Donglin Sun

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.

Transcystic Approach with Micro-incision of the Cystic Duct and Its Confluence Part in Laparoscopic Common Bile Duct Exploration

BACKGROUND Laparoscopic transcystic common bile duct exploration has become a safe and ideal treatment of common bile duct stones. This study was designed to explore the clinical value of modified laparoscopic transcystic common bile duct exploration as a first line of treatment for patients with common bile duct stones. PATIENTS AND METHODS A retrospective, case-control study of clinically comparable groups of patients who underwent the laparoscopic transcystic approach with micro-incision of the cystic duct and its confluence part in common bile duct exploration (LTM-CBD) (n=110) and laparoscopic common bile duct exploration (LCBD) (n=100) under the care of one surgeon was performed. All clinical data were analyzed retrospectively. RESULTS There was no significant difference in terms of operation time between the two groups (P>.05). Postoperative hospital stay and abdominal drainage time were shorter in the LTM-CBD group than in the LCBD group (P<.05). Postoperative bile leakage was seen in 1 case (1 of 110) in the LTM-CBD group and 10 cases (10 of 100) in the LCBD group (P<.05). Twenty patients underwent T-tube drainage in the LCBD group, and primary closure was performed in the other patients; however, all cases in the LTM-CBD group underwent primary closure. The median follow-up was 12 months; 2 patients in the LCBD group who suffered from bile leakage presented with obstructive jaundice due to bile duct stenosis 6 months postoperatively. CONCLUSIONS LTM-CBD, which can avoid postoperative T-tube drainage, decrease complications, shorten hospitalization time, and enhance the existing quality, is a minimally invasive, safe, and effective treatment.

Long Noncoding RNA PVT1 Promotes EMT and Cell Proliferation and Migration Through Downregulating p21 in Pancreatic Cancer Cells

Background and Aim: Long noncoding RNA-plasmacytoma variant translocation 1 is identified to be highly expressed and exhibits oncogenic activity in a variety of human malignancies, including pancreatic cancer. However, little is known about the overall biological role and mechanism of plasmacytoma variant translocation 1 in pancreatic cancer so far. In this study, we investigated the effect of plasmacytoma variant translocation 1 on pancreatic cancer cell proliferation and migration as well as epithelial–mesenchymal transition. Methods: Pancreatic cancer tissue specimens and cell line were used in this study, with normal tissue and cell line acting as control. Results: It showed that plasmacytoma variant translocation 1 expression was significantly upregulated in pancreatic cancer tissues or cell line compared to normal groups. Plasmacytoma variant translocation 1 downregulation significantly inhibited zinc finger E-box-binding protein 1/Snail expression but promoted p21 expression, and it also inhibited the cell proliferation and migration. Additionally, p21 downregulation enhanced, and p21 overexpression repressed, zinc finger E-box-binding protein 1/Snail expression and cells proliferation in PANC-1 cells. However, p21 downregulation reversed the effect of plasmacytoma variant translocation 1 downregulation on zinc finger E-box-binding protein 1/Snail expression and cell proliferation and migration. Conclusion: Plasmacytoma variant translocation 1 promoted epithelial–mesenchymal transition and cell proliferation and migration through downregulating p21 in pancreatic cancer cells.

Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2

Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Although microRNAs are involving in the carcinogenesis and development of pancreatic cancer, little information is known regarding the role of miR-663b in pancreatic cancer. In this study, the expression of miR-663b in pancreatic cancer cells was down-regulated by hypermethylation in its putative promoter region, and overexpression of miR-663b repressed cell proliferation, invasion and migration, and induced apoptosis in pancreatic cancer cells. Bioinformatics analysis, luciferase report assay and rescue experiments showed that insulin-like growth factor 2 (IGF2) was a direct target of miR-663b. Results from clinical samples showed that the expression level of miR-663b correlated with the pathological grading, and the expression of miR-663b was down-regulated and was inversely correlated with IGF2 expression level in pancreatic cancer tissues. More importantly, the long non-coding RNA, HOX transcript antisense RNA (HOTAIR), was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter. Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. In summary, our studies demonstrated that miR-663b is epigenetically repressed by HOTAIR and exerts its tumor-suppressive function via targeting IGF2 in pancreatic cancer.

Rare case of omentum-wrapped abscess caused by a fish bone penetrating the terminal ileum

Accidentally ingested foreign bodies, for the most part, pass through the gastrointestinal tract, but can cause several complications. Perforation is rare, but can occur in any segment of the gastrointestinal tract. Intestinal perforations due to foreign bodies are rarely diagnosed preoperatively as clinical symptoms are non-specific and they can mimic other abdominal conditions. We describe a case of a 48-year-old patient who was admitted to the emergency room because of severe abdominal pain of 5 d duration. A computed tomography scan showed an undefined liquid collection involving a linear image 35 mm in size, suggestive of a foreign body. On laparotomy, an abscess containing a fish bone was resected. As fish bone ingestion is usually not remembered by the patient, the diagnosis can be delayed. The preoperative diagnosis is frequently acute abdomen of unknown cause. A low threshold of suspicion along with a good clinical history and radiological studies are extremely important in order to make a correct diagnosis.

