In this review, we summarise new insights into the fundamental cell biology of CD133 and discuss the involvement of CD133 in metastasis, metabolism, tumourigenesis, drug-resistance, apoptosis and autophagy.
Tumours with the infiltrating pattern were associated with high FIGO grade (P = 0.002), reduced ER and PR, and CD44 expression (P = 0.014, 0.026, and 0.030, respectively); those with a MELF pattern showed LN metastasis (P < 0.001), lymphovascular invasion (P = 0.011), and reduced ER, CD44, and CD133 expression (P = 0.036, 0.006, and 0.016, respectively).
In this review, we summarize the latest findings about the implication of CD133 in breast tumors, highlighting its role in tumor cells with a triple negative phenotype in which it directly regulates the expression of proteins involved in metastasis and drug resistance.
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.
While expression of CSC markers CD44, CD133 and aldehyde dehydrogenase 1 (ALDH1) in locoregional gastroesophageal cancer is known to be associated with poorer clinical outcomes, the significance of CSC marker expression in distal metastatic disease is unknown.
The data showed that the presence of VM and high ZEB1 expression was associated with higher Gleason score, TNM stage, and lymph node and distant metastases as well as with the expression of vimentin and CD133 in prostate cancer tissues.
At present, transmembrane glycoprotein CD133 highly expressed pancreatic cancer stem cells (PCSCs), with the features of chemotherapeutic/radiotherapeutic resistance and exclusive tumorigenic potential, are considered as the primary cause of metastasis and recurrence in pancreatic cancer, and therefore are an effective target in the disease treatment.
This trial showed the feasibility, controllable toxicities, and effective activity of CART-133 transfer for treating patients with CD133-postive and late-stage metastasis malignancies.
In this study, we focused on colon cancer with peritoneal metastasis and investigated the association between the expression of CD133, aldehyde dehydrogenase-1 (ALDH1) and leucine-rich repeating G-protein coupled receptor-5 (Lgr5), and disease prognosis.
Up-regulated p53, p16, p21, E-cadherin, CD80, MICA, MICB and Fas, together with down-regulated MMP-9, vimentin, VEGF, TGF-β, CD47 and CD133 in genome edited cells indicate that the genome editing system can inhibit cancerous cell growth, prevent tumor invasion and metastasis, reverse tumor-induced immune suppression, and inhibit cancer stemness.
Cytoplasmic and nuclear CD133 expression in CRAC cells and TMEs may play an important role in early CRAC carcinogenesis, while decreased CD133 nuclear expression in CRAC cells may contribute to CRAC metastasis.
High sensitive immune CD133 PLGA magnetic spheres platform is constructed to isolate and enrich lung cancer stem cells in order to study their biological characteristics, such as their proliferation, self-renewal and invasion and metastasis in vitro.
Altogether, CD133-induced TM4SF5 expression and function were important for liver cancer sphere growth and may be a promising target to block metastasis.
Distant metastasis and Enneking staging were significantly correlated with CD133-positive expression in osteosarcoma patients (P < 0.05), and the proportion of CD133-positive expression was high in both distant metastasis and Enneking staging.
Moreover, the overexpression of the miR‑181b‑5p in A549 cells and CD133+/CD326+ cells resulted in the downregulation of the E-cadherin and increased invasion and metastasis in vitro and in vivo.
The T allele of CD133rs3130 predicted a worse survival for gastric cancer patients receiving tumorectomy (hazard ratio: 1.28; 95% CI: 1.04-1.58; p = 0.020), independent from tumor node metastasis stage, vessel invasion and postoperational chemotherapy.