Low-molecular-mass secretome profiling identifies C–C motif chemokine 5 as a potential plasma biomarker and therapeutic target for nasopharyngeal carcinoma

Lin, Shio Jean; Chang, Kai‐Ping; Hsu, Chia-Wei; Chi, Lang‐Ming; Chien, Kun-Yi; Li, Ying; Tsai, Ming–Hung; Lin, Yung Hsiang; Yu, Jau‐Song

doi:10.1016/j.jprot.2013.09.013

Cited by 28 publications

(23 citation statements)

References 60 publications

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“…Chemokine (C‐C motif) ligand 5 (CCL5, also known as RANTES [regulated upon activation, normal T‐cell‐expressed and secreted]), has been originally identified as an inducer that can recruit leukocytes to sites of inflammation (Mackay, 2001). It is secreted by various cell types, including platelets, immune cells, fibroblasts, and endothelial and epithelial cells (Lin et al, ). Increased levels of CCL5 have been demonstrated in various types of cancers and CCL5 has been reported to play a promoter role in cancer progression (Lin et al, ; Kato et al, ).…”

mentioning

confidence: 99%

Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1

Kan

et al. 2015

J. Cell. Physiol.

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Tumor micro-environment is a critical factor in the development of cancer. The aim of this study was to investigate the inflammatory cytokines secreted by tumor-associated dendritic cells (TADCs) that contribute to enhanced migration, invasion, and epithelial-to-mesenchymal transition (EMT) in colon cancer. The administration of recombinant human chemokine (C-C motif) ligand 5 (CCL5), which is largely expressed by colon cancer surrounding TADCs, mimicked the stimulation of TADC-conditioned medium on migration, invasion, and EMT in colon cancer cells. Blocking CCL5 by neutralizing antibodies or siRNA transfection diminished the promotion of cancer progression by TADCs. Tumor-infiltrating CD11c(+) DCs in human colon cancer specimens were shown to produce CCL5. The stimulation of colon cancer progression by TADC-derived CCL5 was associated with the up-regulation of non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1), which subsequently increased the expression of Snail. Blocking MALAT-1 significantly decreased the TADC-conditioned medium and CCL5-mediated migration and invasion by decreasing the enhancement of Snail, suggesting that the MALAT-1/Snail pathway plays a critical role in TADC-mediated cancer progression. In conclusion, the inhibition of CCL5 or CCL5-related signaling may be an attractive therapeutic target in colon cancer patients.

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mentioning

confidence: 99%

Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1

Kan

et al. 2015

J. Cell. Physiol.

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“…The protein expression that varied significantly between the two cell lines is displayed in Table 1 . Today, low-molecular-mass proteins secretome profiling represents an attractive pool for cancer biomarker discovery [ 100 ]. Therefore, to seek potential plasma biomarkers and therapeutic targets for NPC, conditioned media of NPC-TW02, NPC-TW04, and NPC-BM1 cells were used with tricine-SDS-gel-assisted fractionation in conjunction with LC-MS/MS [ 100 ].…”

Section: Current Proteomic Research Into Npcmentioning

confidence: 99%

“…Today, low-molecular-mass proteins secretome profiling represents an attractive pool for cancer biomarker discovery [ 100 ]. Therefore, to seek potential plasma biomarkers and therapeutic targets for NPC, conditioned media of NPC-TW02, NPC-TW04, and NPC-BM1 cells were used with tricine-SDS-gel-assisted fractionation in conjunction with LC-MS/MS [ 100 ]. As a result, 35 low-molecular-mass proteins (<15 kDa) were identified as candidate NPC biomarkers, and the plasma C–C motif chemokine 5 showed good power (AUC 0.801) in discriminating NPC patients from healthy controls.…”

Section: Current Proteomic Research Into Npcmentioning

confidence: 99%

A Review: Proteomics in Nasopharyngeal Carcinoma

Chen

Liang

Zhu

2015

IJMS

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Although radiotherapy is generally effective in the treatment of major nasopharyngeal carcinoma (NPC), this treatment still makes approximately 20% of patients radioresistant. Therefore, the identification of blood or biopsy biomarkers that can predict the treatment response to radioresistance and that can diagnosis early stages of NPC would be highly useful to improve this situation. Proteomics is widely used in NPC for searching biomarkers and comparing differentially expressed proteins. In this review, an overview of proteomics with different samples related to NPC and common proteomics methods was made. In conclusion, identical proteins are sorted as follows: Keratin is ranked the highest followed by such proteins as annexin, heat shock protein, 14-3-3σ, nm-23 protein, cathepsin, heterogeneous nuclear ribonucleoproteins, enolase, triosephosphate isomerase, stathmin, prohibitin, and vimentin. This ranking indicates that these proteins may be NPC-related proteins and have potential value for further studies.

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“…Interaction between chemotactants and their receptors leads to multiple intracellular events that allow extravasation of cells from circulation and directional migration toward the area with the highest chemotactic gradient (Alexeev et al., 2013). Chemokine (C-C motif) ligand 5 (CCL5, also known as RANTES [regulated upon activation, normal T cell-expressed and secreted]), is secreted by various cell types including platelets, immune cells, fibroblasts, and endothelial and epithelial cells (Lin et al., 2013), and has been originally identified as an inducer that can recruit leukocytes to sites of inflammation (Donlon et al., 1990). After binding to its receptors, namely CCR1, CCR3, and CCR5, CCL5 induces phosphorylation of mitogen-activated protein kinase and other signaling pathways involved in the regulation of various cellular functions, such as proliferation, migration, and differentiation (Aldinucci and Colombatti, 2014, Marques et al., 2013).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Modification of the CCL5/CCR1/ERK Axis Enhances Glioma Targeting in Dedifferentiation-Reprogrammed BMSCs

et al. 2017

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SummaryThe success of stem cell-mediated gene therapy in cancer treatment largely depends on the specific homing ability of stem cells. We have previously demonstrated that after in vitro induction of neuronal differentiation and dedifferentiation, bone marrow stromal cells (BMSCs) revert to a primitive stem cell population (De-neu-BMSCs) distinct from naive BMSCs. We report here that De-neu-BMSCs express significantly higher levels of chemokines, and display enhanced homing abilities to glioma, the effect of which is mediated by the activated CCL5/CCR1/ERK axis. Intriguingly, we find that the activated chemokine axis in De-neu-BMSCs is epigenetically regulated by histone modifications. On the therapeutic front, we show that De-neu-BMSCs elicit stronger homing and glioma-killing effects together with cytosine deaminase/5-fluorocytosine compared with unmanipulated BMSCs in vivo. Altogether, the current study provides an insight into chemokine regulation in BMSCs, which may have more profound effects on BMSC function and their application in regenerative medicine and cancer targeting.

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Low-molecular-mass secretome profiling identifies C–C motif chemokine 5 as a potential plasma biomarker and therapeutic target for nasopharyngeal carcinoma

Cited by 28 publications

References 60 publications

Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1

Chemokine (C-C Motif) Ligand 5 is Involved in Tumor-Associated Dendritic Cell-Mediated Colon Cancer Progression Through Non-Coding RNA MALAT-1

A Review: Proteomics in Nasopharyngeal Carcinoma

Epigenetic Modification of the CCL5/CCR1/ERK Axis Enhances Glioma Targeting in Dedifferentiation-Reprogrammed BMSCs

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