Systematic review and meta-analysis of the prognostic value of CXCR2 in solid tumor patients

CXC chemokine receptor-2 (CXCR2) expression is associated with the prognosis of multiple cancers. We performed a meta-analysis to determine the association between the CXCR2 expression in tumor tissue and patient prognosis. We compiled related literature from PubMed, Embase, and Web of Science (last updated July 31, 2017). A total of 4012 patients with solid tumors from 21 studies were included to evaluate the association between CXCR2 and overall survival, recurrence-free survival, or disease-free survival. High CXCR2 expression was significantly associated with poor overall survival (pooled HR = 1.82; 95% CI = 1.63–2.03; P < 0.001), recurrence-free survival (pooled HR = 1.40; 95% CI = 1.21–1.62; P < 0.001), and disease-free survival (pooled HR = 1.89; 95% CI = 1.05–3.40; P = 0.033), especially in patients with digestive system neoplasms. Thus high CXCR2 expression in tumor tissue appears predictive of a poor prognosis in patients with solid tumors. Further studies will be required to determine whether CXCR2 blockade has a favorable effect on the prognosis of patients with cancer.

LncRNA DLX6-AS1 promoted cancer cell proliferation and invasion by attenuating the endogenous function of miR-181b in pancreatic cancer

BackgroundPancreatic cancer, one of the most aggressive malignancies, ranks the fourth cause of cancer-related death worldwide. Aberrantly expressed long non-coding RNAs (lncRNAs) functioned as oncogenes or tumor suppressors in pancreatic cancer. This study aimed to determine the expression of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in pancreatic cancer tissues and to explore the DLX6-AS1-related pathway in pancreatic cancer.Materials and methodsThe gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot assay. CCK-8 assay, colony formation assay and Transwell migration and invasion assays were used to examine cell proliferation, migration and invasion. Luciferase reporter assay was used to confirm the binding between DLX6-AS1and its potential targets. In vivo study used the mouse xenograft model to test the anti-tumor effect of DLX6-AS1 knockdown.ResultsThe high expression of DLX6-AS1 was observed in pancreatic cancer tissues, and high expression of DLX6-AS1 was positively correlated with larger tumor size, advanced TNM stage and lymph node metastasis. Knockdown of DLX6-AS1 dramatically impaired cancer cell proliferation, migration and invasion. MiR-181b was the downstream target of DLX6-AS1. Knockdown of miR-181b reversed the suppression of cell viability, migration and invasion abilities caused by DLX6-AS1 knockdown. MiR-181b was found to target Zinc finger E-box-binding homeobox 2 and to modulate epithelial-mesenchymal transition. Furthermore, DLX6-AS1 knockdown inhibited tumor growth and tumor metastasis in vivo.ConclusionCollectively, our data suggested that DLX6-AS1 promotes cancer cell proliferation and invasion by attenuating the endogenous function of miR-181b in pancreatic cancer.

MiR-216b inhibits pancreatic cancer cell progression and promotes apoptosis by down-regulating KRAS

Introduction Pancreatic cancer is a highly lethal malignancy with high invasion metastasis, which is difficult to diagnose and treat. MicroRNA-216b (miR-216b) plays an important role in many types of tumors. In this study, we explore how miR-216b affected human pancreatic cancer cell development by targeting KRAS. Material and methods Expression level of miR-216b and KRAS in tissue samples and cells were detected by RT-PCR and western blot. Immunohistochemical assay analysed the expressions of KRAS protein in tumor and adjacent tissues. The target relationship between miR-216b and KRAS was validated by dual-luciferase reporter assay. Pancreatic cancer cell proliferation, migration, invasion and apoptosis abilities of cells transfected with miR-216b mimics and KRAS-siRNA, Panc-1 were detected by MTT assay, transwell assay and flow cytometry assay respectively. Prognosis of patients with different expression levels of miR-216b and KRAS were analyzed by Kaplan-Meier survival analysis and Cox proportional hazards regression model. Results The expression of miR-216b in pancreatic cancer tissue and cell line was down-regulated (p < 0.01), while KRAS expression was up-regulated (p < 0.01) compared with adjacent normal tissues. Both the expressions of miR-216b and KRAS have a strong influence on prognosis of the pancreatic cancer patients (p = 0.024 and p = 0.017). The dual-luciferase reporter assay verified that miR-216b directly targeted KRAS in pancreatic cancer cells. Overexpression of miR-216b reduced the expression of mRNA and protein of KRAS (p = 0.013 and p = 0.003), but silencing KRAS had no effect on miR-216b expression (p = 0.706). By silencing KRAS or up-regulation of miR-216b could suppress cell proliferation, migration and invasion of pancreatic cancer cells and promote apoptosis. Conclusions MiR-216b might inhibit pancreatic cancer cell progression and stimulate apoptosis by silencing KRAS.

Case of spontaneous splenic rupture caused by ectopic pregnancy in the spleen

Splenic ectopic pregnancy refers to the implantation of the oosperm in the spleen. If not diagnosed early, the results of this phenomenon would almost certainly be splenic rupture, which is equivalent to the spontaneous rupture of the spleen. If the patient has no history of trauma, it is difficult to diagnose this condition early and an explicit diagnosis is often obtained by exploratory laparotomy. We report the case of a 27‐year‐old woman who was admitted to the hospital due to abdominal pain and hemorrhagic shock. Under emergency general anesthesia, gynecologist and hepatobiliary surgeons worked together to conduct an exploratory laparotomy. It was confirmed during surgery that this was ectopic pregnancy in the spleen, which caused rupture of the spleen. Hence, splenectomy was conducted. Postoperative recovery was good.