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Conference Paper: Dexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomid
Title | Dexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomid |
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Authors | |
Issue Date | 2014 |
Publisher | Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/ |
Citation | The 2014 Annual Meeting of Experimental Biology (EB 2014), San Diego, CA., 26-30 April 2014. In The FASEB Journal, 2014, v. 28 suppl. 1, p. abstract no. LB642 How to Cite? |
Abstract | Dexmedetomidine(DEX), an alpha-2 adrenergic agonist which can affect cell-to-cell gap junctions(GJ), is used as an adjuvant analgesic and sedatives in patients with cancer pain, especially in neural cancer patients who concomitantly receiving chemotherapy. GJ may increase the sensitivity of tumor cells to chemotherapeutic agents (Oncol Rep. 2014;31:540-550). It is unknown whether or not DEX may affect the sensitivity of gliocytoma (U87 cell, which richly expresses the GJ protein Connexin43) to temozolomide (TEM, an anticancer agent for gliocytoma) and if DEX exerts its effect via affecting GJ. U87 cells were treated with TEM, respectively at high density (which form GJ) or low density (without GJ formation), for 1 hour in the absence or presence of 3 hours DEX pretreatment prior to applying TEM. TEM toxicity (i.e., reduction of clonogenic cell survival), was assayed by “Standard Clony-forming assay” and GJ function was examined by “Parachute' dye-coupling assay. TEM toxicity was greater at high density than at low density cells (P<0.01), while either oleamide (a GJ inhibitor) or Cx43 siRNA reduced TEM toxicity. Similarly, DEX reduced GJ function and compromised TEM treatment effects, manifested as increases in clonogenic cell survivals at high but not at low cell density. We concluded that DEX reduced TEM cytotoxicity through inhibiting GJ function in gliocytoma. |
Description | Conference Theme: Transforming the Future through Science Session: Pharmacology and Experimental Therapeutics - Toxicology |
Persistent Identifier | http://hdl.handle.net/10722/204768 |
ISSN | 2023 Impact Factor: 4.4 2023 SCImago Journal Rankings: 1.412 |
DC Field | Value | Language |
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dc.contributor.author | Wang, L | en_US |
dc.contributor.author | Zhang, S | - |
dc.contributor.author | Huang, H | - |
dc.contributor.author | Xia, W | - |
dc.contributor.author | Xia, Z | - |
dc.date.accessioned | 2014-09-20T00:39:20Z | - |
dc.date.available | 2014-09-20T00:39:20Z | - |
dc.date.issued | 2014 | en_US |
dc.identifier.citation | The 2014 Annual Meeting of Experimental Biology (EB 2014), San Diego, CA., 26-30 April 2014. In The FASEB Journal, 2014, v. 28 suppl. 1, p. abstract no. LB642 | en_US |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10722/204768 | - |
dc.description | Conference Theme: Transforming the Future through Science | - |
dc.description | Session: Pharmacology and Experimental Therapeutics - Toxicology | - |
dc.description.abstract | Dexmedetomidine(DEX), an alpha-2 adrenergic agonist which can affect cell-to-cell gap junctions(GJ), is used as an adjuvant analgesic and sedatives in patients with cancer pain, especially in neural cancer patients who concomitantly receiving chemotherapy. GJ may increase the sensitivity of tumor cells to chemotherapeutic agents (Oncol Rep. 2014;31:540-550). It is unknown whether or not DEX may affect the sensitivity of gliocytoma (U87 cell, which richly expresses the GJ protein Connexin43) to temozolomide (TEM, an anticancer agent for gliocytoma) and if DEX exerts its effect via affecting GJ. U87 cells were treated with TEM, respectively at high density (which form GJ) or low density (without GJ formation), for 1 hour in the absence or presence of 3 hours DEX pretreatment prior to applying TEM. TEM toxicity (i.e., reduction of clonogenic cell survival), was assayed by “Standard Clony-forming assay” and GJ function was examined by “Parachute' dye-coupling assay. TEM toxicity was greater at high density than at low density cells (P<0.01), while either oleamide (a GJ inhibitor) or Cx43 siRNA reduced TEM toxicity. Similarly, DEX reduced GJ function and compromised TEM treatment effects, manifested as increases in clonogenic cell survivals at high but not at low cell density. We concluded that DEX reduced TEM cytotoxicity through inhibiting GJ function in gliocytoma. | - |
dc.language | eng | en_US |
dc.publisher | Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/ | - |
dc.relation.ispartof | The FASEB Journal | en_US |
dc.title | Dexmedetomidine suppresses gap junctional intercellular communication and attenuates the sensitivity of gliocytoma to temozolomid | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | en_US |
dc.identifier.authority | Xia, Z=rp00532 | en_US |
dc.identifier.hkuros | 235645 | en_US |
dc.identifier.volume | 28 | en_US |
dc.identifier.issue | suppl. 1 | en_US |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0892-6638 | - |