Ping-Pong—Tumor and Host in Pancreatic Cancer Progression

Mu, Wei; Wang, Zhe; Zöller, Margot

doi:10.3389/fonc.2019.01359

Cited by 26 publications

(22 citation statements)

References 763 publications

(630 reference statements)

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“…[214] "In the healthy pancreas, PSCs are in the quiescent state and retain vitamin A-containing lipid droplets". [232,233] "PSC, quiescent in the healthy pancreas. During pancreatic injury, PSC develop a myofibroblast phenotype expressing αSMA1, actively proliferate and migrate.…”

Section: Favoring Quiescence (Cell Dormancy)-a Valid Therapeutic Stramentioning

confidence: 99%

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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Starting from the recent identification of CD36 and CD97 as a novel marker combination of fibroblast quiescence in lung during fibrosis, we aimed to survey the literature in search for facts about the separate (or concomitant) expression of clusters of differentiation CD36 and CD97 in either tumor- or pancreatic-cancer-associated cells. Here, we provide an account of the current knowledge on the diversity of the cellular functions of CD36 and CD97 and explore their potential (common) contributions to key cellular events in oncogenesis or metastasis development. Emphasis is placed on quiescence as an underexplored mechanism and/or potential target in therapy. Furthermore, we discuss intricate signaling mechanisms and networks involving CD36 and CD97 that may regulate different subpopulations of tumor-associated cells, such as cancer-associated fibroblasts, adipocyte-associated fibroblasts, tumor-associated macrophages, or neutrophils, during aggressive pancreatic cancer. The coexistence of quiescence and activated states in cancer-associated cell subtypes during pancreatic cancer should be better documented, in different histological forms. Remodeling of the local microenvironment may also change the balance between growth and dormant state. Taking advantage of the reported data in different other tissue types, we explore the possibility to induce quiescence (similar to that observed in normal cells), as a therapeutic option to delay the currently observed clinical outcome.

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Section: Favoring Quiescence (Cell Dormancy)-a Valid Therapeutic Stramentioning

confidence: 99%

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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“…These re-activated cells are nurtured by extracellular niches, which crosstalk and support positive cytoprotective signals such as Wnt and Notch [96,[141][142][143][144][145] . As Mu et al [15] described, tumor progression is driven by the cross-interaction between tumor cells, primarily CSCs and surrounding stromal cells as well as distant organs, in which tumor-derived extracellular vesicles (TEX) play a major and important role. Mu et al [15] report that the PCSC markers Tspan8, alpha6beta4, CD44v6, CXCR4, LRP5/6, LRG5, claudin, EpCAM, and CD133 participate in the metastatic cascade at different stages, often via PDAC TEX.…”

Section: Metastasis and Csc Populationmentioning

confidence: 99%

“…Another major problem limiting our ability to treat PDAC is the existence of rare populations of pancreatic cancer stem cells (PCSCs) or cancer-initiating cells in pancreatic tumors; PCSCs may represent sub-populations of tumor cells resistant to therapy which are most crucial for driving invasive tumor growth [9][10][11][12][13] . The PCSCs express a wide array of markers such as CD44, CD24, epithelial specific antigen (ESA), CD133, c-mesenchymal to epithelial transition (c-MET), CXCR4, PD2/Paf1, and ALDH1 [14][15][16][17] . These cells are capable of regenerating the cellular heterogeneity associated with the primary tumor when xenografted into mice [13][14][15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

“…The PCSCs express a wide array of markers such as CD44, CD24, epithelial specific antigen (ESA), CD133, c-mesenchymal to epithelial transition (c-MET), CXCR4, PD2/Paf1, and ALDH1 [14][15][16][17] . These cells are capable of regenerating the cellular heterogeneity associated with the primary tumor when xenografted into mice [13][14][15][16][17] . Therefore, the presence of PCSCs has prognostic relevance and influences the therapeutic response of tumors.…”

Section: Introductionmentioning

confidence: 99%

“…Metastasis is the major cause of high PDAC mortality. As Mu et al [15] recently described, tumor progression is driven by the cross-interaction between tumor cells, primarily cancer stem cells (CSCs) (or cancer-initiating cells) and surrounding stromal cells as well as distant organs, in which tumor-derived extracellular vesicles (TEX) play a major and important role. Mu et al [15] report that the PCSC markers Tspan8, alpha6beta4, CD44v6, CXCR4, LRP5/6, LRG5, claudin7, EpCAM, and CD133, participate in a metastatic cascade at various steps, often via PDAC CSC-TEX.…”

Section: Introductionmentioning

confidence: 99%

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Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis formation, and drug resistance

