Girdin Research Articles

Expression and clinical significance of CD133 and Girdin in children with nephroblastoma

Objective To explore the expression of CD133 and Girdin in children with nephroblastoma. Methods The nephroblastoma tissues and adjacent non-cancerous tissues in 58 patients with nephroblastoma treated in Guangdong Woman and Children Hospital and Affiliated Hospital of Guangdong Medical University and confirmed pathologically from April 2011 to March 2019 were collected. The expression of CD133 and Girdin in nephroblastoma tissues and adjacent non-cancerous tissues was detected by immunohistochemistry. Results The positive expression rate of CD133 in nephroblastoma tissues was significantly higher than that in adjacent non-cancerous tissues (46.55% vs. 17.24%, t=11.469, P<0.01). The positive expression rate of CD133 was related with histology grade and TNM stage of nephroblastoma (respectively, t=4.254, 4.244, P<0.05). The positive expression rate of Girdin in nephroblastoma tissues was significantly higher than that in adjacent non-cancerous tissues (70.69% vs. 43.10%, t=8.999, P<0.01). The positive expression rate of Girdin was related with histology grade, diameter of tumor, TNM stage and lymph node metastasis of nephroblastoma (respectively, t=4.411, 6.307, 4.172, 6.355, P<0.05). Conclusion The CD133 and Girdin were highly expressed in nephroblastoma tissues, and CD133 and Girdin can be used as diagnostic index to evaluate the prognosis of patients with nephroblastoma. Key words: CD133; Girdin; Children; Nephroblastoma

Girdin regulates the migration and invasion of pancreatic cancer cell Aspc-1

Girdin regulates the migration and invasion of pancreatic cancer cell Aspc-1

Expression of Girdin gene in hepatocellular carcinoma cells and inhibition of its expression on biological characteristics

Objective To investigate the Expression of Girdin gene in hepatocellular carcinoma cells and inhibition of its expression on proliferation and apoptosis of cells. Methods The expression of Girdin protein in HL-7702 normal liver cells and liver cancer Huh7, HepG2, MHCC97H, HCCLM3 cells were detected by Western blotting; Girdin small interfering RNA (siRNA) were transfected into HCCLM3 cells by Lipofectamine™2000, and set the negative control group and blank control group, the expression of proliferation cell nuclear antigen (Ki-67), cysteinyl aspartate-specific protease (Caspase)-3, B cell lymphoma/leukemia-2 associated X protein (bax), phosphorylation of janus kinase 2 (JAK2) and signal transducer and activators of transcription 3 (STAT3) protein were detected by Western blotting; cells activity were detected by cell counting kit-8 (CCK-8) assay in transfected 24, 48 and 72 h; cell apoptosis were detected by flow cytometry in transfected 48 h. Results The expression of Girdin in HepG2 (0.355±0.043), HCCLM3 (0.599±0.068), MHCC97H (0.462±0.055), Huh7 (0.378±0.049) HCC cells was significantly higher than that in normal liver cells HL-7702 (0.112±0.013, PHepG2=0.001; PHCCLM3=0.000; PMHCC97H=0.000; PHuh7=0.001); cell activity in Girdin-siRNA group in 24 h (0.247±0.032), 48 h (0.477±0.043) and 72 h (0.666±0.073) were significantly lower than the control group (0.385±0.045), (0.711±0.068), (0.936±0.096), the apoptosis rate (16.18±1.38)% in 48 h was significantly higher than the blank control group (1.87±0.39)%, the expression of Ki-67 (0.162±0.019), p-JAK2 (0.096±0.011) and p-STAT3 (0.057±0.009) protein were significantly lower than the control group (0.626±0.073), (0.170±0.021), (0.145±0.018), the expression of Caspase-3 (0.257±0.032) and bax (0.279±0.032) protein were significantly higher than the control group (0.120±0.013, 0.135±0.015) (PKi-67=0.000; Pp-JAK2=0.006; Pp-STAT3=0.002; PCaspase-3=0.002; Pbax=0.002). Conclusion Girdin gene is highly expressed in hepatocellular carcinoma cells and inhibiting of Girdin expression by RNA interference can reduce the proliferation and induce apoptosis of cancer cells by down regulating the JAK2/STAT3 signal. Key words: Girdin gene; Hepatocellular carcinoma; Proliferation; Apoptosis; Janus kinase 2/signal transducer and activators of transcription 3 signaling pathway

