By activating matrix metalloproteinase-7, shear stress promotes chondrosarcoma cell motility, invasion and lung colonization

Guan, Pei Pei; Yu, Xin; Guo, Jian Jun; Wang, Yue; Wang, Tao; Li, Jia Yi; Κωνσταντόπουλος, Κωνσταντίνος; Wang, Zhan You; Wang, Pu

doi:10.18632/oncotarget.3274

Cited by 48 publications

(40 citation statements)

References 71 publications

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“…A recent study of chondrosarcoma cell lines reported that interstitial flow and fluid shear stress induced MMP‐7 expression and thereby enhanced invasion via the PI3‐K, ERK1/2 and p38 signaling pathway . This is similar to the pathway investigated by Shi et al .…”

Section: Discussionsupporting

confidence: 75%

Heparan sulfate proteoglycans mediate renal carcinoma metastasis

Qazi

Shi

Song

et al. 2016

Intl Journal of Cancer

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The surface proteoglycan/glycoprotein layer (glycocalyx) on tumor cells has been associated with cellular functions that can potentially enable invasion and metastasis. In addition, aggressive tumor cells with high metastatic potential have enhanced invasion rates in response to interstitial flow stimuli in vitro. Our previous studies suggest that heparan sulfate (HS) in the glycocalyx plays an important role in this flow mediated mechanostransduction and upregulation of invasive and metastatic potential. In this study, highly metastatic renal cell carcinoma cells were genetically modified to suppress HS production by knocking down its synthetic enzyme NDST1. Using modified Boyden chamber and microfluidic assays, we show that flow-enhanced invasion is suppressed in HS deficient cells. To assess the ability of these cells to metastasize in vivo, parental or knockdown cells expressing fluorescence reporters were injected into kidney capsules in SCID mice. Histological analysis confirmed that there was a large reduction (95%) in metastasis to distant organs by tumors formed from the NDST1 knockdown cells compared to control cells with intact HS. The ability of these cells to invade surrounding tissue was also impaired. The substantial inhibition of metastasis and invasion upon reduction of HS suggests an active role for the tumor cell glycocalyx in tumor progression.

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Section: Discussionsupporting

confidence: 75%

Heparan sulfate proteoglycans mediate renal carcinoma metastasis

Qazi

Shi

Song

et al. 2016

Intl Journal of Cancer

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“…The C‐terminal domain of HSPG2, Dm IV‐3, can be cleaved by MMP7, which will favor cell dispersion and migration (Grindel et al, ). Although there was no evidence for the direct regulation of MMP7 activities by substrate stiffness, the other mechanical stimulus, matrix stress, induced the activation of MMP7 in chondrosarcoma cells (Guan et al, ). The results of that study showed that shear stress could resulted in accumulation of cyclic AMP, which in turn, led to the increased expression of MMP7 by the activation of several intracellular signaling pathways, including PI3‐kinase, ERK, and p38.…”

Section: Discussionmentioning

confidence: 99%

Substrate stiffness regulated migration and angiogenesis potential of A549 cells and HUVECs

Zhao

Xue

et al. 2017

Journal Cellular Physiology

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Tumor tissue tends to stiffen during solid tumor progression. Substrate stiffness is known to alter cell behaviors, such as proliferation and migration, during which angiogenesis is requisite. Mono- and co-culture systems of lung cancer cell line A549 and human umbilical vein endothelial cells (HUVECs), on polydimethylsiloxane substrates (PDMS) with varying stiffness, were used for investigating the effects of substrate stiffness on the migration and angiogenesis of lung cancer. The expressions of matrix metalloproteinases (MMPs) and angiogenesis-related growth factors were up-regulated with the increase of substrate stiffness, whereas that of tissue inhibitor of matrix metalloproteinase (TIMPs) were down-regulated with increasing substrate stiffness. Our data not only suggested that stiff substrate may promote the migration and angiogenesis capacities of lung cancer, but also suggested that therapeutically targeting lung tumor stiffness or response of ECs to lung tumor stiffness may help reduce migration and angiogenesis of lung tumor.

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“…When exerted directly on cancer cells, shear stress can increase cells’ invasive and metastatic potential. Wang P and Guan PP et al indicated that shear stress with 2 dyn/cm 2 increased the release of cyclic AMP and interleukin-1β via the induction of MMPs (MMP-1, MMP-7 and MMP-12) in PI3-K and ERK1/2-dependent manner, which significantly promoted motility and invasion of chondrosarcoma cells [39, 40]. …”

Section: Discussionmentioning

confidence: 99%

Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells

et al. 2016

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Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation.

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By activating matrix metalloproteinase-7, shear stress promotes chondrosarcoma cell motility, invasion and lung colonization

Cited by 48 publications

References 71 publications

Heparan sulfate proteoglycans mediate renal carcinoma metastasis

Heparan sulfate proteoglycans mediate renal carcinoma metastasis

Substrate stiffness regulated migration and angiogenesis potential of A549 cells and HUVECs

Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells

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