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Effects of lysophosphatidic acid (LPA) signaling via LPA receptors on cellular functions associated with ATP reduction in osteosarcoma cells treated with ethidium bromide
Lysophosphatidic acid (LPA) signaling via LPA receptors (LPA 1 to LPA 6 ) exhibits a variety of malignant properties in cancer cells. Intracellular ATP depletion leads to the development of necrosis and apoptosis. The present study aimed to evaluate the effects of LPA receptor-mediated signaling on...
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| Published in: | Journal of bioenergetics and biomembranes 2022-04, Vol.54 (2), p.109-117 |
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| container_end_page | 117 |
| container_issue | 2 |
| container_start_page | 109 |
| container_title | Journal of bioenergetics and biomembranes |
| container_volume | 54 |
| creator | Kurisu, Rio Takamoto, Miyu Minami, Kanako Ueda, Nanami Yamada, Marina Shima, Nanami Otani, Tomoka Sakai, Yuma Kondo, Daisuke Tsujiuchi, Toshifumi |
| description | Lysophosphatidic acid (LPA) signaling via LPA receptors (LPA
1
to LPA
6
) exhibits a variety of malignant properties in cancer cells. Intracellular ATP depletion leads to the development of necrosis and apoptosis. The present study aimed to evaluate the effects of LPA receptor-mediated signaling on the regulation of cancer cell functions associated with ATP reduction. Long-term ethidium bromide (EtBr) treated (MG63-EtBr) cells were established from osteosarcoma MG-63 cells. The intracellular ATP levels of MG63-EtBr cells were significantly lower than that of MG-63 cells.
LPAR2
,
LPAR3
,
LPAR4
and
LPAR6
gene expressions were elevated in MG63-EtBr cells. The cell motile and invasive activities of MG63-EtBr cells were markedly higher than those of MG-63 cells. The cell motile activity of MG-63 cells was increased by LPA
4
and LPA
6
knockdowns. In cell survival assay, cells were treated with cisplatin (CDDP) every 24 h for 3 days. The cell survival to CDDP of MG63-EtBr cells was lower than that of MG-63 cells. LPA
2
knockdown decreased the cell survival to CDDP of MG-63 cells. The cell survival to CDDP of MG-63 cells was inhibited by (2 S)-OMPT (LPA
3
agonist). Moreover, the cell survival to CDDP of MG-63 cells was enhanced by LPA
4
and LPA
6
knockdowns. These results indicate that LPA signaling via LPA receptors is involved in the regulation of cellular functions associated with ATP reduction in MG-63 cells treated with EtBr. |
| doi_str_mv | 10.1007/s10863-022-09933-8 |
| format | article |
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1
to LPA
6
) exhibits a variety of malignant properties in cancer cells. Intracellular ATP depletion leads to the development of necrosis and apoptosis. The present study aimed to evaluate the effects of LPA receptor-mediated signaling on the regulation of cancer cell functions associated with ATP reduction. Long-term ethidium bromide (EtBr) treated (MG63-EtBr) cells were established from osteosarcoma MG-63 cells. The intracellular ATP levels of MG63-EtBr cells were significantly lower than that of MG-63 cells.
