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Objective：This study aims to examine the expression of ZBTB3 in human glioblastoma (GBM) tissues and cell lines, and to explore the effects of ZBTB3 on the proliferation and clonal formation of GBM cells and their regulatory mechanism. Methods：The expression of ZBTB3 in tumor tissues of GBM patients was analyzed by GEPIA2 database. The mRNA and protein expression levels of ZBTB3 in GBM cell lines (U251, U373, U87) were detected by RT⁃PCR, qPCR and Western blot, and U87 cell line was identified with the highest expression of ZBTB3. CCK ⁃ 8 and clonal formation assay were used to examine the effects of silencing ZBTB3 on the proliferation and clonal formation of U87 cells. U87 cells were treated with p38MAPK, AMPK and Akt1 inhibitors, and the phosphorylation levels of p38MAPK, AMPK and Akt1 were detected by Western blot. ZBTB3 mRNA and protein levels were detected by RT ⁃ PCR, qPCR and Western blot. Cell proliferation and clone formation were examined by CCK ⁃ 8 and clone formation assay. Results：The expression of ZBTB3 in tumor tissues of GBM patients was significantly higher than that in normal tissues. The expression levels of ZBTB3 in U251, U373 and U87 cell lines were examined, and the highest expression in U87 cells was observed. Silencing ZBTB3 markedly inhibited the proliferation and clonal formation of U87 cells. AMPK inhibition could not only obviously reduce the expression level of ZBTB3 in U87 cells, but also markedly attenuate the proliferation and clonal formation of U87 cells. Conclusion：The expression of ZBTB3 is obviously increased in GBM tissues and cells, and the AMPK ⁃ up ⁃ regulated ZBTB3 expression promotes the proliferation and clonal formation of GBM cells. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

OBJECTIVE: Ovarian cancer is the most common malignant tumor in female reproductive system. Metformin is an orally taken hypoglycemic agent, which is extensively applied in the clinic. Clinical trials find that there may be a certain degree of action of the metformin in inhibiting malignant tumors. This paper aims to investigate the inhibitory effect and mechanism of metformin on human ovarian cancer cells. MATERIALS AND METHODS: Through in vitro cell experiment, the influences of metformin on the proliferation, colony formation and apoptosis of ovarian carcinoma cells were studied. Ovarian cancer cells SKOV-3 and A2780 in logarithmic growth phase were selected and cell proliferation was measured by MTT method. The metformin was processed for 48 h to calculate the survival rate of cells. Also, metformin was processed for 24 h and two weeks or stained with crystal violet, after which Quantity One (Bio-Rad, Hercules, CA, USA) method was used to quantitatively analyze the cell clone formation, meanwhile, the FCM (flow cytometry) was used for the detection and analysis. RESULTS: Intervened by metformin with different concentrations for 48 h, the cell viabilities of SKOV-3 and A2780 cells were respectively reduced by 19.49 ± 2.92%, 45.41 ± 7.95%, 53.84 ± 5.53%, 64.04 ± 4.36% and 11.45 ± 3.12%, 35.42 ± 7.55%, 43.77 ± 5.77%, 53.05 ± 5.55% as compared with that in the control group with statistical significances. After processed by metformin with different concentrations for two weeks, the cells clone numbers of SKOV-3 and A2780 were significantly reduced. Treatment of metformin on SKOV-3 and A2780 cells of human ovarian cancer showed significant apoptosis. CONCLUSIONS: The metformin has the inhibitory effect on the cells of human ovarian cancer, which may be through inducing ovarian cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

The purpose of the research was aimed to explore the inhibition effect of 3,5,4'-trimethoxy-trans-stilbene (BTM) on human gastric cancer cells and its mechanism. The results indicated the higher the concentration of trimethoxystilbene was, the higher the inhibition rates on MKN-45 and MGC-803 cell lines were, with a significant dose-depending relationship. The half maximum inhibitory concentration of cisplatin on MKN-45 and MGC-803 cell lines treated with 20 μmol/l trimethoxystilbene were significantly lower than that of the control group (0 mol/l), showing that the cisplatin IC50 of MGC-803 cell lines could be reduced by trimethoxystilbene. In addition, the combination of trimethoxystilbene and cisplatin can obviously induce apoptosis of MKN-45 and MGC-803 cells, which is much higher than that of the single use of the two. The higher the concentration of trimethoxystilbene was, the higher the apoptosis rates of MKN-45 and MGC-803 cells were, there was a significant dose-effect relationship. And with the increased concentration of the drug, the proportion of G0/G1 was increased in a certain concentration effect relationship, suggesting that the G2/M phase of cisplatin resistant gastric cancer cell was blocked by trimethoxystilbene. Besides, trimethoxystilbene combined with cisplatin significantly inhibited the expression of anti-apoptotic protein Bcl-2, and increased the expression of Pro apoptotic protein Bax. [ABSTRACT FROM AUTHOR]