MicroRNA-128 acts as a suppressor in the progression of gastrointestinal stromal tumor by targeting B-lymphoma Mo-MLV insertion region 1

Introduction The critical role of microRNA-128 (miR-128) in gastrointestinal-related diseases has been documented. In the current study, we tried to clarify the specific role miR-128 in gastrointestinal stromal tumor (GIST) and the underlying mechanism. Methods Differentially expressed genes in GIST were identified following bioinformatics analysis. Then, expression patterns of miR-128 and B-lymphoma Mo-MLV insertion region 1 (BMI-1) in clinical tissue samples and cell lines were characterized, followed by validation of their correlation. GIST-T1 cells were selected and transfected with different mimic, inhibitor, or siRNA plasmids, after which the biological functions were assayed. Results We identified low miR-128 and high BMI-1 expression in GIST tissues of 78 patients and 4 GIST cell lines. Ectopic expression of miR-128 or silencing of BMI-1 suppressed the malignant potentials of GIST-T1 cells. As a target of miR-128, BMI-1 re-expression could partly counteract the suppressive effect of miR-128 on the malignancy of GIST-T1 cells. Conclusion Our study provided evidence that miR-128-mediated silencing of BMI-1 could prevent malignant progression of GIST, highlighting a promising anti-tumor target for combating GIST (AU)

MicroRNA-128 acts as a suppressor in the progression of gastrointestinal stromal tumor by targeting B-lymphoma Mo-MLV insertion region 1.

INTRODUCTION: The critical role of microRNA-128 (miR-128) in gastrointestinal-related diseases has been documented. In the current study, we tried to clarify the specific role miR-128 in gastrointestinal stromal tumor (GIST) and the underlying mechanism. METHODS: Differentially expressed genes in GIST were identified following bioinformatics analysis. Then, expression patterns of miR-128 and B-lymphoma Mo-MLV insertion region 1 (BMI-1) in clinical tissue samples and cell lines were characterized, followed by validation of their correlation. GIST-T1 cells were selected and transfected with different mimic, inhibitor, or siRNA plasmids, after which the biological functions were assayed. RESULTS: We identified low miR-128 and high BMI-1 expression in GIST tissues of 78 patients and 4 GIST cell lines. Ectopic expression of miR-128 or silencing of BMI-1 suppressed the malignant potentials of GIST-T1 cells. As a target of miR-128, BMI-1 re-expression could partly counteract the suppressive effect of miR-128 on the malignancy of GIST-T1 cells. CONCLUSION: Our study provided evidence that miR-128-mediated silencing of BMI-1 could prevent malignant progression of GIST, highlighting a promising anti-tumor target for combating GIST.

A preliminary study on the role of Bacteroides fragilis in stent encrustation.

OBJECTIVE: To preliminarily study the characteristics of bacterial flora distribution in the urine of ureteral stent encrustation patients as well as the relation between Bacteroides and stent encrustation. METHODS: Patients undergoing ureteral stenting were included in the study and divided into encrustation group and non-encrustation group based on the condition of stent encrustation. The urine of patients was collected to undergo 16s DNA test to compare the bacterial flora distribution characteristics of the two groups. The bacterial genus with highest abundance in the urine of encrustation group was used for animal experiment. A rat model with a foreign body in the bladder was created, in which the rats were injected with the aforesaid bacterial genus. A control group injected with normal saline was also formed. The incidence of foreign body tube encrustation between the two groups was compared. RESULTS: The urine collected from the patients in encrustation group contained a variety of bacteria, while dominant bacteria genera included g_Lactobacillus (23.1%), g_Bacteroides (18.8%) and g_norank_Bacteroides (17.1%). While the urine from the non-encrustation group was less diverse in bacteria flora, as the major bacteria genera were g_Escherichia-Shigella (32.2%), g_Enterococcus (24.9%) and g_Pseudomonas (18.2%). Bacteroidetes in the encrustation group were significantly higher, therefore Bacteroides fragilis in this genus was adopted for animal experiment, resulting in a higher incidence of foreign body tube encrustation in the bladder among rats. CONCLUSION: The present study enriches our knowledge about ureteral stent encrustation and reveals that the target regulation of urine bacteria is worth further research and clinical application.

MiRNA-409-3p enhances cisplatin-sensitivity of ovarian cancer cells by blocking the autophagy mediated by Fip200.

Background: Efficacy of chemotherapy for ovarian cancer (OC) is usually affected by various factors,especially the chemoresistance of ovarian cancer cells. Downregulation of miR-409-3p has been found in a variety of tumors. However, the role of miR-409-3p in chemo-resistant OC cells still remains unknown. The aim of this study was to investigate the effect of miR-409-3p on cisplatin-resistant OC cells and to elucidate the mechanism by which enhances cisplatin-sensitivity of OC cells. Methods: Expression of miR-409-3p in OC cells was assessed by qRT-PCR. MTS and clone formation assays were used to validate cell proliferation. Flow cytometry was performed for apoptosis analysis. Western blot assay was used to assess the alterations of signaling pathway related proteins. BALB/c nude mouse xenograft model was used to evaluate the role of miR-409-3p in cisplatin-resistant OC cells in vivo. Results: We found that miR-409-3p was apparently downregulated in the OC cells compared with normal ovarian cells. Results also showed that compared with the cisplatinsensitive cells, in cisplatin-resistant cells, miR-409-3p was decreased with an obvious increasing autophagic activity. In addition, based on the bioinformatics analysis, miR-409-3p was supposed to bind with Fip200. Our results demonstrated that in miR-409-3p overexpression cells, significant decreases were seen in protein expression of Fip200 and autophagic activity, which might be caused by conjugation between overexpressed miR-409-3p and 3'-UTR in Fip200 mRNA. Moreover, under the miR-409-3p overexpression, we found that cisplatin-sensitive and cisplatin-resistant ovarian cancer cells were more sensitive to the chemotherapeutics, which could be reversed by Fip2000. Further, we found that chemosensitivity in tumor cells was augmented by miR-409-3p overexpression, and Fip200 acted as a key link in interrupting the chemotherapy-induced autophagy. Conclusions: Results mentioned above revealed that miR-409-3p can ameliorate cisplatin-sensitivity of ovarian cancer cells through blocking the autophagy mediated by Fip200.

Relationship of cytopathology and cervical infection to outcome of in-vitro fertilization and embryo transfer.

OBJECTIVE: To determine whether a relationship exists between in-vitro fertilization and embryo transfer (IVF-ET) outcome and cervical infection or presence of human papillomavirus (HPV). METHOD: Cervical scrapes, digital colposcopies, and cervical biopsies were performed in 1044 Chinese women undergoing IVF for tubal infertility or, in their partners, abnormal semen. The pregnant (n=415) and nonpregnant (n=629) groups differed neither in clinical signs of cervical inflammation nor in rate of HPV detection. RESULTS: There were no associations between IVF-ET outcome and infection rate, degree of cytopathologic abnormality, detection of HPV, or results of digital colposcopy and cervical biopsy. Cytologic results did not correlate with any of the clinical parameters of IVF-ET. CONCLUSIONS: No association was found between IVF-ET outcome and cervical infection, cytopathologic result, HPV detection, or result from the colposcopy or biopsy. Extensive testing and treatment for cervical infection do not appear necessary in IVF-ET candidates.