Expression of Girdin in brain tissues of Alzheimer's disease

To investigate the expression of Girdin and its significance in Alzheimer's disease (AD). Fifty-nine autopsy cases from Department of Pathology, Beijing Hospital from January 1988 to December 2013, including 35 AD cases and 24 non-AD cases as control. Girdin and amyloid β-protein (Aβ) expression was evaluated immunohistochemically by EnVision method. The correlation between Girdin and Aβ was analyzed. Girdin expression was localized in the nucleus and/or cytoplasm. The expression rates of Girdin were 20.0% (7/35) in the AD group and 83.3% (20/24) in the non-AD group, respectively. The difference was significant (Yates's correction for continuity χ(2)=20.527, P<0.05). Girdin expression and Aβ deposition also correlated significantly (P<0.05). Girdin shows reduced expression in AD, and is correlated positively with Aβ deposition. This suggests that Girdin may play an important role in the occurrence and development of AD.

Expression of Girdin protein and its correlation with tumor's invasion and metastasis in colorectal carcinoma

Objective To investigate the expression of Girdin protein in colorectal carcinoma, and explore its relationship with clinical characteristics and tumor's invasion and metastasis. Methods Eightyfour cases of colorectal carcinoma specimens, 40 cases of colorectal adenoma and 30 cases of tumoradjacent mucosal tissues were collected, and the expression levels of Girdin protein were detected by immumihistochemistry Envision two-step methods. The relationship between Girdin expression and clinicopathological characteristics was analyzed. Results The positive expression rate of Girdin protein in colorectal carcinoma was 42.9%, which was significantly higher than that in tumor- adjacent mucosa, adenoma with low grade inraepithelial neoplasia(LGIN)and adenoma with high grade inraepithelial neoplasia(HGIN)respectively(χ2= 15.752,P 0.05). Follow- up study results showed that the five- year overall survival rate in Girdin negative group(83.3%)was higher than that in Twist positive group(21.7%)significantly(P<0.01). Conclusion Girdin protein expression is up- regulated in colorectal carcinoma and correlated with tumor's invasion and metastasis. Key words: Colorectal neooplasms; Girdin; Neooplasms metasasis

Effect of Girdin on apoptosis of human glioblastoma cells

Objective To investigate the effects of Girdin on apoptosis of LN229 glioblastoma cells by Girdin small RNA interference (RNAi) technology and the molecular mechanisms. Methods Girdin expression was knocked down in LN229 glioblastoma cells by Girdin small interfering RNA (siRNA). The expression levels of Girdin, cytochrome C (Cyt-C) and Bad proteins in glioblastoma LN229 cells were detected by Western blotting. Stable clones were used to measure cells survival ratio by proliferation assay and methyl thiazol tetrazolium ( MTT) assay. Flow Cytometry was used to examine the content of Cyt-C in siGirdin/LN229 and scr/LN229. 20 male athymic Nu/Nu mice were subcutaneously injected with siGirdin/LN229 or scr/LN229 cells respectively to study the growth of tumor in each group. Results Western blotting showed that the expression of Girdin was decreased significantly. The relative intensity of Cyt-C and Bad in siGirdin/LN229 cells was 3. 57 ±0.43 and 4. 78 ± 1. 03 respectively, and the relative intensity of Cyt-C and Bad in scr/LN229 was 1. 13 ±0. 11,1. 78 ±0.20 respectively (P＜0. 05). The mean fluorescence density of Cyt-C in siGirdin/LN229 and scr/LN229 by flow cytometry was 12 531.00 ±1412. 98 and 183. 67 ±41. 55 respectively. Meanwhile, the number of siGirdin/LN229 cells was obviously decreased as compared with control group in proliferation assay. The number of siGirdin/LN229 cells on the 6th day was (15. 08 ± 1.17) x 104, and that of scr/LN229 cells was (53. 93 ± 6. 26) x 104. MTT assay revealed the survival rate of siGirdin/LN229 on the 5th day was (323. 15 ± 57. 01) % , and that of scr/LN229 was (640.67 ±59.66)%, P＜0.05. Additionally, the volume of xenograft tumors in siGirdin/LN229 group was decreased significantly as compared with control group. The volume of xenograft tumors in siGirdin/LN229 group was (36.42 ±2. 00) mm3, and that in scr/LN229 group was (262. 42 ±24. 12) mm3 at the 7.5th week. Conclusion Girdin plays a critical role in apoptosis of glioblastoma cells. Inhibition of Girdin by siRNA could promote the apoptosis of glioblastoma LN229 cells through the release of Cyt-C from mitochondria and up-regulation of Bad. Key words: Glioma; Girdin; Apoptosis

DISC1 drives development through girdin

DISC1 drives development through girdin