E2F1 silencing inhibits migration and invasion of osteosarcoma cells via regulating DDR1 expression

Wang, Zhaofeng; Sun, Xianjie; Bao, Yi; Mo, Juanfen; Du, Hengchao; Hu, Jichao; Zhang, Xingen

doi:10.3892/ijo.2017.4165

Cited by 36 publications

(29 citation statements)

References 36 publications

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“…For instance, DDR1 inhibited cell migration and invasion in a chariollantoic membrane (CAM) assay [91]. Furthermore, in gastric cancer cells [34] or in osteosarcoma cells, DDR1 is involved in tumor growth in xenograft mouse model [40]. The role of DDR1 in EMT in vivo remains unclear as most studies focus on tumor growth and needs to be investigated further.…”

Section: In Vivomentioning

confidence: 99%

Multitasking discoidin domain receptors are involved in several and specific hallmarks of cancer

Henriet

Sala

Hammoud

et al. 2018

Cell Adhesion & Migration

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Discoidin domain receptors, DDR1 and DDR2, are two members of collagen receptor family that belong to tyrosine kinase receptor subgroup. Unlike other matrix receptor-like integrins, these collagen receptors have not been extensively studied. However, more and more studies are focusing on their involvement in cancer. These two receptors are present in several subcellular localizations such as intercellular junction or along type I collagen fibers. Consequently, they are involved in multiple cellular functions, for instance, cell cohesion, proliferation, adhesion, migration and invasion. Furthermore, various signaling pathways are associated with these multiple functions. In this review, we highlight and characterize hallmarks of cancer in which DDRs play crucial roles. We discuss recent data from studies that demonstrate the involvement of DDRs in tumor proliferation, cancer mutations, drug resistance, inflammation, neo-angiogenesis and metastasis. DDRs could be potential targets in cancer and we conclude this review by discussing the different ways to inhibits them.

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Section: In Vivomentioning

confidence: 99%

Multitasking discoidin domain receptors are involved in several and specific hallmarks of cancer

Henriet

Sala

Hammoud

et al. 2018

Cell Adhesion & Migration

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“…The region was a GC-rich sequence (86% GC), and a number of E2F1 binding sites (13 sites) were top-ranked ( Figure 2B). Increased E2F1 expression has been reported to be associated with cell migration and tumor development [18][19][20]. Indeed, MG cells expressed E2F1 mRNA and protein to a much greater degree compared with non-MG cells ( Figure 2C,D).…”

Section: Promoter Array Of Short C9orf3 Transcriptmentioning

confidence: 78%

The MicroRNA-23b/27b/24 Cluster Facilitates Colon Cancer Cell Migration by Targeting FOXP2

Nishida

Kuwano

Rokutan

2020

Cancers

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Acquisition of cell migration capacity is an early and essential process in cancer development. The aim of this study was to identify microRNA gene expression networks that induced high migration capacity. Using colon cancer HCT116 cells subcloned by transwell-based migrated cell selection, microRNA array analysis was performed to examine the microRNA expression profile. Promoter activity and microRNA targets were assessed with luciferase reporters. Cell migration capacity was assessed by either the transwell or scratch assay. In isolated subpopulations with high migration capacity, the expression levels of the miR-23b/27b/24 cluster increased in accordance with the increased expression of the short C9orf3 transcript, a host gene of the miR-23b/27b/24 cluster. E2F1-binding sequences were involved in the basic transcription activity of the short C9orf3 expression, and E2F1-small-interfering (si)RNA treatment reduced the expression of both the C9orf3 and miR-23b/27b/24 clusters. Overexpression experiments showed that miR-23b and miR-27b promoted cell migration, but the opposite effect was observed with miR-24. Forkhead box P2 (FOXP2) mRNA and protein levels were reduced by both/either miR-23b and miR-27b. Furthermore, FOXP2 siRNA treatment significantly promoted cell migration. Our findings demonstrated a novel role of the miR-23b/27b/24 cluster in cell migration through targeting FOXP2, with potential implications for the development of microRNA-based therapy targeted at inhibiting cancer migration.

