Objective To find out the pathogenicity of bacterial L-forms.Methods β-glucuronidase activities of both E.coli and their L-forms were determined with modified Fishman's method. The endotoxin content in 3 kinds of Gram negtive bacteria and their L-forms were measured with the limulus lysate test. Under ultrasonography, percutaneous transhepatic cholecystic punctures were performed on 2 groups of 10 healthy dogs. E.coli and their L-forms were respectively injected into the gallbladders of the 2 groups. 48 hours later, the gallbladder bile was obtained through puncture and cultured. After 6 months, all the animals were killed. Their bile was cultured and the gallbladders were pathologically analysed.Results Endotoxin existed in L-forms of Gram negtive bacteria (about 1/3-1/2 of the original forms). L-forms of E.coli also produced β-glucuronidase (58.67% activity of the original forms). A half of the E.coli which had stayed in the canine gallbladders for 48 hours have been transformed into L-forms by the action of bile and other factors. The L-forms existed in the gallbladder bile longer than 6 months. The gallbladders showed chronic infections: mild atrophy of mucosa, white blood cell and lymph cell infiltration in submucosa and slight fiberosis of the gallbladder walls. Bacterial L-forms were found in mucosa cells.Conclusions Bacterial L-forms can also produce pathogenical materials, but the amount is less than that of the original bacterial forms. Both bacterial forms and L-forms can lead to chronic infection of the canine gallbladders.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.

Krüppel-like factors (KLFs) play extremely important roles in genesis and development of tumors. Simultaneously, KLFs have been proven to affect the proliferation, differentiation and migration of hepatocellular carcinoma cells. Nine members in the KLFs family (KLF2, KLF4, KLF5, KLF6, KLF8, KLF9, KLF10, KLF14 and KLF17) are involved in the occurrence and development of hepatocellular carcinoma in various ways as an oncogene and tumor suppressor gene. Therefore, the KLFs family will hopefully become biological therapeutic targets for hepatocellular carcinoma.