scholarly journals Isoliquiritin Apioside Suppresses in vitro Invasiveness and Angiogenesis of Cancer Cells and Endothelial Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Aeyung Kim ◽  
Jin Yeul Ma
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
In Vitro Invasiveness

scholarly journals The Functional Implications of Endothelial Gap Junctions and Cellular Mechanics in Vascular Angiogenesis

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 237 ◽  
Author(s):  
Takayuki Okamoto ◽  
Haruki Usuda ◽  
Tetsuya Tanaka ◽  
Koichiro Wada ◽  
Motomu Shimaoka
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Gap Junctions ◽  
Gap Junction ◽  
Cancer Cells ◽  
Tumor Development ◽  
Tube Formation ◽  
Cellular Mechanics

Angiogenesis—the sprouting and growth of new blood vessels from the existing vasculature—is an important contributor to tumor development, since it facilitates the supply of oxygen and nutrients to cancer cells. Endothelial cells are critically affected during the angiogenic process as their proliferation, motility, and morphology are modulated by pro-angiogenic and environmental factors associated with tumor tissues and cancer cells. Recent in vivo and in vitro studies have revealed that the gap junctions of endothelial cells also participate in the promotion of angiogenesis. Pro-angiogenic factors modulate gap junction function and connexin expression in endothelial cells, whereas endothelial connexins are involved in angiogenic tube formation and in the cell migration of endothelial cells. Several mechanisms, including gap junction function-dependent or -independent pathways, have been proposed. In particular, connexins might have the potential to regulate cell mechanics such as cell morphology, cell migration, and cellular stiffness that are dynamically changed during the angiogenic processes. Here, we review the implication for endothelial gap junctions and cellular mechanics in vascular angiogenesis.

scholarly journals Cancer-Associated Fibroblasts Differentiated by Exosomes Isolated from Cancer Cells Promote Cancer Cell Invasion

2020 ◽  
Vol 21 (21) ◽  
pp. 8153
Author(s):  
Kimin Kim ◽  
Yeh Joo Sohn ◽  
Ruri Lee ◽  
Hye Ju Yoo ◽  
Ji Yoon Kang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cell Types ◽  
Cancer Drug ◽  
Cancer Microenvironment ◽  
Cancer Associated Fibroblasts ◽  
Cancer Cell Invasion

Cancer-associated fibroblasts (CAFs) in the cancer microenvironment play an essential role in metastasis. Differentiation of endothelial cells into CAFs is induced by cancer cell-derived exosomes secreted from cancer cells that transfer molecular signals to surrounding cells. Differentiated CAFs facilitate migration of cancer cells to different regions through promoting extracellular matrix (ECM) modifications. However, in vitro models in which endothelial cells exposed to cancer cell-derived exosomes secreted from various cancer cell types differentiate into CAFs or a microenvironmentally controlled model for investigating cancer cell invasion by CAFs have not yet been studied. In this study, we propose a three-dimensional in vitro cancer cell invasion model for real-time monitoring of the process of forming a cancer invasion site through CAFs induced by exosomes isolated from three types of cancer cell lines. The invasiveness of cancer cells with CAFs induced by cancer cell-derived exosomes (eCAFs) was significantly higher than that of CAFs induced by cancer cells (cCAFs) through physiological and genetic manner. In addition, different genetic tendencies of the invasion process were observed in the process of invading cancer cells according to CAFs. Our 3D microfluidic platform helps to identify specific interactions among multiple factors within the cancer microenvironment and provides a model for cancer drug development.

scholarly journals Transendothelial Migration of Melanoma Cells Involves N-Cadherin-mediated Adhesion and Activation of the β-Catenin Signaling Pathway

2005 ◽  
Vol 16 (9) ◽  
pp. 4386-4397 ◽  
Author(s):  
Jianfei Qi ◽  
Ning Chen ◽  
Junfu Wang ◽  
Chi-Hung Siu
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Transendothelial Migration ◽  
Melanoma Cells ◽  
Dominant Negative ◽  
Vitro Assay ◽  
Multistep Process ◽  
Adhesive Interactions

