Wrightgross9669
Estrogen evidently exerts a protective role against gastric cancer. Accordingly, we evaluated the relationship between the expression of the estrogen receptor ER-α36 and the clinicopathologic features in gastric cancer. ER-α36 expression levels differed among the tumor center, invasion front, and vascular metastases. The effects of E2β (17β-Estradiol, E2β) on invasion ability in SGC7901, High36 (with ER-α36 upregulation), and Low36 (with ER-α36 downregulation) cells were evaluated using Transwell assays. Furthermore, the c-Src signaling pathway was inhibited using PP2 and the effects on E2β-induced increases in E-cadherin, MMP2, and MMP9 were evaluated using western blotting. ER-α36, c-Src, MMP2, and E-cadherin levels were also evaluated in tumor xenografts. We found that 0.1 nM E2β promoted gastric cancer cell invasion by reducing E-cadherin expression and increasing MMP2 and MMP9 levels. The upregulation of ER-α36 promoted gastric cancer cell invasion and the downregulation of ER-α36 reduced the invasive ability of cells. The levels of ER-α36, c-Src, and MMP2 were the highest in tumor xenografts using High36 cells, intermediate in tumor xenografts using SGC7901 cells, and lowest in tumor xenografts using Low36 cells. The opposite results were obtained for E-cadherin expression. ER-α36 enhanced gastric cancer cell invasion by the activation of membrane-initiated c-Src signaling pathways. In particular, treatment with E2β and ER-α36 influenced gastric cancer cell invasion. Furthermore, c-Src was involved in the ER-α36-mediated estrogen signaling pathway and cell invasion.
The function of Interleukin-6 (IL-6) in the regenerative process is not fully understood. The aim was to show the IL-6 role in hepatocyte regeneration by identifying the proliferative rate of hepatocytes following partial hepatectomy.
Eighty male adult Sprague-Dawley rats were categorized into two equivalent groups (n = 40 rats); non-treated, and treated group with IL-6 of 35 µg/100 gm body weight according to lethality study for a four-day observation. Both groups were subjected to 70% hepatic resection. Liver specimens were taken for histo/immunohistochemical studies. Five measures were investigated histopathologically; binucleation, mitoses, thickening of the hepatic plate, ductular reaction, and presence of inflammatory cells. Ki-67 labeling index was evaluated using mouse anti-Ki-67 antibody.
In non-treated group; binucleation and multinucleation were noted in 12 cases (30%), bizarre cells with abnormal mitoses 16 cases (42%), and thickening of liver cell plate 18 cases (45%), in contrast to 32 (80%), 30 (75%) and 28 (70%), in treated group. Patches of inflammatory infiltrate were more marked in the treated group. Ki-67 labeling index was higher in the treated group (
-value 0.00001). The degree of Ki-67 reactivity in the treated group was negative 6 (15%), weak 6 (15%), moderate 16 (40%) and strong 12 (30%) compared with 18 (45%), 13 (32.5%), 6 (15%) and strong 3 (7.5%) in non-treated group.
IL-6 is valuable in the induction of liver cell regeneration. Correlation with biochemical assay and flow cytometric studies is recommended.
IL-6 is valuable in the induction of liver cell regeneration. Correlation with biochemical assay and flow cytometric studies is recommended.
To improve the understanding of epithelioid glioblastoma (E-GBM) and provide accurate basis for clinical diagnosis, treatment, and prognosis through the analysis of clinicopathologic characteristics, immunohistochemical expression, molecular characteristics, and prognosis of E-GBM.
The clinicopathologic characteristics of 33 cases of E-GBM in our hospital from January 2015 to September 2019 were analyzed retrospectively. Kaplan Meier method was used for survival analysis. Multivariate Cox regression analysis was used to screen the independent risk factors affecting the survival time of patients.
Among 33 patients with E-GBM, 16 were male and 17 were female. The age ranged from 9 to 67 years old, with the median age of 36 years old and the average age of 38 years old. The tumor size (calculated by the largest diameter) 1-6 cm, average size 3.5 cm. The ratio of smoking and non-smoking is 1716. All the tumors were located in the cerebral hemisphere, and 26 cases (78.79%) of brain MR showed that the tumors ion and 1p/19q co-deletion were not found in any cases.
E-GBM is a highly invasive and rare malignant nervous system tumor, with poor prognosis and lack of clinical specificity. Immunohistochemically, the higher expression of CK, GFAP and Ki67 proliferation index is more conducive to the diagnosis and differential diagnosis of E-GBM. Smoking, brain MR showing tumor invasion of cortex, TERT mutation, radiotherapy, and chemotherapy are independent risk factors affecting the prognosis (survival time) of patients.
E-GBM is a highly invasive and rare malignant nervous system tumor, with poor prognosis and lack of clinical specificity. Immunohistochemically, the higher expression of CK, GFAP and Ki67 proliferation index is more conducive to the diagnosis and differential diagnosis of E-GBM. Smoking, brain MR showing tumor invasion of cortex, TERT mutation, radiotherapy, and chemotherapy are independent risk factors affecting the prognosis (survival time) of patients.Aberrant expression of microRNAs may contribute to the initiation and progression of various types of human cancer and they may also constitute biomarkers for cancer diagnosis and treatment. However, the specific function of miR-194 in hepatocellular carcinoma (HCC), and the potential mechanism of its involvement in HCC were unclear. In the present study, we found that miR-194 inhibited CADM1 protein level expression by inhibiting mRNA translation of CADM1; the expression of CADM1 was low in liver cancer cells and tumor tissues, and the high expression of miR-194 was closely related to HCC. MiR-194 promoted proliferation, invasion, migration, and cell cycle progression of HCC cells, and such promotion effect was inhibited by CADM1. In addition, miR-194 may play a tumor-promoting action in a HCC xenograft tumor model. These results suggested that miR-194 may promote the occurrence and development of HCC by inhibiting CADM1. UK 5099 Therefore, miR-194 may be a promising novel therapy for diagnosis of hepatocellular carcinoma.
