A rare case of concurrent intrahepatic splenosis and pancreatic adenocarcinoma following splenectomy.

We present an extremely rare case of intrahepatic splenosis (IHS). On admission and examination, the patient was diagnosed with hepatocellular carcinoma and postoperative injury or inflammatory lesions of the pancreas, based on image analysis. Postoperative histopathology showed that the lesions of the liver and diaphragm were of splenic origin, and the pancreatic lesion was identified as a moderately differentiated adenocarcinoma.

Exosome-Based Theranostics for Liver Diseases.

Exosomes are small extracellular vesicles that can be secreted by any type of cell, released into almost all biological fluids, and extracted from anybody fluid such as blood, urine, saliva, and amniotic fluid. The theranostic role of exosome in liver diseases has been widely studied in recent years. In this review, we briefly introduce the biological characteristics of exosomes and then focus on the theranostics of exosomes in liver diseases, specifically gene delivery associated with liver diseases.

Targeted activation of reverses hepatic fibrosis via exosome-mediated delivery of CRISPR/dCas9-SAM system.

Hepatic fibrosis is one of the most common conditions worldwide, and yet no effective antifibrotic therapy is available. This study aimed to reverse hepatic fibrosis via exosome-mediated delivery of the CRISPR/dCas9-SAM system. The authors constructed a modified-exosome delivery system targeting hepatic stellate cells (HSCs), and constructed the CRISPR/dCas9-SAM system inducing HSCs convert into hepatocyte-like cells and .

CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges.

Hepatic fibrosis is a pathological reaction of tissue damage and repair caused by various pathogenic factors acting on liver. At present, there is no effective anti-fibrotic specific therapy. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system is a new generation of gene editing technology.

Hepatic Stellate Cell: A Double-Edged Sword in the Liver.

Hepatic stellate cells (HSCs) are located in the space of Disse, between liver sinusoidal endothelia cells (LSECs) and hepatocytes. They have surprised and excited hepatologists for their biological characteristics. Under physiological quiescent conditions, HSCs are the major vitamin A-storing cells of the liver, playing crucial roles in the liver development, regeneration, and tissue homeostasis.

Hepatic stellate cell reprogramming via exosome-mediated CRISPR/dCas9-VP64 delivery.

Hepatic stellate cells (HSCs) play a crucial role in the progression of liver fibrosis, which can be considered as the specific therapeutic target of anti-fibrotic treatment. Targeted induction of HSCs to hepatocytes via delivery of clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (dCas9) system holds promise for hepatic fibrosis treatment. Our study here revealed that CRISPR/dCas9-VP64 system encapsulated in AML12 cell-derived exosomes could efficiently and successfully be delivered into the HSCs.

Post-transcriptional up-regulation of PDGF-C by HuR in advanced and stressed breast cancer.

Breast cancer is a heterogeneous disease characterized by multiple genetic alterations leading to the activation of growth factor signaling pathways that promote cell proliferation. Platelet-derived growth factor-C (PDGF-C) is overexpressed in various malignancies; however, the involvement of PDGF-C in breast cancers and the mechanisms underlying PDGF-C deregulation remain unclear. Here, we show that PDGF-C is overexpressed in clinical breast cancers and correlates with poor prognosis.

HuR: a promising therapeutic target for angiogenesis.

Multiple angiogenic factors and inhibitors are becoming potential therapeutic targets for ischemia diseases and cancer. Posttranscriptional regulation through the untranslated region of mRNA is emerging as a critical regulating level in nearly all the biological processes. As a kind of RNA binding proteins, HuR plays important role in augmenting the hypoxic or inflammatory signal, stabilizing the resultant angiogenic factors and promoting the proliferation and migration of endothelial cells.