10mg·kg-1.d-1)对肥胖小鼠进行灌胃,一个月后检测肥胖小鼠及灌胃组肥胖小鼠的葡萄糖耐量,骨密度及骨组织形态学,并取小鼠原代MSC进行培养,提取其RNA,利用实时定量PCR,检测在MSCs分化过程中成骨及成脂特异性基因的表达量。结果吡格列酮灌胃的肥胖小鼠胰岛素抵抗改善的同时,骨密度虽无明显改变,但骨组织形态学中成骨细胞周长百分率明显增加,原代MSCs的成骨分化基因的表达量明显增加而成脂基因明显下降。结论PPARγ改善胰岛素抵抗的同时,促使MSCs向成骨细胞分化的能力增强,向脂肪细胞分化的能力下降,PPARγ除直接参与调节MSCs的分化外,还可能通过间接作用在MSCs的分化过程中起重要作用。     

过氧化物酶体增殖物激活受体-γ配体抗肿瘤机制的研究进展

过氧化物酶体增殖物激活受体(PPAR-γ)及其配体已成为肿瘤基础研究的热点之一,文中从细胞分化、细胞增殖、细胞凋亡、血管形成及肿瘤侵袭性等方面综述了PPAR-γ配体抗肿瘤机制的研究进展。     

过氧化物酶体增殖物激活受体γ激动剂抗转化生长因子-β促器官纤维化作用的研究进展

目的 总结过氧化物酶体增殖物激活受体γ(PPARγ)激动剂抗转化生长因子-(βTGF-β)促器官纤维化作用的研究进展.方法 复习有关PPARγ激动剂抗TGF-β促器官纤维化作用的文献并进行综述.结果 TGF-β是一种主要的促纤维化细胞因子,能促进多种器官的纤维化进程,而PPARγ激动剂则可以有效地阻断TGF-β的信号传导,从而发挥抗器官纤维化的作用.结论 研究PPARγ激动剂主要通过阻断TGF-β信号传导来实现抗器官纤维化的机理,有助于PPARγ激动剂在临床上的推广运用,为治疗器官纤维化疾病提供一种新途径.     

敲减PPARG对乳腺癌MCF-7细胞裸鼠移植瘤生长影响的研究

目的：探讨敲减过氧化物酶体增殖物激活受体γ(PPARG)对乳腺癌MCF-7细胞裸鼠移植瘤生长的影响。方法：体外培养MCF-7细胞,将PPARG-si RNA和NC-si RNA转染进入MCF-7细胞。分别采用CCK-8法和流式细胞术检测细胞增殖和凋亡情况。将转染后的细胞建立裸鼠移植瘤模型。28 d后处死裸鼠,分离瘤体并称重,计算抑瘤率。采用RT-PCR和蛋白印迹法分别检测瘤体中PPARG、β-catenin和MMP-9的m RNA表达和蛋白水平。结果：与空白对照组比较,NC-si RNA组各指标比较差异无统计学意义（P>0.05）;与空白对照组和NC-si RNA组比较,PPARG-si RNA组MCF-7细胞增殖率降低、细胞凋亡率增加（P<0.05）;与空白对照组和NC-si RNA组比较,PPARG-si RNA组移植瘤质量减少,PPARG、NF-κB和MMP-9的m RNA表达和蛋白水平均降低,抑瘤率增加（P<0.05）。结论：敲减PPARG能抑制乳腺癌MCF-7细胞增殖,促进MCF-7细胞凋亡,抑制裸鼠移植瘤生长,发生机制可能与PPARG调控能量代谢有关。