LPAR2
,
LPAR3
,
LPAR4
and
LPAR6
gene expressions were elevated in MG63-EtBr cells. The cell motile and invasive activities of MG63-EtBr cells were markedly higher than those of MG-63 cells. The cell motile activity of MG-63 cells was increased by LPA
4
and LPA
6
knockdowns. In cell survival assay, cells were treated with cisplatin (CDDP) every 24 h for 3 days. The cell survival to CDDP of MG63-EtBr cells was lower than that of MG-63 cells. LPA
2
knockdown decreased the cell survival to CDDP of MG-63 cells. The cell survival to CDDP of MG-63 cells was inhibited by (2 S)-OMPT (LPA
3
agonist). Moreover, the cell survival to CDDP of MG-63 cells was enhanced by LPA
4
and LPA
6
knockdowns. These results indicate that LPA signaling via LPA receptors is involved in the regulation of cellular functions associated with ATP reduction in MG-63 cells treated with EtBr.</description><identifier>ISSN: 0145-479X</identifier><identifier>EISSN: 1573-6881</identifier><identifier>DOI: 10.1007/s10863-022-09933-8</identifier><identifier>PMID: 35260987</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenosine Triphosphate - pharmacology ; Animal Anatomy ; Animal Biochemistry ; Apoptosis ; ATP ; Biochemistry ; Biomedical materials ; Bioorganic Chemistry ; Bone cancer ; Bone Neoplasms - drug therapy ; Bone Neoplasms - genetics ; Cancer ; Cell Movement ; Cell survival ; Chemistry ; Chemistry and Materials Science ; Cisplatin ; Depletion ; Ethidium - pharmacology ; Ethidium bromide ; Gene Expression Regulation, Neoplastic ; Histology ; Humans ; Intracellular ; Invasiveness ; Lysophosphatidic acid ; Lysophospholipids - metabolism ; Morphology ; Necrosis ; Organic Chemistry ; Osteosarcoma ; Osteosarcoma - drug therapy ; Osteosarcoma - genetics ; Osteosarcoma cells ; Receptor mechanisms ; Receptors ; Receptors, Lysophosphatidic Acid - genetics ; Receptors, Lysophosphatidic Acid - metabolism ; Reduction ; Sarcoma ; Signaling ; Survival</subject><ispartof>Journal of bioenergetics and biomembranes, 2022-04, Vol.54 (2), p.109-117</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-3538be848586024a4146ee7965c7b3ce39bbfe50bea98d7d38d6adbe03f9b463</citedby><cites>FETCH-LOGICAL-c375t-3538be848586024a4146ee7965c7b3ce39bbfe50bea98d7d38d6adbe03f9b463</cites><orcidid>0000-0002-6890-1417</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35260987$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kurisu, Rio</creatorcontrib><creatorcontrib>Takamoto, Miyu</creatorcontrib><creatorcontrib>Minami, Kanako</creatorcontrib><creatorcontrib>Ueda, Nanami</creatorcontrib><creatorcontrib>Yamada, Marina</creatorcontrib><creatorcontrib>Shima, Nanami</creatorcontrib><creatorcontrib>Otani, Tomoka</creatorcontrib><creatorcontrib>Sakai, Yuma</creatorcontrib><creatorcontrib>Kondo, Daisuke</creatorcontrib><creatorcontrib>Tsujiuchi, Toshifumi</creatorcontrib><title>Effects of lysophosphatidic acid (LPA) signaling via LPA receptors on cellular functions associated with ATP reduction in osteosarcoma cells treated with ethidium bromide</title><title>Journal of bioenergetics and biomembranes</title><addtitle>J Bioenerg Biomembr</addtitle><addtitle>J Bioenerg Biomembr</addtitle><description>Lysophosphatidic acid (LPA) signaling via LPA receptors (LPA
1
to LPA
6
) exhibits a variety of malignant properties in cancer cells. Intracellular ATP depletion leads to the development of necrosis and apoptosis. The present study aimed to evaluate the effects of LPA receptor-mediated signaling on the regulation of cancer cell functions associated with ATP reduction. Long-term ethidium bromide (EtBr) treated (MG63-EtBr) cells were established from osteosarcoma MG-63 cells. The intracellular ATP levels of MG63-EtBr cells were significantly lower than that of MG-63 cells.
LPAR2
,
LPAR3
,
LPAR4
and
LPAR6
gene expressions were elevated in MG63-EtBr cells. The cell motile and invasive activities of MG63-EtBr cells were markedly higher than those of MG-63 cells. The cell motile activity of MG-63 cells was increased by LPA
4
and LPA
6
knockdowns. In cell survival assay, cells were treated with cisplatin (CDDP) every 24 h for 3 days. The cell survival to CDDP of MG63-EtBr cells was lower than that of MG-63 cells. LPA
2
knockdown decreased the cell survival to CDDP of MG-63 cells. The cell survival to CDDP of MG-63 cells was inhibited by (2 S)-OMPT (LPA
3
agonist). Moreover, the cell survival to CDDP of MG-63 cells was enhanced by LPA
