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Objective To investigate the effect of imatinib on the growth of A549 non-small cell lung cancer transplanted tumors and the expression of PDGFB and PDGFRβ proteins in tumor tissues and stroma in nude mice and to explore the underlying tumor suppression mechanism. Methods A transplantation tumor model of A549 non-small cell lung cancer was established in nude mice. The mice were then randomly divided into four groups: control group (0.9%NaCl), low-dose imatinib group (50 mg/(kg·d)), medium-dose imatinib group (100 mg/(kg·d)), and high-dose imatinib group (200 mg/(kg·d)). The effect of different concentrations of imatinib administered by continuous gavage on tumor growth was observed for 28 days. HE staining was performed to observe the pathological changes of tumor tissues. The expression of PDGF/PDGFR pathway-related proteins and the phosphorylation levels of AKT and ERK1/2 proteins in tumor tissues were detected by Western blot analysis. Double immunofluorescence staining was used to detect the expression of PDGFB and PDGFRβ proteins in the tumor stroma. Results Imatinib inhibited the growth of A549 non-small cell lung cancer cells in nude mice, suppressed the expression of PDGFB in tumor tissues, and decreased the phosphorylation levels of PDGFRβ, AKT, and ERK1/2. The expression of PDGFB and PDGFRβ in tumor stromal fibroblasts of the administered group was significantly lower than that of the control group. Conclusion Imatinib exhibits a pronounced inhibitory effect on A549 xenografts of nude mice with non-small cell lung cancer, and its antitumor mechanism may involve the downregulation of PDGFB and PDGFRβ expression in tumor stromal fibroblasts.
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Objective:To study the effects of Docetaxel o n the proliferation of adenoid cystic carcinoma SACC-83 cells of salivary gland. Methods:The inhibitory effects of Docetaxel on the proliferatio n of SACC-83 cells were investigated with cell counting, soft agar clonogenic a ssay, and flow cytometry. Results:With the exposure time of 24, 48 or 72 h the IC 30(nmol/L) of Docetaxel was 1.39,1.26 and 0.47, the I C 50(nmol/L) 13.02, 3.34 and 1.26 respectively; the relative antitumor acti vity (RAA) of the drug against SACC-83 cells was 330, 1 289 and 3 426 respectiv ely. After the cells had been treated for 72 h, the percentages of G 1, S and G 2 phase cells in the cell cycle in the control group were 73.8,19.8 and 6.4, in IC 30 group 65.0, 29.5 and 5.5, in IC 50 group 57.6,42.4 and 0, res pectively. The clonogenesity (%) in control, IC 30 and IC 50 groups we re 36.0?0.5,8.3?2.5 and 0.5?0.3 respectively. Conclusion:Doc etaxel may inhibit the proliferation of SACC-83 cells in a dose and time depend ent way.
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Objective: To select highly metastatic cells from human salivary gland mucoepidermoid carcinoma cell clone Mc3. Methods: In situ transplantation of Mc3 cells into submandibular gland of nude mice, in situ transplantation of Mc3 induced lung metastasized tumor tissue among nude mice and cell culture were employed to obtain the wanted cells. Morphological observation, cell growth analysis, flow cytometry, chromosome staining, clonogenic assay and artificial metastasis test in nude mice were used to characterize the cells. Results: Lung metastasis was observed in 3 out of 10 nude mice after 4 cycles of in situ transplantation of Mc3 cell induced lung metastasized tumor tissue. Epidermoid cells with similar morphology to Mc3 were obtained through cell culture and the cells were named M3SP4. M3SP4 cell induced lung metastatic foci were histologicaly proved to be mucoepidermoid carcinoma. Subdiploid karyotype with human chromosome morphology was observed in M3SP4 and Mc3 cells. The population doubling time (h) of M3SP4 and Mc3 cells was 23.9 and 25.9, the percentage of S phase cells in cell cycle 26.8 and 15.3, clonogenecity (%) 54.6 and 30.2, respectively. The artificial lung metastatic potential of M3SP4 cells was 35% higher than that of Mc3 in nude mice. Conclusion: M3SP4 cells are of human mucoepidermoid carcinoma with higher metastatic potential than Mc3. In situ transplantation of mucoepidermoid carcinoma cells or lung metastasized tumor tissue may maintain the metastatic potential of the cells.
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?Objective:To study the effects of Docetaxel on the proliferation and metastatic potential of mucoepidermoid carcinoma M 3SP 4 cells in vitro and in vivo . Methods:Inhibitory effects of Docetaxel on the proliferation and metastatic potential of mucoepidermoid carcinoma M 3SP 4 cells were investigated with cell counting,cloning assay flow cytometry, tail vein injection and submandibular gland injection of the cells into nude mice. Results:Docetaxel inhibited M 3SP 4 cells growth in a dose and time dependent way. The IC 30 and IC 50 (with 72 h exposure) of Docetaxel were 0.34 nmol/L and 0.63 nmol/L, respectively; the doubling time(h) of the cells treated with the drug at IC 30 for 7 days and of the control were 32.7 h, 43 h, respectively; the clonogenesity(%) of the control and of the cells treated with Docetaxel ( 0.05 nmol/Lor 0.1 nmol/L)were (29.2?1.4)% and (20.2?0.8)% and (2.8?0.4)%, respectively; the number of metastatic foci on lung surface in the nude mice treated with the drug at 30 mg/kg?week and in the controls were 0 and 11?3.4; the weight(g) of submandibular gland in the two groups were 0.31?0.05 and 1.20?0.23 respectively. Conclusion:Docetaxel may inhibit the proliferation and metastatic potential of mucoepidermoid carcinoma M 3SP 4 cells.