The bone marrow metastasis niche in retinoblastoma

Khosravi, Abbas; Shahrabi, Saeid; Shahjahani, Mohammad; Saki, Najmaldin

doi:10.1007/s13402-015-0232-x

Cited by 16 publications

(14 citation statements)

References 95 publications

(87 reference statements)

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“…Other ways through which tumor cells may spread include local tissue invasion and direct seeding into body cavities. Which way tumor cells choose to spread depends on the site of tumor initiation, the aggressiveness of the tumor cells, extrinsic signals and intrinsic tumor micro-environmental conditions including direct cell-cell and cell-matrix interactions within a tumor niche and the presence of paracrine factors mediating the formation of new vessels [ 5 ]. It has been found that solid tumors frequently induce angiogenesis and lymphangiogenesis.…”

Section: Introductionmentioning

confidence: 99%

The role of lymphangiogenesis and angiogenesis in tumor metastasis

2016

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BackgroundMetastasis is the main cause of mortality in cancer patients. Two major routes of cancer cell spread are currently being recognized: dissemination via blood vessels (hematogenous spread) and dissemination via the lymphatic system (lymphogenous spread). Here, our current knowledge on the role of both blood and lymphatic vessels in cancer cell metastasis is summarized. In addition, I will discuss why cancer cells select one or both of the two routes to disseminate and I will provide a short description of the passive and active models of intravasation. Finally, lymphatic vessel density (LVD), blood vessel density (BVD), interstitial fluid pressure (IFP) and tumor hypoxia, as well as regional lymph node metastasis and the recently discovered primo vascular system (PVS) will be highlighted as important factors influencing tumor cell motility and spread and, ultimately, clinical outcome.ConclusionsLymphangiogenesis and angiogenesis are important phenomena involved in the spread of cancer cells and they are associated with a poor prognosis. It is anticipated that new discoveries and advancing knowledge on these phenomena will allow an improvement in the treatment of cancer patients.

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Section: Introductionmentioning

confidence: 99%

The role of lymphangiogenesis and angiogenesis in tumor metastasis

2016

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“…The role of matrix metalloproteinases (MMPs) and dipeptidyl peptidases (DPPs) in invasive and metastatic processes has amply been documented [ 1 , 7 – 9 ]. MMPs are zinc- and calcium-dependent peptidases essential for ECM reorganization.…”

Section: Introductionmentioning

confidence: 99%

TNF-α promotes breast cancer cell migration and enhances the concentration of membrane-associated proteases in lipid rafts

et al. 2016

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PurposeTumor progression is associated with cell migration, invasion and metastasis. These processes are accompanied by the activation of specific proteases that are either linked to cellular membranes or are secreted into extracellular spaces. TNF-α is known to play an important role in various aspects of tumor progression. The aim of this work was to assess the effect of TNF-α on the migration of breast cancer cells and, in addition, to assess its association with the location of membrane-associated proteases in lipid rafts.MethodsWound scratch healing and Transwell migration assays were used to study the effect of TNF-α on the migration of both hormone-dependent and hormone-independent breast cancer-derived cells, i.e., MCF7 and MDA-MB-231, respectively. The expression and secretion of three matrix metalloproteases, MMP9, MMP2 and MT1-MMP, and two dipeptidyl peptidases, CD26 and FAP-α, was investigated using RT-PCR, Western blotting and gelatin zymography. In addition, activation of the MAPK/ERK signaling pathway was investigated by Western blotting.ResultsWe found that a TNF-α-induced enhancement of breast cancer cell migration was accompanied by an increased secretion of MMP9, but not MMP2, into the culture media. We also found that TNF-α upregulated the expression of the dipeptidyl peptidases CD26 and FAP-α in a dose-dependent manner and, in addition, enhanced the concentration of all five proteases in lipid rafts in the breast cancer-derived cells tested, regardless of cell type. Furthermore, we found that TNF-α activated the MAPK/ERK signaling pathway by increasing the ERK1/2 phosphorylation level. Application of the MEK/ERK1/2 inhibitor U-0126 resulted in down-regulation of TNF-α-induced MMP9 secretion and abrogation of the enhanced concentration of proteases in the lipid rafts.ConclusionsFrom our results we conclude that TNF-α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers susceptible to TNF-α stimulation.

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“…Micro-environmental factors may have profound effects on cancer cells, including their metastatic behavior [1][2][3]. Since metastasis is one of the most crucial factors determining the survival of cancer patients, ample attempts have been made to identify key molecular mediators that control metastasis.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide increases the migratory activity of non-small cell lung cancer cells via AKT-mediated integrin αv and β1 upregulation

2016

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Background Previously, nitric oxide (NO) has been found to affect the metastatic behavior of various types of cancer. In addition, it has been found that alterations in integrin expression may have profound effects on cancer cell survival and migration. Here, we aimed at assessing the effects of non-toxic concentrations of NO on human non-small cell lung cancer (NSCLC) cells, including the expression of integrins and the migration of these cells. Methods The cytotoxic and proliferative effects of NO on human NSCLC-derived H460, H292 and H23 cells were tested by MTT assay. The migration capacities of these cells was evaluated by wound healing and transwell migration assays. The expression of integrins and migration-associated proteins was determined by Western blot analyses. Results We found that NO treatment caused a significant increase in the expression of integrin αv and β1 in all three NSCLC-derived cell lines tested. Known migrationassociated proteins acting downstream of these integrins, including focal adhesion kinase (FAK), active RhoA (Rho-GTP) and active cell division control 42 (Cdc42-GTP), were found to be significantly activated in response to NO. In addition, we found that NO-treated cells showed an increased motility and that this motility was associated with a significant increase in the number of filopodia per cell. We also found that NO-treated cells exhibited increased active protein kinase G (PKG), protein kinase B (AKT) and FAK expression levels. Using a pharmacological approach, we found that the integrinmodulating effect of NO is most likely brought about by a PKG/AKT-dependent mechanism, since the observed changes in integrin expression were abolished by AKT inhibitors, but not by FAK inhibitors. Conclusion Our data suggest a novel role of NO in the regulation of integrin expression and, concomitantly, the migratory capacity of NSCLC cells.

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The bone marrow metastasis niche in retinoblastoma

Abstract: The various BM metastasis-related molecular changes identified to date may be instrumental for a better diagnosis, prognosis and classification of Rb patients, as well as for the development of novel comprehensive (targeted) therapies.

Cited by 16 publications

References 95 publications

The role of lymphangiogenesis and angiogenesis in tumor metastasis

The role of lymphangiogenesis and angiogenesis in tumor metastasis

TNF-α promotes breast cancer cell migration and enhances the concentration of membrane-associated proteases in lipid rafts

Nitric oxide increases the migratory activity of non-small cell lung cancer cells via AKT-mediated integrin αv and β1 upregulation

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