61 Interactions Between Breast Cancer Stem Cells and their Niche Govern Metastatic Colonization of the Lung

Malanchi, Ilaria; Santamaria-Martínez, Albert; Susanto, Evelyn; Peng, Hua; Lehr, Hans‐Anton; Delaloye, J.-F.; Huelsken, Joerg

doi:10.1016/s0959-8049(12)70765-7

Cited by 4 publications

(4 citation statements)

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“…Instead, various stimuli including prominent inflammatory signaling via transcription factors NF-kB and STAT3 in cancer cells can drive their stemness, increase the proportion of CSCs among the tumor cell population and thereby elevate the invasive potential (Kryczek et al, 2014;Schwitalla et al, 2013a). The same effects can originate from mesenchymal-cancer interactions (Del Pozo Martin et al, 2015;Malanchi et al, 2011), and mesenchymal and stromal cells can be regulated by inflammatory signals.…”

Section: Inflammation Tumor Progression and Metastasismentioning

confidence: 99%

Inflammation and Cancer: Triggers, Mechanisms, and Consequences

2019

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Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here, we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression, and metastasis. We discuss how tumor-promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis, or tissue repair and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatiotemporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for further development of anti-cancer therapies.

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Section: Inflammation Tumor Progression and Metastasismentioning

confidence: 99%

Inflammation and Cancer: Triggers, Mechanisms, and Consequences

2019

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“…Metastasis, although infrequent [1], remains the leading cause of cancer-related mortality (90%) in patients [2].Over the past decades, various mechanisms of metastasis have been revealed, including cancer cell intrinsic factors that endow the cells with sufficient motility/invasiveness [3][4][5], and the supportive microenvironment within the primary tumor as well as the metastatic sites that favors cancer cell survival, outgrowth and escape from immunosurveillance [6][7][8], yet so far cancer metastasis can neither be prevented at the early stage in high-risk patients nor eradicated during overt metastasis, highlighting an unmet medical need to develop new treatment regimens that effectively block metastatic cascade locally and systemically.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Extracellular Traps: A New Player in Cancer Metastasis and Therapeutic Target

Yang

Liu

2021

J Exp Clin Cancer Res

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Neutrophil Extracellular Traps (NETs) are neutrophil-derived extracellular scaffolds, which typically consist of fibrous decondensed chromatins decorated with histones and granule proteins. Initially discovered as a host defence mechanism of neutrophil against pathogens, they have also been implicated in the progression of sterile inflammation-associated diseases such as autoimmune disease, diabetes, and cancer. In this review, we highlight and discuss the more recent studies on the roles of NETs in cancer development, with a special focus on cancer metastasis. Moreover, we present the strategies for targeting NETs in pre-clinical models, but also the challenging questions that need to be answered in the field.

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“…For example, in the tumor microenvironment, ECM proteins can directly promote oncogenic transformation and metastasis, and influence stromal cell behaviors, such as angiogenesis and inflammation, resulting in formation of a protumorigenic microenvironment (9). In distant organs, ECM proteins have been shown to contribute to metastatic niches that maintain cancer cell stemness and enable cancer cell outgrowth (10,11). The matrisome is defined as both core ECM proteins, including collagens, glycoproteins and proteoglycans, and ECM-associated proteins, such as ECM regulators (e.g., proteases and their inhibitors, cross-linking agents), ECM-affiliated proteins (e.g., mucins, lectins, annexins), and secreted factors (e.g., growth factors, chemokines; ref.…”

Section: Introductionmentioning

confidence: 99%

Cancer Cell–Derived Matrisome Proteins Promote Metastasis in Pancreatic Ductal Adenocarcinoma

et al. 2020

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The prognosis for pancreatic ductal adenocarcinoma (PDAC) remains poor despite decades of effort. The abundant extracellular matrix (ECM) in PDAC comprises a major fraction of the tumor mass and plays various roles in promoting resistance to therapies. However, nonselective depletion of ECM has led to poor patient outcomes. Consistent with that observation, we previously showed that individual matrisome proteins derived from stromal cells correlate with either long or short patient survival. In marked contrast, those derived from cancer cells correlate strongly with poor survival. Here, we studied three cancer cell-derived matrisome proteins that are significantly overrepresented during PDAC progression, AGRN (agrin), SER-PINB5 (serine protease inhibitor B5), and CSTB (cystatin B). Using both overexpression and knockdown experiments, we demonstrate that all three are promoters of PDAC metastasis. Furthermore, these proteins operate at different metastatic steps. AGRN promoted epithelial-to-mesenchymal transition in primary tumors, whereas SERPINB5 and CSTB enhanced late steps in the metastatic cascade by elevating invadopodia formation and in vivo extravasation. All three genes were associated with a poor prognosis in human patients and high levels of SERPINB5, secreted by cancer cells and deposited in the ECM, correlated with poor patient prognosis. This study provides strong evidence that cancer cell-derived matrisome proteins can be causal in promoting tumorigenesis and metastasis and lead to poor patient survival. Therefore, compared with the bulk matrix, mostly made by stromal cells, precise interventions targeting cancer cell-derived matrisome proteins, such as AGRN, SERPINB5, and CSTB, may represent preferred potential therapeutic targets.Significance: This study provides insights into the biological roles of cancer cell-derived matrisome proteins in PDAC and supports the notion that these proteins are protumorigenic and better therapeutic targets.

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61 Interactions Between Breast Cancer Stem Cells and their Niche Govern Metastatic Colonization of the Lung

Cited by 4 publications

References 0 publications

Inflammation and Cancer: Triggers, Mechanisms, and Consequences

Inflammation and Cancer: Triggers, Mechanisms, and Consequences

Neutrophil Extracellular Traps: A New Player in Cancer Metastasis and Therapeutic Target

Cancer Cell–Derived Matrisome Proteins Promote Metastasis in Pancreatic Ductal Adenocarcinoma

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