Stromal cell-derived factor-1α and macrophage migration-inhibitory factor induce metastatic behavior in CXCR4-expressing colon cancer cells

Shin, Han Na; Moon, Hyun Hye; Ku, Ja Lok

doi:10.3892/ijmm.2012.1141

Cited by 27 publications

(29 citation statements)

References 44 publications

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“…Although several studies have assessed the antimetastatic effects of CXCR4 inhibitors in different cancer types [83–98], only few have investigated their effects in lung cancer. TF14016, a small peptidic inhibitor of CXCL12 receptor CXCR4, has been recently shown to suppress metastases of small-cell lung cancer cells in mice [99].…”

Section: Antagonist Of Cxcr4-mediated Brain Metastasismentioning

confidence: 99%

CXCR4/CXCL12 in Non-Small-Cell Lung Cancer Metastasis to the Brain

Cavallaro

2013

IJMS

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Lung cancer represents the leading cause of cancer-related mortality throughout the world. Patients die of local progression, disseminated disease, or both. At least one third of the people with lung cancer develop brain metastases at some point during their disease, even often before the diagnosis of lung cancer is made. The high rate of brain metastasis makes lung cancer the most common type of tumor to spread to the brain. It is critical to understand the biologic basis of brain metastases to develop novel diagnostic and therapeutic approaches. This review will focus on the emerging data supporting the involvement of the chemokine CXCL12 and its receptor CXCR4 in the brain metastatic evolution of non-small-cell lung cancer (NSCLC) and the pharmacological tools that may be used to interfere with this signaling axis.

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Section: Antagonist Of Cxcr4-mediated Brain Metastasismentioning

confidence: 99%

CXCR4/CXCL12 in Non-Small-Cell Lung Cancer Metastasis to the Brain

Cavallaro

2013

IJMS

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“…MIF‐induced migration of T cells and B cells is Giα dependent . In colon cancer cells, MIF/CXCR4 signaling promotes an aggressive phenotype by inducing the invasion and metastasis of cancer cells . Similarly, the MIF/CXCR4 interaction was recently shown to mediate the recruitment of mesenchymal stem cells to tumors and enhance invasion capacity in a pulmonary metastasis model .…”

Section: Signaling Pathways Of Cxcr4 Receptor/ligand Familymentioning

confidence: 99%

“…In complex with CD44, MIF/CD74 interaction promotes cell survival via ERK1/2 and Akt phosphorylation . MIF has been shown to recruit many types of cell, including T cells, B cells, endothelial progenitor cells, mesenchymal stem cells, and cancer cells …”

Section: Signaling Pathways Of Cxcr4 Receptor/ligand Familymentioning

confidence: 99%

“…Metastatic cancer cells utilize the similar pathways of cellular migration as stem/progenitor cells during wound repair and tissue regeneration . Through interaction with CXCL12 and MIF, CXCR4‐dependent signaling enhances cancer cell proliferation and metastasis . Apart from this, organs and tissues such as brain, lung, liver, lymph nodes, and bone can secrete high levels of CXCL12 to facilitate migration and invasion by recruiting CXCR4‐expressing cancer cells along a CXCL12 gradient .…”

Section: Therapeutic Potential For Intervention With Cxcl12/cxcr4 Axismentioning

confidence: 99%

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Harnessing CXCR4 antagonists in stem cell mobilization, HIV infection, ischemic diseases, and oncology

Tsou

Huang²,

Song

et al. 2017

Medicinal Research Reviews

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CXCR4 antagonists (e.g., Plerixafor ) have been successfully validated as stem cell mobilizers for peripheral blood stem cell transplantation. Applications of the CXCR4 antagonists have heralded the era of cell-based therapy and opened a potential therapeutic horizon for many unmet medical needs such as kidney injury, ischemic stroke, cancer, and myocardial infarction. In this review, we first introduce the central role of CXCR4 in diverse cellular signaling pathways and discuss its involvement in several disease progressions. We then highlight the molecular design and optimization strategies for targeting CXCR4 from a large number of case studies, concluding that polyamines are the preferred CXCR4-binding ligands compared to other structural options, presumably by mimicking the highly positively charged natural ligand CXCL12. These results could be further justified with computer-aided docking into the CXCR4 crystal structure wherein both major and minor subpockets of the binding cavity are considered functionally important. Finally, from the clinical point of view, CXCR4 antagonists could mobilize hematopoietic stem/progenitor cells with long-term repopulating capacity to the peripheral blood, promising to replace surgically obtained bone marrow cells as a preferred source for stem cell transplantation.