Safa

2020

JCMT

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Metastasis, tumor progression, and chemoresistance are the major causes of death in patients with pancreatic ductal adenocarcinoma (PDAC). Tumor dissemination is associated with the activation of an epithelial-tomesenchymal transition (EMT) process, a program by which epithelial cells lose their cell polarity and cell-tocell adhesion, and acquire migratory and invasive abilities to become mesenchymal stem cells (MSC). These MSCs are multipotent stromal cells capable of differentiating into various cell types and trigger the phenotypic transition from an epithelial to a mesenchymal state. Therefore, EMT promotes migration and survival during cancer metastasis and confers stemness features to particular subsets of cells. Furthermore, a major problem limiting our ability to treat PDAC is the existence of rare populations of pancreatic cancer stem cells (PCSCs) or cancer-initiating cells in pancreatic tumors. PCSCs may represent sub-populations of tumor cells resistant to therapy which are most crucial for driving invasive tumor growth. These cells are capable of regenerating the cellular heterogeneity associated with the primary tumor when xenografted into mice. Therefore, the presence of PCSCs has prognostic relevance and influences the therapeutic response of tumors. PCSCs express markers of cancer stem cells (CSCs) including CD24, CD133, CD44, and epithelial specific antigen as well as the drug transporter ABCG2 grow as spheroids in a defined growth medium. A major difficulty in studying tumor cell dissemination and metastasis has been the identification of markers that distinguish metastatic cancer cells from cells that are normally circulating in the bloodstream or at sites where these cells metastasize. Evidence highlights a linkage between CSC and EMT. In this review, The current understanding of the PCSCs, signaling pathways regulating these cells, PDAC heterogeneity, EMT mechanism, and links between EMT and metastasis in PCSCs

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The Role of ECM Remodeling, EMT, and Adhesion Molecules in Cancerous Neural Invasion: Changing Perspectives

Mukherjee

Wai

et al. 2022

Advanced Biology

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the nerve, is often used synonymously with the term PNI. It is important to differentiate between these two terms as the former can be determined using imaging techniques as it is apparent both clinically and radiologically whereas the latter is more of a histological diagnosis. [4,5] The presence of PNI in malignant neoplasms serves as a marker for poor clinical prognosis and higher mortality rate among patients. PNI is most commonly detected in the aggressive pancreatic, prostate, head and neck, colorectal and gastric cancers. [6] Importantly, in some of these cancers, PNI is the only method of metastasis and it can exist independently without vascular and lymphatic invasion. [2,7] In head and neck, the prevalence of PNI varies between 25-80% when compared to non-PNI cases, whereas in pancreatic cancer, 90% of patients exhibit PNI. [8,9] Furthermore, multiple population-based studies carried out over the years have reported no significant difference in the development of PNI based on age, gender, ethnicity/race or other demographic risk factors like smoking history. [10,11,12] Knowledge of the structure and composition of the nerve and its perineural niche is integral to understanding PNI. The peripheral nerves are primarily composed of Schwann cells, fibroblasts, blood vessels along with axon bundles. The Schwann cells are essential for the maintenance of the axons as well as for the production of myelin in the peripheral nervous system. [13] The innermost endoneurium is composed of the extracellular matrix (ECM), fibroblasts and collagen. It is a delicate layer of connective tissue which wraps around the axon and capillaries. The axons are supported and protected by endoneurial cells which are found in this layer. [14] The perineurium has one or more layers of flat epithelial-like cells which group the axons and endoneurium into fascicles. The presence of tight and adherens junctions (AJs) in the epithelial layer adds to the robustness of this layer thereby providing a permeable, but selective barrier between the surrounding axons and tissues. [15] And finally, the outermost epineurium consists of a dense connective tissue layer composed of elastin fibers and collagen which surround the entire nerve bundle. [16] Numerous blood vessels can also be found in this layer as they serve as the vascular supply to the nerve. Based on the structure of the nerve, Leibig et al. [17] combined past and present definitions and defined PNI as the presence of cancer cells along the nerves Perineural invasion (PNI) refers to the cancerous invasion of nerves. It provides an alternative route for metastatic invasion and can exist independently in the absence of lymphatic or vascular invasion.It is a prominent characteristic of specific aggressive malignancies where it correlates with poor prognosis. The clinical significance of PNI is widely recognized despite a lack of understanding of the molecular mechanisms underlying its pathogenesis. The interaction between the nerve and the cancer cells is the most pivotal PNI step which...

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Ping-Pong—Tumor and Host in Pancreatic Cancer Progression

Cited by 26 publications

References 763 publications

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis formation, and drug resistance

The Role of ECM Remodeling, EMT, and Adhesion Molecules in Cancerous Neural Invasion: Changing Perspectives

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