Carcinogenetic initiation contributed by EpCAM+ cancer cells in orthotopic HCC models of immunocompetent and athymic mice
Objective: The expression of the epithelial cell adhesion molecule (EpCAM) is correlated with a poor prognosis, and treatment failure early tumor recurrence of hepatocellular carcinoma (HCC) patients. The tumor microenvironment determine the fate of tumor cancer stem cell-start (CSC); However, very limited studies that seek to evaluate CSC tumorigenesis in the liver microenvironment. Here, we have systematically investigated the role of EpCAM + cancer cells in tumor initiation in an orthotopic model of HCC.
Result: control mice and mice with bland steatosis failed to develop tumors. In rats with steatohepatitis, EpCAM + CSC has demonstrated a significant improvement in terms of the ability of tumor initiation and growth, as compared to non-CSC EpCAM- inoculation (p <0.005). For Hep3B inoculation, high-EpCAM group has demonstrated tumor growth was significantly higher compared with EpCAM-Low (p <0.005). For HepG2 inoculation, both high EpCAM and EpCAM-Low group confirmed the same tumor incidence and growth.
Methods: Diet-induced compromised microenvironments fatty liver was established to mimic the clinical and patient non-alcoholic steatohepatitis (NASH) and the ability of tumorigenic cells Hepa1-6 evaluated. CSC is enriched by the cultural round and labeled with copGFP for EpCAM + CSC and with mCherry for non-CSC. FACS-sorted cells were inoculated into the left lobe of the liver, and the tumor growth was monitored by high frequency ultrasound. The Hep3B and HepG2 cell subpopulations in terms of EpCAM-low and high EpCAM was evaluated in an orthotopic model of athymic mice.
Conclusion: NASH micro EpCAM + CSC began promoting tumorigenesis in a mouse model of immunocompetent. EpCAM showed differential expression of different tumor biology in athymic mouse model.
Carcinogenetic initiation contributed by EpCAM+ cancer cells in orthotopic HCC models of immunocompetent and athymic mice
Multimodal imaging of stem cell-derived bulge of hair follicles in a mouse model of traumatic brain injury.
traumatic brain injury (TBI) is a devastating event therapy is currently limited. Stem cell transplantation may lead to recovery of function through different mechanisms, such as the replacement of cells through differentiation, angiogenesis stimulation and support for micro environment. Adult hair follicle bulge-derived stem cells (HFBSCs) has a capacity of neuronal differentiation, it is easy to harvest and relatively immune-privileged, which makes them potential candidates for autologous stem cell-based therapies.
In this study, we apply the in vivo multimodal techniques of optical and magnetic resonance imaging to investigate the behavior of HFBSCs mouse in a mouse model of TBI. HFBSCs stated Luc2 and copGFP and examined for their differentiation capacity in vitro. Furthermore, HFBSCs transduced, loaded with ferumoxytol, transplanted next TBI lesions (cortical region) in nude mice, two days after the injury. Brains were fixed for immunohistochemistry 58 days after transplantation. Luc2- and copGFP-express, HFBSCs ferumoxytol-loaded show sufficient differentiation potential of neurons in the brain lesions revealed vitro.
Bioluminescence HFBSCs survival and magnetic resonance imaging identified their localization in the field of transplantation. Immunohistochemistry showed that the transplanted cells stained for nestin and Neurofilament protein (NF-Pan). Cells also expressed laminin and fibronectin extracellular matrix but the mass was not detected.
pCDH-MSCV-MCS-EF1-Puro cDNA Cloning and Expression Vector
Description: Clone your gene of interest into this AAV Expression Vector, then co-transfect along with AAV packaging vectors into a packaging host cell line such as 293AAV.
Description: The ANPRA/Aequorin expression vector is designed to co-express human atrial natriuretic peptide receptor A (ANPRA, also called natriuretic peptide receptor A/guanylate cyclase A) and jellyfish (Aequorea victoria) Aequorin in mammalian cells.
Description: GFP-Rac1 Expression Vector Set contains 3 vectors: Rac wild type, T17N dominant negative mutant, and Q61L constitutively active mutant. Each vector also contains a GFP reporter sequence.
Description: GFP-RhoA Expression Vector Set contains 3 vectors: RhoA wild type, T19N dominant negative mutant, and Q63L constitutively active mutant. Each vector also contains a GFP reporter sequence.
Description: GFP-Cdc42 Expression Vector Set contains 3 vectors: Cdc42 wild type, T17N dominant negative mutant, and Q61L constitutively active mutant. Each vector also contains a GFP reporter sequence.
Description: Active Rac1 Expression Vector Set contains 3 vectors expressing different constitutively active mutants of Rac1: Q61L, Q61L/F37A, and Q61L/Y40C.
Description: Clone your gene of interest into this AAV Expression Vector, then co-transfect along with AAV packaging vectors into a packaging host cell line such as 293AAV.
Description: Clone your gene of interest into this AAV Expression Vector, then co-transfect along with AAV packaging vectors into a packaging host cell line such as 293AAV.
Description: Clone your gene of interest into this AAV Expression Vector, then co-transfect along with AAV packaging vectors into a packaging host cell line such as 293AAV.
Description: Clone your gene of interest into this AAV Expression Vector, then co-transfect along with AAV packaging vectors into a packaging host cell line such as 293AAV.
Description: Active H-Ras Expression Vector Set contains 3 vectors expressing different constitutively active mutants of H-Ras: V12, V12S35, and V12C40.
Description: Baculovirus cassette vector pAc-l-CH3 for the expression of human, humanized or chimeric IgG(lambda) in insect cells and secretion of assembled antibodies into the supernatant.
After 58 days, ferumoxytol could be detected in HFBSCs in parts of the brain tissue. These results indicate that HFBSCs able to survive after transplantation of the brain and suggest that these cells may undergo differentiation towards neural cell lineages, which support the potential use for cell-based therapy for TBI.