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“…However, both epithelial-and mesenchymal-derived cells have been shown to express either one or both receptors in physiological and pathological conditions [11][12][13][14][15][16][17][18][19][20][21] . Consistently, both DDR1 and DDR2 are expressed in cancers of epithelial 18,19,[22][23][24][25][26][27][28][29][30] and mesenchymal 17,31,32 origin. Functionally, DDRs are thought to mediate tumour cell-collagen interactions at various stages of cancer progression, where they initiate signal transduction pathways that regulate epithelial-to-mesenchymal transition (EMT), cell proliferation and survival, and metastatic dissemination 3,33 .…”

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confidence: 68%

“…Thus, the HT1080 cell system is a dependable xenograft model to elucidate the contribution of factors to tumour growth and experimental lung metastases. Importantly, like other mesenchymal cell lines and tumours 17,31,32,46 , HT1080 cells express DDR1 and DDR2 26,[47][48][49][50] . In vivo, fibrosarcomas are characterized by an abundant collagen matrix, which has been suggested to promote malignancy 51,52 .…”

mentioning

confidence: 96%

“…Functionally, DDRs are thought to mediate tumour cell-collagen interactions at various stages of cancer progression, where they initiate signal transduction pathways that regulate epithelial-to-mesenchymal transition (EMT), cell proliferation and survival, and metastatic dissemination 3,33 . Indeed, in mouse models of cancer, DDR1 and DDR2 were shown to play a role in tumour growth and/or metastases of epithelial 21,23,29,30,[34][35][36][37][38][39][40][41][42][43][44][45] and mesenchymal 32 cancers. Thus, significant experimental evidence supports a role for DDRs in promotion of cancer progression.…”

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confidence: 99%

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Discoidin Domain Receptors, DDR1b and DDR2, Promote Tumour Growth within Collagen but DDR1b Suppresses Experimental Lung Metastasis in HT1080 Xenografts

Wasinski

Sohail

Bonfil

et al. 2020

Sci Rep

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the Discoidin Domain Receptors (DDRs) constitute a unique set of receptor tyrosine kinases that signal in response to collagen. Using an inducible expression system in human HT1080 fibrosarcoma cells, we investigated the role of DDR1b and DDR2 on primary tumour growth and experimental lung metastases. Neither DDR1b nor DDR2 expression altered tumour growth at the primary site. However, implantation of DDR1b-or DDR2-expressing HT1080 cells with collagen I significantly accelerated tumour growth rate, an effect that could not be observed with collagen I in the absence of DDR induction. Interestingly, DDR1b, but not DDR2, completely hindered the ability of HT1080 cells to form lung colonies after intravenous inoculation, suggesting a differential role for DDR1b in primary tumour growth and lung colonization. Analyses of tumour extracts revealed specific alterations in Hippo pathway core components, as a function of DDR and collagen expression, that were associated with stimulation of tumour growth by DDRs and collagen I. Collectively, these findings identified divergent effects of DDRs on primary tumour growth and experimental lung metastasis in the HT1080 xenograft model and highlight the critical role of fibrillar collagen and DDRs in supporting the growth of tumours thriving within a collagen-rich stroma. The DDRs constitute a unique subfamily of receptor tyrosine kinases (RTKs) that signal in response to collagens, and therefore they represent the only RTKs that are directly activated upon contact of cells with their collagenous matrix 1-6. The DDR subfamily comprises two kinases: DDR1 and DDR2 1,2,7. The DDR1 subfamily includes six isoforms generated by alternative splicing, while there is only one form of DDR2. Among the DDR1 isoforms, DDR1a, DDR1b, and DDR1c are full length, highly homologous receptors, with the only structural difference being the presence of 37 additional residues, including two additional tyrosine residues, within the intracellular region of DDR1b and DDR1c, suggesting that these species may activate different downstream signalling pathways 1. DDR1d and DDR1e are truncated, kinase-deficient receptors of unknown function 8. DDR1f contains a full kinase domain but lacks most of the extracellular domains 9. Structurally, the DDRs are type I transmembrane

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E2F1 silencing inhibits migration and invasion of osteosarcoma cells via regulating DDR1 expression

Cited by 36 publications

References 36 publications

Multitasking discoidin domain receptors are involved in several and specific hallmarks of cancer

Multitasking discoidin domain receptors are involved in several and specific hallmarks of cancer

The MicroRNA-23b/27b/24 Cluster Facilitates Colon Cancer Cell Migration by Targeting FOXP2

Discoidin Domain Receptors, DDR1b and DDR2, Promote Tumour Growth within Collagen but DDR1b Suppresses Experimental Lung Metastasis in HT1080 Xenografts

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