Objective:To investigate the effect of GBP3 on replication of adult T-lymphocytic leukemia virus type 1(HTLV-1).Methods:Expression of GBP3 in HTLV-1-infected HeLa cell and THP1 cell was detected by Western blot.The knock-down efficiency of siRNAs targeting GBP3 in HeLa and THP1 cells was evaluated by Western blot.Effects of GBP3 overexpression or knockdown on expression of HTLV-1 proviral transcripts Tax,px,HBZ,Gag,ENV,5'UTR,and viral proteins Tax,p19 were investigated by RT-qPCR and Western blot.GTPase-defective mutant of GBP3,GBP3K51A was constructed to explore whether the effects of GBP3 on HTLV-1 infection were dependent on its GTPase activity.Results:GBP3 expression was upregulated in HTLV-1 infected HeLa and THP1 cells.GBP3 overexpression decreased expression of HTLV-1 proviral transcripts and viral proteins,whereas the knockdown of GBP3 has the opposite effects.Overexpression of GBP3K51A increased expression of HTLV-1 proviral transcripts and viral proteins.Conclusion:HTLV-1 virus infection can induce expression of GBP3;overexpression of GBP3 inhibits virus replication and may depend on GTPase.

Objective:To investigate the effect of GBP3 on replication of adult T-lymphocytic leukemia virus type 1(HTLV-1).Methods:Expression of GBP3 in HTLV-1-infected HeLa cell and THP1 cell was detected by Western blot.The knock-down efficiency of siRNAs targeting GBP3 in HeLa and THP1 cells was evaluated by Western blot.Effects of GBP3 overexpression or knockdown on expression of HTLV-1 proviral transcripts Tax,px,HBZ,Gag,ENV,5'UTR,and viral proteins Tax,p19 were investigated by RT-qPCR and Western blot.GTPase-defective mutant of GBP3,GBP3K51A was constructed to explore whether the effects of GBP3 on HTLV-1 infection were dependent on its GTPase activity.Results:GBP3 expression was upregulated in HTLV-1 infected HeLa and THP1 cells.GBP3 overexpression decreased expression of HTLV-1 proviral transcripts and viral proteins,whereas the knockdown of GBP3 has the opposite effects.Overexpression of GBP3K51A increased expression of HTLV-1 proviral transcripts and viral proteins.Conclusion:HTLV-1 virus infection can induce expression of GBP3;overexpression of GBP3 inhibits virus replication and may depend on GTPase.

Purpose To investigate the expression of chiti-nase-3-like protein 1(CHI3L1)in esophageal squamous cell carcinoma(ESCC)and its correlations between CHI3L1 and molecules associated with the Wnt/β-catenin signaling pathway.Methods Paraffin-embedded tissue specimens from 119 ESCC patients and 60 normal esophageal tissues were retrospectively selected.Immunohistochemistry was used to detect the protein expression levels of CHI3L1 and Wnt/β-catenin signaling path-way related molecules in the above tissues,and the ectopic pro-tein expression levels of CHI3L1,TCF4,Cyclin D1,APC andβ-catenin in ESCC patients'tissues and normal esophageal tis-sues were compared.The survival of ESCC patients was followed up.Results Compared with normal esophageal tissue,the pos-itive rates of CHI3L1,TCF4,Cyclin D1 and β-catenin in ESCC were higher(63.0％,69.7％,68.1％and 67.2％,respec-tively),and the positive rates of APC were lower(41.2％).The expression levels of CHI3L1,TCF4,Cyclin D1 and β-cate-nin were positively correlated with each other(P＜0.05),but negatively correlated with APC(P＜0.05).CHI3L1 protein was associated with ESCC tumor volume,invasion depth,lymph node metastasis,and pTNM stage(P＜0.05).High expression of CHI3L1,TCF4,Cyclin D1 or abnormal high expression of β-catenin protein was associated with poor prognosis in ESCC pa-tients,suggesting shortened survival time(Log-rank=10.121,Log-rank=34.896,Log-rank=34.923,Log-rank=4.082,all P＜0.05).Conclusion In ESCC,the high expression of CHI3L1 is closely related to the activation of Wnt/β-catenin sig-naling pathway,suggesting that CHI3L1 may participate in the occurrence and development of ESCC through abnormal activa-tion of Wnt/β-catenin signaling pathway.

Purpose To investigate the expression of chiti-nase-3-like protein 1(CHI3L1)in esophageal squamous cell carcinoma(ESCC)and its correlations between CHI3L1 and molecules associated with the Wnt/β-catenin signaling pathway.Methods Paraffin-embedded tissue specimens from 119 ESCC patients and 60 normal esophageal tissues were retrospectively selected.Immunohistochemistry was used to detect the protein expression levels of CHI3L1 and Wnt/β-catenin signaling path-way related molecules in the above tissues,and the ectopic pro-tein expression levels of CHI3L1,TCF4,Cyclin D1,APC andβ-catenin in ESCC patients'tissues and normal esophageal tis-sues were compared.The survival of ESCC patients was followed up.Results Compared with normal esophageal tissue,the pos-itive rates of CHI3L1,TCF4,Cyclin D1 and β-catenin in ESCC were higher(63.0％,69.7％,68.1％and 67.2％,respec-tively),and the positive rates of APC were lower(41.2％).The expression levels of CHI3L1,TCF4,Cyclin D1 and β-cate-nin were positively correlated with each other(P＜0.05),but negatively correlated with APC(P＜0.05).CHI3L1 protein was associated with ESCC tumor volume,invasion depth,lymph node metastasis,and pTNM stage(P＜0.05).High expression of CHI3L1,TCF4,Cyclin D1 or abnormal high expression of β-catenin protein was associated with poor prognosis in ESCC pa-tients,suggesting shortened survival time(Log-rank=10.121,Log-rank=34.896,Log-rank=34.923,Log-rank=4.082,all P＜0.05).Conclusion In ESCC,the high expression of CHI3L1 is closely related to the activation of Wnt/β-catenin sig-naling pathway,suggesting that CHI3L1 may participate in the occurrence and development of ESCC through abnormal activa-tion of Wnt/β-catenin signaling pathway.

Objective: To investigate the clinicopathological features, diagnosis, and differential diagnosis of gallbladder sarcomatoid carcinoma. Methods: The clinical manifestations and the microscopic and immunohistochemical characteristics of six patients with gallbladder sarcomatoid carcinoma were analyzed with a follow-up period. Related literature was reviewed. Results:Immunohistochemical markers of gallbladder sarcomatoid carcinoma with spindle cell morphology were epithelial and mesenchymal positivity. Conclusion: Gallbladder sarcomatoid carcinoma could be firmly diagnosed by microscopic morphology and immunohistochemistry. Radical resection is currently used to treat such patients. However, more cases with longer follow-up period are needed to discover better treatments and improve the survival of these patients.