4
and LPA
6
knockdowns. These results indicate that LPA signaling via LPA receptors is involved in the regulation of cellular functions associated with ATP reduction in MG-63 cells treated with EtBr.</description><subject>Adenosine Triphosphate - pharmacology</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Apoptosis</subject><subject>ATP</subject><subject>Biochemistry</subject><subject>Biomedical materials</subject><subject>Bioorganic Chemistry</subject><subject>Bone cancer</subject><subject>Bone Neoplasms - drug therapy</subject><subject>Bone Neoplasms - genetics</subject><subject>Cancer</subject><subject>Cell Movement</subject><subject>Cell survival</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cisplatin</subject><subject>Depletion</subject><subject>Ethidium - pharmacology</subject><subject>Ethidium bromide</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Histology</subject><subject>Humans</subject><subject>Intracellular</subject><subject>Invasiveness</subject><subject>Lysophosphatidic acid</subject><subject>Lysophospholipids - metabolism</subject><subject>Morphology</subject><subject>Necrosis</subject><subject>Organic Chemistry</subject><subject>Osteosarcoma</subject><subject>Osteosarcoma - drug therapy</subject><subject>Osteosarcoma - genetics</subject><subject>Osteosarcoma cells</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>Receptors, Lysophosphatidic Acid - genetics</subject><subject>Receptors, Lysophosphatidic Acid - metabolism</subject><subject>Reduction</subject><subject>Sarcoma</subject><subject>Signaling</subject><subject>Survival</subject><issn>0145-479X</issn><issn>1573-6881</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u1DAQxi0EokvhBTggS1zKIdSOE8c5rqryR1qpPeyhN8uxJ7uukjh4HFBfiafEu1uoxKGnkWZ-3zej-Qh5z9lnzlhziZwpKQpWlgVrWyEK9YKseN2IQirFX5IV41VdVE17d0beIN4zxhSr2WtyJupSslY1K_L7uu_BJqShp8MDhnkfcN6b5J231Fjv6MXmdv2Jot9NZvDTjv70huYWjWBhTiFm6UQtDMMymEj7ZbLJhwmpQQzWmwSO_vJpT9fb26xxy3FM_UQDJghoog2jORogTRGeBJD2-YplpF0Mo3fwlrzqzYDw7rGek-2X6-3Vt2Jz8_X71XpTWNHUqRC1UB2oStVKsrIyFa8kQNPK2jadsCDaruuhZh2YVrnGCeWkcR0w0bddJcU5uTjZzjH8WACTHj0ezjMThAV1KfMaVUreZPTjf-h9WGL-04GqpBScVyxT5YmyMSBG6PUc_Wjig-ZMH4LUpyB1DlIfg9Qqiz48Wi_dCO6f5G9yGRAnAPNo2kF82v2M7R-a-Kvo</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Kurisu, Rio</creator><creator>Takamoto, Miyu</creator><creator>Minami, Kanako</creator><creator>Ueda, Nanami</creator><creator>Yamada, Marina</creator><creator>Shima, Nanami</creator><creator>Otani, Tomoka</creator><creator>Sakai, Yuma</creator><creator>Kondo, Daisuke</creator><creator>Tsujiuchi, Toshifumi</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6890-1417</orcidid></search><sort><creationdate>20220401</creationdate><title>Effects of lysophosphatidic acid (LPA) signaling via LPA receptors on cellular functions associated with ATP reduction in osteosarcoma cells treated with ethidium bromide</title><author>Kurisu, Rio ; Takamoto, Miyu ; Minami, Kanako ; Ueda, Nanami ; Yamada, Marina ; Shima, Nanami ; Otani, Tomoka ; Sakai, Yuma ; Kondo, Daisuke ; Tsujiuchi, Toshifumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-3538be848586024a4146ee7965c7b3ce39bbfe50bea98d7d38d6adbe03f9b463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenosine Triphosphate - pharmacology</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Apoptosis</topic><topic>ATP</topic><topic>Biochemistry</topic><topic>Biomedical materials</topic><topic>Bioorganic Chemistry</topic><topic>Bone cancer</topic><topic>Bone Neoplasms - drug therapy</topic><topic>Bone Neoplasms - genetics</topic><topic>Cancer</topic><topic>Cell Movement</topic><topic>Cell survival</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Cisplatin</topic><topic>Depletion</topic><topic>Ethidium - pharmacology</topic><topic>Ethidium bromide</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Histology</topic><topic>Humans</topic><topic>Intracellular</topic><topic>Invasiveness</topic><topic>Lysophosphatidic acid</topic><topic>Lysophospholipids - metabolism</topic><topic>Morphology</topic><topic>Necrosis</topic><topic>Organic Chemistry</topic><topic>Osteosarcoma</topic><topic>Osteosarcoma - drug therapy</topic><topic>Osteosarcoma - genetics</topic><topic>Osteosarcoma cells</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Receptors, Lysophosphatidic Acid - genetics</topic><topic>Receptors, Lysophosphatidic Acid - metabolism</topic><topic>Reduction</topic><topic>Sarcoma</topic><topic>Signaling</topic><topic>Survival</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kurisu, Rio</creatorcontrib><creatorcontrib>Takamoto, Miyu</creatorcontrib><creatorcontrib>Minami, Kanako</creatorcontrib><creatorcontrib>Ueda, Nanami</creatorcontrib><creatorcontrib>Yamada, Marina</creatorcontrib><creatorcontrib>Shima, Nanami</creatorcontrib><creatorcontrib>Otani, Tomoka</creatorcontrib><creatorcontrib>Sakai, Yuma</creatorcontrib><creatorcontrib>Kondo, Daisuke</creatorcontrib><creatorcontrib>Tsujiuchi, Toshifumi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest - 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Academic</collection><jtitle>Journal of bioenergetics and biomembranes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kurisu, Rio</au><au>Takamoto, Miyu</au><au>Minami, Kanako</au><au>Ueda, Nanami</au><au>Yamada, Marina</au><au>Shima, Nanami</au><au>Otani, Tomoka</au><au>Sakai, Yuma</au><au>Kondo, Daisuke</au><au>Tsujiuchi, Toshifumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of lysophosphatidic acid (LPA) signaling via LPA receptors on cellular functions associated with ATP reduction in osteosarcoma cells treated with ethidium bromide</atitle><jtitle>Journal of bioenergetics and biomembranes</jtitle><stitle>J Bioenerg Biomembr</stitle><addtitle>J Bioenerg Biomembr</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>54</volume><issue>2</issue><spage>109</spage><epage>117</epage><pages>109-117</pages><issn>0145-479X</issn><eissn>1573-6881</eissn><abstract>Lysophosphatidic acid (LPA) signaling via LPA receptors (LPA
1
to LPA
6
) exhibits a variety of malignant properties in cancer cells. Intracellular ATP depletion leads to the development of necrosis and apoptosis. The present study aimed to evaluate the effects of LPA receptor-mediated signaling on the regulation of cancer cell functions associated with ATP reduction. Long-term ethidium bromide (EtBr) treated (MG63-EtBr) cells were established from osteosarcoma MG-63 cells. The intracellular ATP levels of MG63-EtBr cells were significantly lower than that of MG-63 cells.
LPAR2
,
LPAR3
,
LPAR4
and
LPAR6
gene expressions were elevated in MG63-EtBr cells. The cell motile and invasive activities of MG63-EtBr cells were markedly higher than those of MG-63 cells. The cell motile activity of MG-63 cells was increased by LPA
4
and LPA
6
knockdowns. In cell survival assay, cells were treated with cisplatin (CDDP) every 24 h for 3 days. The cell survival to CDDP of MG63-EtBr cells was lower than that of MG-63 cells. LPA
2
knockdown decreased the cell survival to CDDP of MG-63 cells. The cell survival to CDDP of MG-63 cells was inhibited by (2 S)-OMPT (LPA
3
agonist). Moreover, the cell survival to CDDP of MG-63 cells was enhanced by LPA
4
and LPA
6
knockdowns. These results indicate that LPA signaling via LPA receptors is involved in the regulation of cellular functions associated with ATP reduction in MG-63 cells treated with EtBr.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35260987</pmid><doi>10.1007/s10863-022-09933-8</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-6890-1417</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0145-479X |
| ispartof | Journal of bioenergetics and biomembranes, 2022-04, Vol.54 (2), p.109-117 |
| issn | 0145-479X 1573-6881 |
| language | eng |
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| source | Springer Nature |
| subjects | Adenosine Triphosphate - pharmacology Animal Anatomy Animal Biochemistry Apoptosis ATP Biochemistry Biomedical materials Bioorganic Chemistry Bone cancer Bone Neoplasms - drug therapy Bone Neoplasms - genetics Cancer Cell Movement Cell survival Chemistry Chemistry and Materials Science Cisplatin Depletion Ethidium - pharmacology Ethidium bromide Gene Expression Regulation, Neoplastic Histology Humans Intracellular Invasiveness Lysophosphatidic acid Lysophospholipids - metabolism Morphology Necrosis Organic Chemistry Osteosarcoma Osteosarcoma - drug therapy Osteosarcoma - genetics Osteosarcoma cells Receptor mechanisms Receptors Receptors, Lysophosphatidic Acid - genetics Receptors, Lysophosphatidic Acid - metabolism Reduction Sarcoma Signaling Survival |
| title | Effects of lysophosphatidic acid (LPA) signaling via LPA receptors on cellular functions associated with ATP reduction in osteosarcoma cells treated with ethidium bromide |
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