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Targeted Therapy for Cancer Stem Cells
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Rama Krishna Nimmakayala, Saswati Karmakar, Garima Kaushik, Sanchita Rauth, Srikanth Barkeer, Saravanakumar Marimuthu, Moorthy P. Ponnusamy
CD44 like CD133 is a transmembrane glycoprotein that facilitates cell-cell and cell to ECM interactions and is found to be overexpressed in several cancers. Study on patient-derived AML blasts has revealed that treatment with anti-human CD44 monoclonal antibody to stimulate myeloid differentiation alters stem cell fate, and impedes homing to the microenvironment niche [81]. Doxorubicin and cyclophosphamide, in combination with anti-human CD44 antibody, have shown synergistic anti-cancerous activity in breast cancer and prevent relapse of aggressive breast cancer [82]. Another study by Tang et al. [83] used a mouse IgG1 anti-human CD44 receptor antibody on MiaPaCa-2 cells and was shown to inhibit CSCs tumorsphere formation, also decreasing tumor growth, metastasis and recurrence in pancreatic cancer xenografted nude mice.
Angiogenesis in Hematological Malignancies
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Alida C. Weidenaar, Hendrik J. M. de Jonge, Arja ter Elst, Evelina S. J. M. de Bont
Vasculature of tumors is predominantly formed by angiogenesis, but can also be developed by postnatal vasculogenesis: the formation of new blood vessels from EPCs that differentiate into mature ECs (55). These EPCs are defined as CD34+/CD133+/CD177+/KDR+ cells, which originate in the bone marrow. EPC recruitment and mobilization have been positively correlated with an increase in VEGFA levels; in response to increased VEGFA levels at the site of the tumor, an increase in circulating EPCs was seen (Fig. 2) (56–58). Moreover, CD133+ cells differentiate into mature-type adherent ECs and abolish the CD133 expression in response to VEGFA (59). While it has been shown that these bone marrow–derived EPCs contribute to the tumor vessel formation by incorporating into the endothelium (60), a second group of proangiogenic cells was described; this population, rather than the EPCs, was thought to home in specifically to the tumor and was characterized by the expression of CD45+, TEK+, CD31−, and CD11b+ (61). Inhibition of those cells resulted in a significant reduction of tumor angiogenesis and growth. Finally, the existence of a third proangiogenic population was suggested, which is characterized by CD34, CXCR4 and FLT1 expression and is implicated in the initiation and formation of metastases (62).
Resistance Mechanisms of Tumor Cells
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
The above-mentioned factors are able to reprogram a cell back to the state of their origin. Expression of SOX2 and OCT4 factor together with KLF4 and c-MYC seems to be sufficient, as it is the standard technology to create iPS cells (Takahashi and Yamanaka, 2006). These factors steer a small genetic program that allow to reset chromatin back to “start,” like in a fertilized egg cell. Tumor cells are using the same or similar mechanism to gain “immortality.” Every tumor type has a certain set of such proteins which can be found in the isolated cancer stem cells fraction (e.g., CD133 in different tumor entities). CD133 is upregulated by IGF2 and promote cancer stemness (Xu et al., 2018). However, CD133 is also an important tumor migration marker that can be secreted by tumor cells via exosomes to other tumor cells. This vesicular transfer of CD133 to non-stem cells looks like a “transplantation strategy” of the tumor to generate more stem cells (Yang et al., 2018). CD133 plays also an important role for stemness in many brain tumors.
Impact of Aluminium phthalocyanine nanoconjugate on melanoma stem cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Bridgette Mkhobongo, Rahul Chandran, Heidi Abrahamse
Most solid tumour cases evaluated have a lower occurrence of CSCs in their microenvironments. According to xenotransplantation in immune-deficient gene-modified mice, the incidence and proliferation of single human Melanoma CSCs in Melanoma tumours can reach 27% [12]. Some of the prime Malignant Melanoma antigenic stem cell markers have been recognised as CD20 [13], CD133 [14] ,ABCB5 [11], CD271 [15] ,and ALDH1A [16]. Prominin-1, also known as CD133, is a pentaspan transmembrane protein found in plasma membrane protrusions, including microvilli play a crucial role in membrane receptor communication [17]. Subsequent to implantation into immune-deficient mice, CD133 expressing CSCs demonstrated self-rejuvenation capability and the potential to produce a histologically comparable tumour [18]. The expression of CD133 has been linked to chemo-resistance and improved metastatic capacity in a variety of human malignancies [19], despite the mechanisms underlying this being unknown.
The shifting paradigm of colorectal cancer treatment: a look into emerging cancer stem cell-directed therapeutics to lead the charge toward complete remission
Published in Expert Opinion on Biological Therapy, 2021
Jessica Kopenhaver, Madison Crutcher, Scott A. Waldman, Adam E. Snook
Also named AC133 or prominin-1, CD133 is a transmembrane glycoprotein expressed in hematopoietic cells, endothelial cells, and neuroepithelial cells [60]. Although the exact function of CD133 is not yet understood, it is speculated to be involved in membrane topology organization or cell–cell interactions [61]. Expression of the transmembrane glycoprotein has been noted in a variety of cancers, including those originating from the colon, brain, ovaries, liver, prostate, and pancreas [62]. CD133+ CRC cells show stem cell characteristics, such as self-renewal and multi-directional differentiation potential [46]. These cells also are resistant to radiation and chemotherapy [63]. Indeed, CD133 positivity has been considered a specific marker of primary colorectal CSCs, and its expression is associated with the degree of differentiation and tumor size in adenomas [62]. A number of studies in the past have used CD133 as their main colorectal CSC biomarker, finding that CD133+ cells have higher tumorigenicity than CD133- cells, and have better colony-forming efficiency [45,63]. However, several publications have cast doubt on the credibility of CD133 as an exclusive stem cell marker. One study found that ALDH+/CD133- cells were still tumorigenic, and others have stated that CD133- intestinal cells show a more aggressive cancerous phenotype than their CD133+ counterparts [64–67]. Given this data, CD133 may still be used as a colorectal CSC marker, but should not be relied upon for CSC isolation.
CD133: beyond a cancer stem cell biomarker
Published in Journal of Drug Targeting, 2019
Amir Barzegar Behrooz, Amir Syahir, Syahida Ahmad
The precise physiological function of CD133 is not clear, but its ubiquitous presence indicates its importance. As discussed above, it is found in plasma membrane protrusions that contain cholesterol-rich membrane microdomains, and these protrusions are associated with the presence of prominosomes. Prominosomes are extracellular vesicles that are attached to the plasma membrane that contains prominin proteins and are often thought of as being organisers of the plasma membrane [4,35]. One of the most common uses for CD133 is in the identification and isolation of stem cells from body tissues, not only in normal cells such as brain [36], kidney [37], prostate [18], bone marrow [19], liver [6,20], sarcoma [20], pancreas [20] and skin [20] but also in cancer cells from brain [21], liver [11,20], pancreas [20], lung [20], skin [20], sarcoma [20], prostate [20,38], colon [36] and ovary [36]. In other words, CD133 is a biomarker that can be used to identify stem cells in both normal and cancerous tissues.