Regulation of cancer stem cell properties by CD9 in human B-acute lymphoblastic leukemia

Yamazaki, Hiroto; Xu, C. Wilson; Naito, Motohiko; Nishida, Hayato; Okamoto, Toshihiro; Ghani, Farhana Ishrat; Iwata, Satoshi; Inukai, Takeshi; Sugita, Kanji; Morimoto, Chikao

doi:10.1016/j.bbrc.2011.04.098

Cited by 51 publications

(32 citation statements)

References 22 publications

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“…CD9 protein expression is detected in a majority of normal tissues, but its expression is negative or weak in the gall bladder, liver, and lymphoid tissues (http://www.proteinatlas.org/). However, it is a useful marker to identify CSCs in human B-acute lymphoblastic leukemia cells (B-ALL), and is linked to several signaling pathways involved in regulating the CSC properties of B-ALL (126). CD166 (activated leukocyte cell adhesion molecule) is a type I membrane glycoprotein, which is a member of the immunoglobulin superfamily.…”

Section: Csc Surface Markers Expressed On Both Stem Cells and Normal mentioning

confidence: 99%

Cancer stem cell surface markers on normal stem cells

2017

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The cancer stem cell (CSC) hypothesis has captured the attention of many scientists. It is believed that elimination of CSCs could possibly eradicate the whole cancer. CSC surface markers provide molecular targeted therapies for various cancers, using therapeutic antibodies specific for the CSC surface markers. Various CSC surface markers have been identified and published. Interestingly, most of the markers used to identify CSCs are derived from surface markers present on human embryonic stem cells (hESCs) or adult stem cells. In this review, we classify the currently known 40 CSC surface markers into 3 different categories, in terms of their expression in hESCs, adult stem cells, and normal tissue cells. Approximately 73% of current CSC surface markers appear to be present on embryonic or adult stem cells, and they are rarely expressed on normal tissue cells. The remaining CSC surface markers are considerably expressed even in normal tissue cells, and some of them have been extensively validated as CSC surface markers by various research groups. We discuss the significance of the categorized CSC surface markers, and provide insight into why surface markers on hESCs are an attractive source to find novel surface markers on CSCs.

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Section: Csc Surface Markers Expressed On Both Stem Cells and Normal mentioning

confidence: 99%

Cancer stem cell surface markers on normal stem cells

2017

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“…For the sake of achieving a deeper insight into the CSC properties in CD9-expressing cells of B-ALL cell lines, the authors performed detailed assays and showed that CD9 regulates the cancer-related genes, such as TEL/AML1 and E2A/PBX1, in B-ALL and significantly affects Src family proteins involved in diverse biological functions. Furthermore, CD9 + cells of B-ALL exhibited drug-resistance (60). Notably, CD9, as a cancer stem cell marker, may also be applied to human malignant mesothelioma (61).…”

Section: Cd9 and Cancer Stem Cells (Cscs)mentioning

confidence: 99%

Role of motility-related protein-1 in promoting the development of several types of cancer (Review)

Han

Huang

2014

Oncology Letters

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Motility-related protein-1 (CD9), a type of cell surface glycoprotein comprising a four-pass transmembrane domain that forms multimeric complexes with other cell surface proteins, belongs to the tetraspanins family. From previous studies, we know that CD9 is considered to function primarily as a progression and metastasis suppressor in a variety of cancers, including breast, non-small cell lung colon and myeloma. However, an expanding body of literature has shown the contradictory outcome that tetraspanin CD9 is also vital in promoting cancer progression in several types of cancer. This review summarizes the recent studies on CD9 and concludes that it does not always act as a progression and metastasis suppressor. Conversely, in specific cases, CD9 may promote tumor progression through the following three aspects: Facilitating tumor cell transmigration, increasing tumor cell motility and hastening the growth of some cancers. In addition, CD9 appears to be an important marker of cancer stem cells in certain types of tumor.

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“…This poorer outcome could be due to increased asymmetric cell divisions in the PROX1 labeled cell populations within these tumors [152]. Asymmetric cell division has been proposed to contribute to therapy resistance in the slow replicating stem-like TPC populations of other cancer types including gastric cancer and acute lymphoblastic leukemia [153, 154]. Therefore, a similar mechanism may confer poorer outcome to brain tumor patients with malignancies which contain a proportion of asymmetrically dividing stem-like TPC.…”

Section: Tumor Propagating Cellsmentioning

confidence: 99%

Asymmetric cell division: Implications for glioma development and treatment

Lewis

Petritsch²

2013

Translational Neuroscience

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Glioma is a heterogeneous disease process with differential histology and treatment response. It was previously thought that the histological features of glial tumors indicated their cell of origin. However, the discovery of continuous neuro-gliogenesis in the normal adult brain and the identification of brain tumor stem cells within glioma have led to the hypothesis that these brain tumors originate from multipotent neural stem or progenitor cells, which primarily divide asymmetrically during the postnatal period. Asymmetric cell division allows these cell types to concurrently self-renew whilst also producing cells for the differentiation pathway. It has recently been shown that increased symmetrical cell division, favoring the self-renewal pathway, leads to oligodendroglioma formation from oligodendrocyte progenitor cells. In contrast, there is some evidence that asymmetric cell division maintenance in tumor stem-like cells within astrocytoma may lead to acquisition of treatment resistance. Therefore cell division mode in normal brain stem and progenitor cells may play a role in setting tumorigenic potential and the type of tumor formed. Moreover, heterogeneous tumor cell populations and their respective cell division mode may confer differential sensitivity to therapy. This review aims to shed light on the controllers of cell division mode which may be therapeutically targeted to prevent glioma formation and improve treatment response.

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Regulation of cancer stem cell properties by CD9 in human B-acute lymphoblastic leukemia

Cited by 51 publications

References 22 publications

Cancer stem cell surface markers on normal stem cells

Cancer stem cell surface markers on normal stem cells

Role of motility-related protein-1 in promoting the development of several types of cancer (Review)

Asymmetric cell division: Implications for glioma development and treatment

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