Liver cancer stem cell dissemination and metastasis: uncovering the role of NRCAM in hepatocellular carcinoma.

Background: Liver cancer stem cells (LCSCs) play an important role in hepatocellular carcinoma (HCC), but the mechanisms that link LCSCs to HCC metastasis remain largely unknown. This study aims to reveal the contributions of NRCAM to LCSC function and HCC metastasis, and further explore its mechanism in detail.

Methods: 117 HCC and 29 non-HCC patients with focal liver lesions were collected and analyzed to assess the association between NRCAM and HCC metastasis.

Sub-micron microparticles with tunable fluorescence emission obtained via co-self-assembly of amidoximed polymeric ligands and lanthanide ions.

Lanthanide coordinating polymeric microparticles have witnessed increasing research interests during the past decades due to their versatile morphology and tunable fluorescent properties. Herein, we have synthesized an amidoximed block copolymer containing aromatic backbone and pendent amidoxime as well as carboxyl groups, which has been employed as the ligand to sensitize the intrinsic fluorescence emission of lanthanide ions of Tb and Eu. Furthermore, the lanthanide coordinating polymeric microparticles showing tunable green and red emission fluorescence have been prepared via the emulsion confinement co-self-assembly of amidoximed polymeric ligands with Tb and Eu.

Atp8a1 deletion increases the proliferative activity of hematopoietic stem cells by impairing PTEN function.

Purpose: The eukaryotic cell plasma membrane contains several asymmetrically distributed phospholipids, which is maintained by the P4-ATPase flippase complex. Herein, we demonstrated the biological effects and mechanisms of asymmetrical loss in hematopoietic stem cells (HSCs).

Methods: An Atp8a1 knockout mouse model was employed, from which the HSC (long-term HSCs and short-term HSCs) population was analyzed to assess their abundance and function.

TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN.

We report herein that TSPAN32 is a key node factor for Philadelphia (Ph) leukemia pathogenesis. We found that TSPAN32 expression was repressed by BCR-ABL and ectopic TSPAN32 expression upon Imatinib treatment inhibited the proliferation of Ph cell lines. Tspan32 overexpression significantly prevented BCR-ABL induced leukemia progression in a murine model and impaired leukemia stem cell (LSC) proliferation.

HDAC I/IIb selective inhibitor Purinostat Mesylate combined with GLS1 inhibition effectively eliminates CML stem cells.

Purinostat Mesylate (PM) is a novel highly selective and active HDAC I/IIb inhibitor, and the injectable formulation of PM (PMF) based on the compound prescription containing cyclodextrin completely can overcome PM's poor solubility and improves its stability and pharmacokinetic properties. Here, we showed that PM effectively repressed the survival of Ph leukemia cells and CD34 leukemia cells from CML patients . studies demonstrated that PMF significantly prevented BCR-ABL(T315I) induced CML progression by restraining leukemia stem cells (LSCs), which are insensitive to chemotherapy and responsible for CML relapse.

The suppressive functions of Rora in B lineage cell proliferation and BCR/ABL1-induced B-ALL pathogenesis.

RORA plays an important role in regulating circadian rhythms, inflammation, metabolism and cellular development. Herein, we explore the roles of in B cell proliferation and differentiation, as well as in Ph B-ALL. By using Mx-1-Cre mice, was deleted in hematopoietic cells post Pipc induction.

Targeting glutaminase1 and synergizing with clinical drugs achieved more promising antitumor activity on multiple myeloma.

Multiple myeloma (MM) pathogenesis remains incompletely understood and biomarkers predicting treatment response still remain lacking. Here we describe the rational mechanisms of combining targeting glautaminase1 (GLS1) with other chemo-reagents for MM treatment. Gls1 is highly expressed cMYC/KRAS12V-drived plasmacytoma (PCT) cells.