Background: Primary small cell carcinoma (SCC) of the esophagus is a rare and aggressive tumor with poor prognosis. In this study, we report the clinicopathological characteristics of 21 cases of small cell carcinoma of the esophagus treated at the Cancer Center of Sun Yat-Sen University, with particular focus on the histologic and immunohistochemical findings.

Emodin-induced hepatotoxicity in vivo and in vitro has been gaining increasing attention. However, the exact molecular pathways underlying these effects remain poorly clarified. The aim of the present study was to evaluate the cytotoxic effect of emodin on HepaRG cells and to define the underlying mechanism. The results demonstrated that emodin evidently inhibited HepaRG cell growth in a dose- and time-dependent manner by blocking cell cycle progression in the S and G2/M phase and by inducing apoptosis. Emodin treatment also resulted in generation of reactive oxygen species (ROS), which abrogated mitochondrial membrane potential (MMP). The above effects were all suppressed by antioxidants, such as N-acetylcysteine (NAC). Further studies by western blot analysis howed that emodin upregulated p53, p21, Bax, cyclin E, cleaved caspase-3, 8 and 9, and cleaved poly(ADP-ribose)polymerase (PARP). However, the protein expression of Bcl-2, cyclin A and CDK2 was downregulated. Taken together, our results suggest that emodin induces apoptosis via the mitochondrial apoptosis pathway through cell cycle arrest and ROS generation in HepaRG cells.

The cytologic pickup of NPC was substantially lower than that obtained on biopsy. More importantly, NPIN was uncommon. Therefore, a screening test that depends on the collection of cells for the microscopic diagnosis of NPIN and NPC is unlikely to have a major impact on the incidence of NPC. Furthermore, obtaining a good cytologic specimen from the nasopharynx is not simple, and this further limits this technique for mass screening purposes. The concept of a cytologic test for NPC, similar to the Pap test for the prevention of uterine cervix cancer, has still to be realized.

Nasopharyngeal carcinoma (NPC) is one of the most common cancers in southern China

MicroRNAs play vital regulatory roles in various type of tumorigenesis. We aimed to explore the functional microRNAs that might play as therapeutic targets in hepatocellular carcinoma (HCC). In this study, our results revealed that microRNA-106b was significantly increased in HCC tumor tissues. However, miR-106b knockdown remarkably suppressed the growth and increased the apoptosis of Hub-7 HCC cells. Biological analysis indicated that miR-106b directly targeted toZinc finger and BTB domain-containing protein 7A (Zbtb7a) to regulate the apoptosis of Hub-7 cells. Extensively, Zbtb7a overexpression reversed Huh-7 cell apoptosis and growth in vitro. Furthermore, in vivo studies confirmed that miR-106b inhibition or Zbtb7a overexpression retarded the growth of Hub-7 xenograft tumor in nude mice. In conclusion, we provide the evidence for the regulatory role of miR-106b in HCC, which is causally linked to targeting of Zbtb7a. This study may provide miR-106b as a potential therapeutic strategy for HCC.

A mechanical stimulation plays a pivotal role in maintaining normal cartilage function. Our objective was to reveal the mechanism of action of the tension-sensitive molecule miR-455-5p in the degeneration of endplate chondrocytes and to identify whether the transforming growth factor beta (TGF-β)/SMAD signaling pathway has a regulatory effect on it. The expression profiles of members of the TGF-β/SMAD pathway, miR-455-5p, and RUNX2 were determined by microRNA microarray analysis, reverse transcription quantitative polymerase chain reaction, luciferase reporter assay, and Western blot analysis. Intermittent cyclic mechanical tension (ICMT) induced the degeneration of endplate chondrocytes without affecting their viability. The tension-sensitive molecule miR-455-5p specifically bound to RUNX2, a gene involved in the degeneration of endplate chondrocytes. Activation of the TGF-β/SMAD signaling pathway upregulated miR-455-5p expression and thus inhibited RUNX2 levels. Therefore, the TGF-β/SMAD signaling pathway inhibits the ICMT-induced degeneration of endplate chondrocytes by regulating the miR-455-5p/RUNX2 axis.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Rationale:Ectopic hepatocellular carcinoma (HCC) is a rare disease that mostly originates from an ectopic liver.Patient concerns:The patient was admitted with upper abdominal distention for 3 months, which aggravated after meal.Diagnoses:A contrast-enhanced computed tomography (CT) scan revealed multiple abdominal masses. After exploratory laparotomy and histological examination, the patient was diagnosed as ectopic HCC.Interventions:Exploratory laparotomy was performed for the purpose of diagnosis and treatment.Outcomes:The tumors were excised by surgery and his symptom of upper abdominal distention was disappeared. A second surgery was performed for tumor recurrence and the patient died with total survival time of 22 months.Lessons:Ectopic HCC was usually in clinically silent, unless compression symptoms or intra-abdominal bleeding appeared. It did not have any typical character features in CT or Magnetic resonance imaging, may present with multiple abdominal masses. Surgery resection seems to be one of the effective treatments for ectopic HCC, though it is detected with multiple tumors.