Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration.
Store-operated Ca(2+) entry (SOCE) is a major mechanism of Ca(2) (+) import from extracellular to intracellular space, involving detection of Ca(2+) store depletion in endoplasmic reticulum (ER) by stromal interaction molecule (STIM) proteins, which then translocate to plasma membrane and activate O...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089292&type=printable |
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| author | Masanari Umemura Erdene Baljinnyam Stefan Feske Mariana S De Lorenzo Lai-Hua Xie Xianfeng Feng Kayoko Oda Ayako Makino Takayuki Fujita Utako Yokoyama Mizuka Iwatsubo Suzie Chen James S Goydos Yoshihiro Ishikawa Kousaku Iwatsubo |
| author_facet | Masanari Umemura Erdene Baljinnyam Stefan Feske Mariana S De Lorenzo Lai-Hua Xie Xianfeng Feng Kayoko Oda Ayako Makino Takayuki Fujita Utako Yokoyama Mizuka Iwatsubo Suzie Chen James S Goydos Yoshihiro Ishikawa Kousaku Iwatsubo |
| author_sort | Masanari Umemura |
| collection | DOAJ |
| description | Store-operated Ca(2+) entry (SOCE) is a major mechanism of Ca(2) (+) import from extracellular to intracellular space, involving detection of Ca(2+) store depletion in endoplasmic reticulum (ER) by stromal interaction molecule (STIM) proteins, which then translocate to plasma membrane and activate Orai Ca(2+) channels there. We found that STIM1 and Orai1 isoforms were abundantly expressed in human melanoma tissues and multiple melanoma/melanocyte cell lines. We confirmed that these cell lines exhibited SOCE, which was inhibited by knockdown of STIM1 or Orai1, or by a pharmacological SOCE inhibitor. Inhibition of SOCE suppressed melanoma cell proliferation and migration/metastasis. Induction of SOCE was associated with activation of extracellular-signal-regulated kinase (ERK), and was inhibited by inhibitors of calmodulin kinase II (CaMKII) or Raf-1, suggesting that SOCE-mediated cellular functions are controlled via the CaMKII/Raf-1/ERK signaling pathway. Our findings indicate that SOCE contributes to melanoma progression, and therefore may be a new potential target for treatment of melanoma, irrespective of whether or not Braf mutation is present. |
| format | Article |
| id | doaj-art-7a368dd04b7c4abb94f989a5d40c5cbc |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-7a368dd04b7c4abb94f989a5d40c5cbc2025-08-20T02:15:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8929210.1371/journal.pone.0089292Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration.Masanari UmemuraErdene BaljinnyamStefan FeskeMariana S De LorenzoLai-Hua XieXianfeng FengKayoko OdaAyako MakinoTakayuki FujitaUtako YokoyamaMizuka IwatsuboSuzie ChenJames S GoydosYoshihiro IshikawaKousaku IwatsuboStore-operated Ca(2+) entry (SOCE) is a major mechanism of Ca(2) (+) import from extracellular to intracellular space, involving detection of Ca(2+) store depletion in endoplasmic reticulum (ER) by stromal interaction molecule (STIM) proteins, which then translocate to plasma membrane and activate Orai Ca(2+) channels there. We found that STIM1 and Orai1 isoforms were abundantly expressed in human melanoma tissues and multiple melanoma/melanocyte cell lines. We confirmed that these cell lines exhibited SOCE, which was inhibited by knockdown of STIM1 or Orai1, or by a pharmacological SOCE inhibitor. Inhibition of SOCE suppressed melanoma cell proliferation and migration/metastasis. Induction of SOCE was associated with activation of extracellular-signal-regulated kinase (ERK), and was inhibited by inhibitors of calmodulin kinase II (CaMKII) or Raf-1, suggesting that SOCE-mediated cellular functions are controlled via the CaMKII/Raf-1/ERK signaling pathway. Our findings indicate that SOCE contributes to melanoma progression, and therefore may be a new potential target for treatment of melanoma, irrespective of whether or not Braf mutation is present.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089292&type=printable |
| spellingShingle | Masanari Umemura Erdene Baljinnyam Stefan Feske Mariana S De Lorenzo Lai-Hua Xie Xianfeng Feng Kayoko Oda Ayako Makino Takayuki Fujita Utako Yokoyama Mizuka Iwatsubo Suzie Chen James S Goydos Yoshihiro Ishikawa Kousaku Iwatsubo Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. PLoS ONE |
| title | Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. |
| title_full | Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. |
| title_fullStr | Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. |
| title_full_unstemmed | Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. |
| title_short | Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration. |
| title_sort | store operated ca2 entry soce regulates melanoma proliferation and cell migration |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089292&type=printable |
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