ABSTRACT
BACKGROUND: Biliary dilatation is a rare disease involving intrahepatic and extrahepatic biliary tract abnormalities. With the development of imaging technology, an increasing number of special cases have been diagnosed, which poses a challenge to the traditional classification method. CASE PRESENTATION: A 50-year-old woman was admitted to the hospital due to right upper quadrant pain for more than 10 days. The patient had previous episodes of similar symptoms, which were relieved after symptomatic treatment at a local community hospital. After the symptoms developed, she underwent a computed tomography scan at the local hospital, which showed biliary dilatation; thus, she was referred to our hospital for further treatment. After admission, her magnetic resonance imaging examination also suggested biliary dilatation, but abnormal signals were found in her duodenum. First, a duodenal diverticulum was considered. Later, endoscopic ultrasonography was conducted, and the results suggested that the dilated biliary tract had herniated into the duodenum. This type of lesion is most closely classified as a Todani type III lesion. The patient finally underwent choledochectomy and RouxenY hepaticojejunostomy, and the postoperative pathology was consistent with our preoperative diagnosis. The patient was followed up for approximately 2 years, and no obvious postoperative complications were found. CONCLUSIONS: The manifestations of this case are relatively rare and involve one of the undiscussed categories of the Todani classification system; therefore, this case has certain clinical value. Moreover, there is no report similar to this experience in the previous literature.
Subject(s)
Bile Ducts, Extrahepatic , Biliary Tract Surgical Procedures , Duodenal Diseases , Dilatation , Duodenal Diseases/diagnostic imaging , Duodenal Diseases/etiology , Duodenal Diseases/therapy , Female , Humans , Middle Aged , ProlapseABSTRACT
BACKGROUND: Pancreatic cancer (PC) is a highly lethal malignancy worldwide. Our previous study indicated that overexpression of USP34 could promote tumor growth in PC cells. Therefore, this study aimed to further investigate the role of USP34 during the tumorigenesis of PC. METHODS: The level of USP34 in PANC-1 and MiaPaCa-2 cells transfected with USP34-shRNAs was detected by RT-qPCR. Moreover, transwell migration and Annexin V/PI analysis were conducted to detect cell migration and apoptosis, respectively. RESULTS: In this study, downregulation of USP34 markedly inhibited proliferation and migration, and induced apoptosis in PANC-1 cells. Moreover, silencing of USP34 obviously downregulated the levels of PRR11 and p-p38 in PANC-1 cells. An in vivo study in nude mice bearing PANC-1 cell xenografts confirmed these results. CONCLUSION: Downregulation of USP34 could inhibit proliferation and migration in PANC-1 cells via inhibiting PRR11, and inactivating p38 MAPK signaling. Therefore, USP34 might be a potential therapeutic target for the treatment of PC.
ABSTRACT
Autophagy plays a protective role in colorectal carcinoma. Arginine ADP-ribosyltransferase 1 (ART1) is an important mono-ADP-ribose transferase, which has been shown to play a role in biological processes such as proliferation and invasion of cancer cells. Interestingly, the role of ART1 in the regulation of autophagy is still not clear. We examined effects of overexpression or knockdown of ART1 by lentiviral transfection on starvation-induced autophagy of colon carcinoma CT26 cell lines in vivo and in vitro. The formation of autophagosome was detected by electron microscopy, acridine orange staining and expression of LC3 B. The molecular contributions of ART1 in regulation of autophagy were detected by western blotting or by co-immunoprecipitation. Additionally, inhibitors were used to study further the signaling pathway of ART1 in the regulation of autophagy. CCK8 assay, plate cloning assay, soft agar assay, examination of subcutaneous transplanted carcinoma in BALB/c mice, flow cytometry and Hoechst33342 staining were used to assess survival and apoptotic ability when starvation-induced autophagy modulated by ART1 was inhibited by 3-MA. Overexpression of ART1 promoted starvation-induced autophagy, which related to increases in the expression of Rac1, NF-κB, PARP-1, LKB1 and p-AMPK and a decrease in the expression of p-P70S6K. Correspondingly, knockdown of ART1 caused the opposite effects. ART1 also interacted with integrin α7. Additionally, changes of protein expressions were further validated following inhibition of Rac1 and PARP-1 in the starvation-induced ART1-GFP CT26 cells. Inhibition of ART1-stimulated starvation-induced autophagy restrained the growth and promoted apoptosis. ART1 is thus relevant in starvation-induced autophagy in colorectal carcinoma and may play essential roles in therapeutic anticancer strategies.
