Upregulation of S100A10 in metastasized breast cancer stem cells

Watanabe, Takashi; Nishimura, Tatsunori; Hayashi, Takanori; Kono, S; Tsuchida, Hitomi; Hirata, Munetsugu; Kijima, Yuko; Takao, Shintaro; Okada, Seiji; Suzuki, Motoshi; Imaizumi, Kazuyoshi; Kawada, Kenji; Minami, Hironobu; Gotoh, Noriko; Shimono, Yohei

doi:10.1111/cas.14659

Cited by 18 publications

(13 citation statements)

References 49 publications

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“…They observed no change in tumor growth at the primary sites but did observe inhibition of metastatic capacity. Our work, therefore, was consistent with other studies showing the importance of S100A10 in breast cancer [ 177 , 193 , 194 , 195 ].…”

Section: Role Of the Anxa2/s100a10 Heterotetramer In Cancersupporting

confidence: 93%

“…After several months the orthotopic tumors and the metastases in the lung tissues are analyzed. These investigators observed that S100A10 was one of the most highly upregulated proteins in the metastasized cancer cells compared to the tumor cancer cells [ 193 ]. These researchers then performed constitutive knockdown of S100A10 in MDA-MB-231 cells followed by orthotopic transplantation in the mammary fat.…”

Section: Role Of the Anxa2/s100a10 Heterotetramer In Cancermentioning

confidence: 99%

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The ANXA2/S100A10 Complex—Regulation of the Oncogenic Plasminogen Receptor

2021

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The generation of the serine protease plasmin is initiated by the binding of its zymogenic precursor, plasminogen, to cell surface receptors. The proteolytic activity of plasmin, generated at the cell surface, plays a crucial role in several physiological processes, including fibrinolysis, angiogenesis, wound healing, and the invasion of cells through both the basement membrane and extracellular matrix. The seminal observation by Albert Fischer that cancer cells, but not normal cells in culture, produce large amounts of plasmin formed the basis of current-day observations that plasmin generation can be hijacked by cancer cells to allow tumor development, progression, and metastasis. Thus, the cell surface plasminogen-binding receptor proteins are critical to generating plasmin proteolytic activity at the cell surface. This review focuses on one of the twelve well-described plasminogen receptors, S100A10, which, when in complex with its regulatory partner, annexin A2 (ANXA2), forms the ANXA2/S100A10 heterotetrameric complex referred to as AIIt. We present the theme that AIIt is the quintessential cellular plasminogen receptor since it regulates the formation and the destruction of plasmin. We also introduce the term oncogenic plasminogen receptor to define those plasminogen receptors directly activated during cancer progression. We then discuss the research establishing AIIt as an oncogenic plasminogen receptor-regulated during EMT and activated by oncogenes such as SRC, RAS, HIF1α, and PML-RAR and epigenetically by DNA methylation. We further discuss the evidence derived from animal models supporting the role of S100A10 in tumor progression and oncogenesis. Lastly, we describe the potential of S100A10 as a biomarker for cancer diagnosis and prognosis.

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Section: Role Of the Anxa2/s100a10 Heterotetramer In Cancersupporting

confidence: 93%

Section: Role Of the Anxa2/s100a10 Heterotetramer In Cancermentioning

confidence: 99%

The ANXA2/S100A10 Complex—Regulation of the Oncogenic Plasminogen Receptor

2021

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“…Moreover, overexpression of p11 in human breast cancer cell line MDA MB 231 resulted in increased organoid-forming, invasive, and metastatic capacity, whereas loss of p11 resulted in a reduced number of organoids. Interestingly, these studies also established that p11 upregulated stem cellrelated genes, such as OCT4, SOX2, and NANOG, in the organoids, suggesting a novel function of p11 in promoting metastasis of CSC [211]. Lu et al, observed that chemotherapy (paclitaxel or carboplatin)-induced p11 is mediated by HIF-1, which further promotes epigenetic modulation and transcriptional activation and expression of pluripotency factors, such as NANOG, SOX2 and KLF4, in breast cancer cell lines.…”

Section: Involvement Of P11 In Biological Processes and Cancermentioning

confidence: 95%

Plasmin and Plasminogen System in the Tumor Microenvironment: Implications for Cancer Diagnosis, Prognosis, and Therapy

Bharadwaj

Holloway

Miller

et al. 2021

Cancers

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The tumor microenvironment (TME) is now being widely accepted as the key contributor to a range of processes involved in cancer progression from tumor growth to metastasis and chemoresistance. The extracellular matrix (ECM) and the proteases that mediate the remodeling of the ECM form an integral part of the TME. Plasmin is a broad-spectrum, highly potent, serine protease whose activation from its precursor plasminogen is tightly regulated by the activators (uPA, uPAR, and tPA), the inhibitors (PAI-1, PAI-2), and plasminogen receptors. Collectively, this system is called the plasminogen activation system. The expression of the components of the plasminogen activation system by malignant cells and the surrounding stromal cells modulates the TME resulting in sustained cancer progression signals. In this review, we provide a detailed discussion of the roles of plasminogen activation system in tumor growth, invasion, metastasis, and chemoresistance with specific emphasis on their role in the TME. We particularly review the recent highlights of the plasminogen receptor S100A10 (p11), which is a pivotal component of the plasminogen activation system.

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“…It was clarified that smoothened (Smo) up-regulated the level of STAT3, accordingly promoting BCSCs maintenancerelated liver metastasis in BC [61]. Besides, S100A10 was discovered to participate in enhancing BCSCs maintenance-related liver metastasis [62]. In addition, combined treatment with JAK2 inhibitors (ruxolitinib and pacritinib) and SMO inhibitors (vismodegib and sonidegib) could served as a suppressor in BCSCs maintenance-related liver metastasis by simultaneously blocking JAK2-STAT3 and SMO-GLI1/tGLI1 signaling pathways [63].…”

Section: Bcscs-related Liver Metastasismentioning

confidence: 99%

Heterogeneity of BCSCs contributes to the metastatic organotropism of breast cancer

Wang

et al. 2021

J Exp Clin Cancer Res

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Breast cancer is one of the most-common female malignancies with a high risk of relapse and distant metastasis. The distant metastasis of breast cancer exhibits organotropism, including brain, lung, liver and bone. Breast cancer stem cells (BCSCs) are a small population of breast cancer cells with tumor-initiating ability, which participate in regulating distant metastasis in breast cancer. We investigated the heterogeneity of BCSCs according to biomarker status, epithelial or mesenchymal status and other factors. Based on the classical “seed and soil” theory, we explored the effect of BCSCs on the metastatic organotropism in breast cancer at both “seed” and “soil” levels, with BCSCs as the “seed” and BCSCs-related microenvironment as the “soil”. We also summarized current clinical trials, which assessed the safety and efficacy of BCSCs-related therapies. Understanding the role of BCSCs heterogeneity for regulating metastatic organotropism in breast cancer would provide a new insight for the diagnosis and treatment of advanced metastatic breast cancer.

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Upregulation of S100A10 in metastasized breast cancer stem cells

Cited by 18 publications

References 49 publications

The ANXA2/S100A10 Complex—Regulation of the Oncogenic Plasminogen Receptor

The ANXA2/S100A10 Complex—Regulation of the Oncogenic Plasminogen Receptor

Plasmin and Plasminogen System in the Tumor Microenvironment: Implications for Cancer Diagnosis, Prognosis, and Therapy

Heterogeneity of BCSCs contributes to the metastatic organotropism of breast cancer

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