Cancer metastasis is a multistep process involving many types of cell-cell interactions, but little is known about the adhesive interactions and signaling events during extravasation of cancer cells. Transendothelial migration of cancer cells was investigated using an in vitro assay, in which melanoma cells were seeded on top of a monolayer of endothelial cells. Attachment of melanoma cells on the endothelium induced a twofold increase in N-cadherin expression in melanoma cells and the redistribution of N-cadherin to the heterotypic contacts. Transendothelial migration was inhibited when N-cadherin expression was repressed by antisense RNA, indicating a key role played by N-cadherin. Whereas N-cadherin and β-catenin colocalized in the contact regions between melanoma cells and endothelial cells during the initial stages of attachment, β-catenin disappeared from the heterotypic contacts during transmigration of melanoma cells. Immunolocalization and immunoprecipitation studies indicate that N-cadherin became tyrosine-phosphorylated, resulting in the dissociation of β-catenin from these contact regions. Concomitantly, an increase in the nuclear level of β-catenin occurred in melanoma cells, together with a sixfold increase in β-catenin-dependent transcription. Transendothelial migration was compromised in cells expressing a dominant-negative form of β-catenin, thus supporting a regulatory role of β-catenin signaling in this process.

scholarly journals Stat5 promotes metastatic behavior of human prostate cancer cells in vitro and in vivo

2010 ◽  
Vol 17 (2) ◽  
pp. 481-493 ◽  
Author(s):  
Lei Gu ◽  
Paraskevi Vogiatzi ◽  
Martin Puhr ◽  
Ayush Dagvadorj ◽  
Jacqueline Lutz ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Human Prostate ◽  
Migration And Invasion ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Metastatic Behavior

There are no effective therapies for disseminated prostate cancer. Constitutive activation of Stat5 in prostate cancer is associated with cancer lesions of high histological grade. We have shown that Stat5 is activated in 61% of distant metastases of clinical prostate cancer. Active Stat5 increased metastases formation of prostate cancer cells in nude mice by 11-fold in an experimental metastases assay. Active Stat5 promoted migration and invasion of prostate cancer cells, and induced rearrangement of the microtubule network. Active Stat5 expression was associated with decreased cell surface E-cadherin levels, while heterotypic adhesion of prostate cancer cells to endothelial cells was stimulated by active Stat5. Activation of Stat5 and Stat5-induced binding of prostate cancer cells to endothelial cells were decreased by inhibition of Src but not of Jak2. Gene expression profiling indicated that 21% of Stat5-regulated genes in prostate cancer cells were related to metastases, while 7.9% were related to proliferation and 3.9% to apoptosis. The work presented here provides the first evidence of Stat5 involvement in the induction of metastatic behavior of human prostate cancer cells in vitro and in vivo. Stat5 may provide a therapeutic target protein for disseminated prostate cancer.

scholarly journals MicroRNA-128 Confers Anti-Endothelial Adhesion and Anti-Migration Properties to Counteract Highly Metastatic Cervical Cancer Cells’ Migration in a Parallel-Plate Flow Chamber

2020 ◽  
Vol 22 (1) ◽  
pp. 215
Author(s):  
Pei-Chin Chuang ◽  
Chun-Wun Lu ◽  
Ching-Chin Tsai ◽  
Shun-Hung Tseng ◽  
Wen-Hong Su
Keyword(s):  
Cervical Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Caski Cell ◽  
Parallel Plate Flow Chamber ◽  
Cervical Cancer Cells ◽  
Vascular Adhesion

Despite the distant metastasis of cervical cancer cells being a prominent cause of mortality, neither the metastasis capacity nor the in vitro conditions mimicking adhesion of cervical cancer cells to endothelial cells have been fully elucidated. Circulating metastatic cancer cells undergo transendothelial migration and invade normal organs in distant metastasis; however, the putative molecular mechanism remains largely uncertain. In this study, we describe the use of an in vitro parallel-plate flow chamber to simulate the dynamic circulation stress on cervical cancer cells and elucidate their vascular adhesion and metastasis. We isolate the viable and shear stress-resistant (SSR) cervical cancer cells for mechanistic studies. Remarkably, the identified SSR-HeLa and SSR-CaSki exhibited high in vitro adhesive and metastatic activities. Hence, a consistently suppressed miR-128 level was revealed in SSR cell clones compared to those of parental wild-type (WT) cells. Overexpressed miR-128 attenuated SSR-HeLa cells’ adherence to human umbilical cord vein endothelial cells (HUVECs); in contrast, suppressed miR-128 efficiently augmented the static adhesion capacity in WT-HeLa and WT-CaSki cells. Hence, amplified miR-128 modestly abolished in vitro SSR-augmented HeLa and CaSki cell movement, whereas reduced miR-128 aggravated the migration speed in a time-lapse recording assay in WT groups. Consistently, the force expression of miR-128 alleviated the SSR-enhanced HeLa and CaSki cell mobility in a wound healing assay. Notably, miR-128 mediated SSR-enhanced HeLa and CaSki cells’ adhesion and metastasis through suppressed ITGA5, ITGB5, sLex, CEACAM-6, MMP9, and MMP23 transcript levels. Our data provide evidence suggesting that miR-128 is a promising microRNA that prevented endothelial cells’ adhesion and transendothelial migration to contribute to the SSR-enhanced adhesion and metastasis progression under a parallel-plate flow chamber system. This indicates that the nucleoid-based miR-128 strategy may be an attractive therapeutic strategy to eliminate tumor cells resistant to circulation shear flow, prevent vascular adhesion, and preclude subsequent transendothelial metastasis.