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“…The process of cancer metastasis includes cancer cell proliferation, local invasion, intravasation and cancer cell survival, extravasation and attachment to secondary organs, and metastatic growth in a new environment (2). CXC chemokine receptor 4 (CXCR4) and its ligand stromal cell-derived factor-1α (SDF-1α, also known as CXCL12) play an important role in cancer growth and dissemination, and CXCR4/SDF-1α is positively correlated with metastasis in many types of cancer including thyroid, lung, ovarian, renal, prostate, breast, pancreatic, gastric and colorectal cancer (3–12).…”

Section: Introductionmentioning

confidence: 99%

The influence of lentivirus-mediated CXCR4 RNA interference on hepatic metastasis of colorectal cancer

Wang

Liu

et al. 2014

International Journal of Oncology

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The aim of this study was to construct a lentiviral vector of CXCR4-siRNA (Lenti-CXCR4-siRNA) and investigate whether the vector can inhibit the growth, migration, invasion and hepatic metastasis of colorectal cancer (CRC). RT-PCR and western blotting were employed to identify the ideal RNA interference sequence. Lenti-CXCR4-siRNA was constructed and transfected into the SW480 cell line. We used RT-PCR and western blotting to measure the expression of CXCR4 RNA and protein, respectively; the MTS assay to assess the proliferation of SW480 cells; transwell chambers to estimate the inhibitory effect on migration and invasion; and the Balb/c nude mouse model of CRC to examine the inhibition of hepatic metastasis. The relative expression of the CXCR4 gene and protein was 5.4 and 18.95%, respectively, in the siCXCR4 group. The genes in the expression plasmid pLenti-CXCR4-siRNA were in the correct order. In the SW480, nonsense control (NC) and the Lenti-CXCR4-siRNA groups CXCR4 RNA levels were, respectively, 0.54±0.06, 1.00±0.03 and 0.11±0.04 (P=0.0001); CXCR4 protein levels were 0.60±0.03, 0.72±0.03 and 0.18±0.02 (P=0.0001); the OD value was 1.38±0.04 (P=0.0050), 1.28±0.05 (P=0.0256) and 0.92±0.06; SW480 cell number in migration test was 32±6.85, 32.63±1.69 and 0.75±0.71 (P=0.0000); SW480 cell number in the invasion test was 29.13±10.3, 30.38±6.09 and 0.63±0.74 (P=0.0000); hepatic metastasis number was 7.10±3.98 (P=0.034), 7.50±4.09 (P=0.019) and (3.50±2.51); hepatic metastasis mean weight (in g) was 2.25±2.51 (P=0.000), 2.11±2.38 (P=0.000) and 1.45±2.07. Lenti-CXCR4-siRNA constructs were correctly constructed and effectively inhibit the expression of CXCR4 RNA and protein, reducing the proliferation, migration, invasion capacity of SW480 cells and hepatic metastasis of CRC.

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Stromal cell-derived factor-1α and macrophage migration-inhibitory factor induce metastatic behavior in CXCR4-expressing colon cancer cells

Cited by 27 publications

References 44 publications

CXCR4/CXCL12 in Non-Small-Cell Lung Cancer Metastasis to the Brain

CXCR4/CXCL12 in Non-Small-Cell Lung Cancer Metastasis to the Brain

Harnessing CXCR4 antagonists in stem cell mobilization, HIV infection, ischemic diseases, and oncology

The influence of lentivirus-mediated CXCR4 RNA interference on hepatic metastasis of colorectal cancer

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