1 Ocak 2015 Dergi makalesi Açık Erişim

Erin, Nuray; Nizam, Esra; Tanriover, Gamze; Koksoy, Sadi

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    "creators": [
      {
        "affiliation": "Akdeniz Univ, Sch Med, Dept Med Pharmacol, TR-07070 Antalya, Turkey", 
        "name": "Erin, Nuray"
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      {
        "affiliation": "Akdeniz Univ, Sch Med, Dept Med Pharmacol, TR-07070 Antalya, Turkey", 
        "name": "Nizam, Esra"
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      {
        "affiliation": "Akdeniz Univ, Sch Med, Dept Histol & Embryol, TR-07070 Antalya, Turkey", 
        "name": "Tanriover, Gamze"
      }, 
      {
        "affiliation": "Akdeniz Univ, Sch Med, Dept Med Microbiol, TR-07070 Antalya, Turkey", 
        "name": "Koksoy, Sadi"
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    "description": "CXCR2 interacts with a wide range of chemokines and CXCR2 antagonists may have therapeutic value for treatment-resistant metastatic carcinomas. We aimed to explore regulation of activity of CXCR2 and its ligand, MIP-2, in metastatic breast carcinoma. We used mouse breast carcinoma cells metastasize to brain (4TBM), liver (4TLM), and heart (4THM) and explored the extra- and intracellular mechanisms effecting MIP-2 secretion using CXCR2 antagonist and inhibitors of downstream signaling molecules. 4TBM, 4TLM, and 4THM cells include cancer stem cell features and metastasize extensively. We also determined kinetics of MIP-2 secretion in 4T1 and non-metastatic 67NR mouse breast carcinoma cells. We found that there is an autocrine-inhibition of MIP-2 secretion. Specifically, metastatic cells selectively express CXCR2 only, and not CXCR1 and attenuating CXCR2 activity with SB225002 increased MIP-2 secretion. This may be due to the inhibition of protein kinase C (PKC) activity since RO318220; a specific inhibitor of PKC also increased MIP-2 secretion. Attenuating CXCR2 activity with SB225002, otherwise suppressed proliferation of 4THM and 4TBM cells. Tumor explants and cancer-associated fibroblasts obtained from 4TLM, 4THM, and 4TBM primary tumors secreted high levels of MIP-2. Surprisingly, CXCR2 expression was low in 4TLM cells demonstrating that liver metastatic cells might be resistant to the anti-tumoral effects of CXCR2 antagonists. Our results demonstrated that resistance to anti-proliferative effects of CXCR2 may also arise from feedback increases in MIP-2 secretion. Activation of PI3 K pathway augments MIP-2 secretion, hence possible resistance to the antitumor effects of CXCR2 antagonists might be prevented with inhibitors of PI3 K.", 
    "doi": "10.1007/s10549-015-3297-3", 
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    "journal": {
      "issue": "1", 
      "pages": "57-69", 
      "title": "BREAST CANCER RESEARCH AND TREATMENT", 
      "volume": "150"
    }, 
    "license": {
      "id": "cc-by"
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    "publication_date": "2015-01-01", 
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      "title": "Dergi makalesi", 
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    "title": "Autocrine control of MIP-2 secretion from metastatic breast cancer cells is mediated by CXCR2: a mechanism for possible resistance to CXCR2 antagonists"
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