Anti-Angiogenic Activity of Rotenoids from the Stems of Derris trifoliata

Planta Medica ◽  
2018 ◽  
Vol 84 (11) ◽  
pp. 779-785 ◽  
Author(s):  
Yanisa Mittraphab ◽  
Nattaya Ngamrojanavanich ◽  
Kuniyoshi Shimizu ◽  
Kiminori Matsubara ◽  
Khanitha Pudhom
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Ex Vivo ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Ex Vivo Model ◽  
Cell Growth And Migration ◽  
Vitro Assay ◽  
Angiogenic Activity

The plants in the genus Derris have proven to be a rich source of rotenoids, of which cytotoxic effect against cancer cells seem to be pronounced. However, their effect on angiogenesis playing a crucial role in both cancer growth and metastasis has been seldom investigated. This study aimed at investigating the effect of the eight rotenoids (1–8) isolated from Derris trifoliata stems on three cancer cells and angiogenesis. Among them, 12a-hydroxyrotenone (2) exhibited potent inhibition on both cell growth and migration of HCT116 colon cancer cells. Further, anti-angiogenic assay in an ex vivo model was carried out to determine the effect of the isolated rotenoids on angiogenesis. Results revealed that 12a-hydroxyrotenone (2) displayed the most potent suppression of microvessel sprouting. The in vitro assay on human umbilical vein endothelial cells was performed to determine whether compound 2 elicits anti-angiogenic effect and its effect was found to occur via suppression of endothelial cells proliferation and tube formation, but not endothelial cells migration. This study provides the first evidence that compound 2 could potently inhibit HCT116 cancer migration and anti-angiogenic activity, demonstrating that 2 might be a potential agent or a lead compound for cancer therapy.

scholarly journals Beneficial or harmful influence of phytosterols on human cells?

2008 ◽  
Vol 100 (6) ◽  
pp. 1183-1191 ◽  
Author(s):  
Blazej Rubis ◽  
Anna Paszel ◽  
Mariusz Kaczmarek ◽  
Magdalena Rudzinska ◽  
Henryk Jelen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Plant Sterols ◽  
Human Organism ◽  
Dependent Manner ◽  
Normal Cells ◽  
Oil Extract ◽  
Dose Dependent ◽  
Human Abdominal Aorta

So far, a protective influence of phytosterols on the human organism and atherogenesis has been suggested. Most studies have concentrated on the cytotoxic efficacy of phytosterols on cancer cells. However, there are only a few reports showing their influence on normal cells. The aim of the present study was to determine whether dietary plant sterols and their thermal processing products could influence the viability of normal, abdominal endothelial cells that play a crucial role in atherogenesis. Thus, we studied the effect of rapeseed oil-extract components, β-sitosterol, cholesterol and their epoxy-derivatives, 5α,6α-epoxy-β-sitosterol and 5α,6α-epoxycholesterol, on the proliferation and viability of human abdominal aorta endothelial cells HAAE-2 in vitro. We showed strong cytotoxic properties of β-sitosterol in HAAE-2 cells (half maximal inhibitory concentration (IC50) = 1·99 (sem 0·56) μm) and, interestingly, a weaker cytotoxic effect of 5α,6α-epoxy-β-sitosterol (IC50>200 μm). Moreover, we observed a significantly stronger cytotoxic activity of β-sitosterol than cholesterol (IC50 = 8·99 (sem 2·74) μm). We also revealed that β-sitosterol as well as cholesterol caused apoptosis, inducing caspase-3 activity in the cells (60 % increase compared with control cells) that corresponded to the DNA fragmentation analysis in a terminal uridine deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling (TUNEL) study. Although absorption of plant sterols is low compared with cholesterol, they can still influence other physiological functions. Since they effectively reduce serum LDL-cholesterol and atherosclerotic risk but also decrease the viability of cancer cells as well as normal cells in a time- and dose-dependent manner in vitro, their influence on other metabolic processes remains to be elucidated.

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