The purpose of the study is to identify the Cancer Stem Cells (CSCs) and to determine their expression profiles in different pathological stages of liver cancer by using multiple markers Methods: In this study, the expression profiles of CD133 and CD13, along with those of stem cell markers Oct4 and SOX2, were analyzed using immunohistochemistry and immunoblotting to clarify the character of CSCs in different stages of liver cancer.
Cluster of differentiation 133 (CD133) is a transmembrane glycoprotein that has been reported as a marker of cancer stem cells or cancer-initiating cells in various cancers.
Moreover, a RNA aptamer against a cancer stem cell (CSC) marker, CD133 was covalently attached to the carboxyl groups of DEX to produce a CD133-PCAD-DMSN@DOX.
Cancer stem cells were identified by CD133 expression levels detected by immunochemistry, real-time polymerase chain reaction, western blot, and flow cytometry.
The CD133 transmembrane protein is a well-recognized stem cell marker that has been used to isolate putative cancer stem cell populations from gastric cancers (GCs).
Low CD8⁺ T Cell Infiltration and High PD-L1 Expression Are Associated with Level of CD44⁺/CD133⁺ Cancer Stem Cells and Predict an Unfavorable Prognosis in Pancreatic Cancer.
Cancer stem cell biomarkers CD51 and CD133 positive populations were reduced and telomerase activities were decreased with the reduced STAT3 binding to hTERT promoters.
Furthermore, the reduction in the amount of CD133-expressing cancer stem-like cell subpopulation was observed following DETA/NO treatment of cells, which was associated with a decreased expression of stem cell markers and attenuation of cell invasiveness.
In this study, the effect of tetrandrine on the proliferation of CD133-positive (CD133) Hep-2 cells was examined to characterize its potential for targeting cancer stem cells in laryngeal cancer.The stem cell population of Hep-2 cells was isolated by magnetic-activated cell sorting against CD133, treated with different concentrations of tetrandrine, and assessed for cell cycle progression, proliferation, and migration.
Both HOXA11-AS silencing and HOXA11 overexpression suppressed the self-renewal, proliferation, migration, and tumorigenicity of HCC stem cells in vivo, as evidenced by the decreased expression of cancer stem cell surface markers (CD133 and CD44) and stemness-related transcription factors (Nanog, Sox2, and Oct4).
As CD133+ CSC population is responsible for radio- and chemo-resistance, which finally determines the cancer recurrences and metastases, identifying the molecular mechanisms which regulate the CD133+ CSC population represents a major target for cancer research.
This study aimed to investigate the effect of CD133 on the proliferation and migration of glioma cells and expressions of genes related to cancer stem cells/tumor stem cells (CSC/TSC) as well as their in-vivo oncogenicity.
In this study, it was attempted to determine: 1) CD133 function; 2) the role of CD133 in cancer; 3) CD133 regulation; 4) the therapeutic role of CD133 in cancers.
Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells.
Compared to the 2D monolayer culture, glioblastoma cells cultured on these 3D Ca-alginate scaffolds showed reduced cell proliferation, increased tumor spheroid formation, enhanced expression of cancer stem cell genes (CD133, SOX2, Nestin, and Musashi-1), and improved expression of differentiation potential-associated genes (GFAP and β-tubulin III).
Since CD133 is a putative cancer stem cell marker for different cancers, associated with decreased survival, we examined resistance of patient-derived CD133(+) and CD133(-) melanoma cells to MAPK inhibitors.