2016
DOI: 10.1016/j.oraloncology.2016.06.008
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Chemokines accentuating protumoral activities in oral cancer microenvironment possess an imperious stratagem for therapeutic resolutions

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Cited by 18 publications
(12 citation statements)
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“…Chemokines can modulate tumor invasion and metastasis by promoting epithelial mesenchymal transition (EMT), upregulating the expression of proteases and downregulating the expression of E-cadherin and integrin through a series of signaling pathways, including the MAPK/ERK/PI3K/ Akt signaling pathways. Furthermore, chemokine receptors expressed by tumor cells can make a response to their corresponding chemokine ligands and migrate directionally towards concentration gradients of chemokine ligands to achieve organ-specific metastases (32,33). Another potential mechanism is that the binding of chemokine ligands to their receptors may induce membrane wrinkling and the formation Chemokine-induced signal transduction in cancer with perineural invasion.…”
Section: Chemokines Promote the Progression Of Cancermentioning
confidence: 99%
“…Chemokines can modulate tumor invasion and metastasis by promoting epithelial mesenchymal transition (EMT), upregulating the expression of proteases and downregulating the expression of E-cadherin and integrin through a series of signaling pathways, including the MAPK/ERK/PI3K/ Akt signaling pathways. Furthermore, chemokine receptors expressed by tumor cells can make a response to their corresponding chemokine ligands and migrate directionally towards concentration gradients of chemokine ligands to achieve organ-specific metastases (32,33). Another potential mechanism is that the binding of chemokine ligands to their receptors may induce membrane wrinkling and the formation Chemokine-induced signal transduction in cancer with perineural invasion.…”
Section: Chemokines Promote the Progression Of Cancermentioning
confidence: 99%
“…Several chemokines derived from bone-tropic tumor cells act as osteolytic factors by inducing bone resorption of osteoclasts and promoting the recruitment and differentiation of osteoclast precursors (14)(15)(16), and the levels of these chemokines in serum or bone marrow are associated with cancer-mediated osteolysis in humans (17,18). In the case of OSCC, various chemokines, including CXCL12/CXCR4, CCL5/CCR5, CXCL8, and CCL2, are known to play critical roles in invasion and metastasis by promoting EMT, MMP expression, and cell dissemination (19)(20)(21). OSCC cell-derived CXCL2 and CXCL13 induce RANKL expression in osteoblastic/stromal cells (22,23), and serum levels of CXCL9 and tissue expression of CCL2 are positively correlated with OSCC bone invasion (24,25).…”
Section: Introductionmentioning
confidence: 99%
“…Chemokines belong to a superfamily of small molecules (8–14 kDa), which could be classified into the four subfamilies: CXC, CC, C, and CX3C based on the sequence of conserved N-terminal cysteine residues 8 . Many studies have proven that chemokines and chemokine receptors are frequently associated with tumor metastases, such as CXCR4, CCR7 and CCR10 in breast and gastric cancer 9 11 , CXCR1 and CXCR5 in pancreatic cancer 12 .…”
Section: Introductionmentioning
confidence: 99%