Bromocriptine, a D2 dopamine receptor (D2R) agonist, is used clinically as a treatment for pituitary tumors of a lactotroph origin. Many questions remain unanswered about the mechanism of this effect. The antiproliferative effect has not been demonstrated in DMS 53 cell line, a Small Cell Lung Cancer (SCLC). In this thesis, we have shown that treatment with NPA (N‑propylnorapomorphine), a dopamine receptor agonist inhibits ERK phosphorylation and proliferation in DMS 53 cells. NPA treatment causes significant increases in DUSP‑1 (MKP‑1), DUSP‑4 (MKP‑2) and DUSP5 mRNA. NPA treatment also correlates with increases in DUSP5 (hVHR3) protein visualized using Western Blot. These three genes were also induced by treatment with exogenous arachidonic acid (AA). In addition, the NPA mediated increases in these genes was inhibited by 5,8,11,14‑eicosatetraynoic acid (ETYA) an AA analog and inhibitor of downstream activity, suggesting NPA induction of these three genes is AA dependent. Ethanol treatment leads to inhibition of the NPA induction of DUSP4 and DUSP5, suggesting phosphatidic acid (PA) produced from Phospholipase D (PLD) is involved in this induction.
","abstract_html":"<p>Bromocriptine, a D2 dopamine receptor (D2R) agonist, is used clinically as a treatment for pituitary tumors of a lactotroph origin. Many questions remain unanswered about the mechanism of this effect. The antiproliferative effect has not been demonstrated in DMS 53 cell line, a Small Cell Lung Cancer (SCLC). In this thesis, we have shown that treatment with NPA (N‑propylnorapomorphine), a dopamine receptor agonist inhibits ERK phosphorylation and proliferation in DMS 53 cells. NPA treatment causes significant increases in DUSP‑1 (MKP‑1), DUSP‑4 (MKP‑2) and DUSP5 mRNA. NPA treatment also correlates with increases in DUSP5 (hVHR3) protein visualized using Western Blot. These three genes were also induced by treatment with exogenous arachidonic acid (AA). In addition, the NPA mediated increases in these genes was inhibited by 5,8,11,14‑eicosatetraynoic acid (ETYA) an AA analog and inhibitor of downstream activity, suggesting NPA induction of these three genes is AA dependent. Ethanol treatment leads to inhibition of the NPA induction of DUSP4 and DUSP5, suggesting phosphatidic acid (PA) produced from Phospholipase D (PLD) is involved in this induction.</p>","abstract_has_math":false,"creators":["Lattimer, Scott Lemar"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Thesis","degree_discipline":"Biomedical Sciences","degree_department":null,"school":null,"contributors":["Susan E. Senogles, Ph.D."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-12-01T08:00:00Z","date_published":"2010-12-01T08:00:00Z","updated_at":"2026-07-24T05:00:11Z","subjects":["Arachidonic Acid","Dopamine","Dusp","ERK","MKP","Proliferation","Medical Cell Biology","Medical Sciences","Medicine and Health Sciences"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dc.uthsc.edu/dissertations/149","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Susan E. Senogles, Ph.D."]},{"key":"dc:creator","label":"Author","values":["Lattimer, Scott Lemar"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2016-06-08T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Arachidonic Acid","Dopamine","Dusp","ERK","MKP","Proliferation","Medical Cell Biology","Medical Sciences","Medicine and Health Sciences"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dc.uthsc.edu/dissertations/149"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Bromocriptine, a D2 dopamine receptor (D2R) agonist, is used clinically as a treatment for pituitary tumors of a lactotroph origin. Many questions remain unanswered about the mechanism of this effect. The antiproliferative effect has not been demonstrated in DMS 53 cell line, a Small Cell Lung Cancer (SCLC). In this thesis, we have shown that treatment with NPA (N‑propylnorapomorphine), a dopamine receptor agonist inhibits ERK phosphorylation and proliferation in DMS 53 cells. NPA treatment causes significant increases in DUSP‑1 (MKP‑1), DUSP‑4 (MKP‑2) and DUSP5 mRNA. NPA treatment also correlates with increases in DUSP5 (hVHR3) protein visualized using Western Blot. These three genes were also induced by treatment with exogenous arachidonic acid (AA). In addition, the NPA mediated increases in these genes was inhibited by 5,8,11,14‑eicosatetraynoic acid (ETYA) an AA analog and inhibitor of downstream activity, suggesting NPA induction of these three genes is AA dependent. Ethanol treatment leads to inhibition of the NPA induction of DUSP4 and DUSP5, suggesting phosphatidic acid (PA) produced from Phospholipase D (PLD) is involved in this induction.
"]},{"key":"dc:title","label":"Title","values":["D2R Dopamine Receptor Mediates Changes in Dual Specificity Phosphatase Expression in a Small Cell Lung Cancer Cell Line"]}]}],"canonical_facts":{"dc:contributor":["Susan E. Senogles, Ph.D."],"dc:creator":["Lattimer, Scott Lemar"],"dc:date.available":["2016-06-08T07:00:00Z"],"dc:description.abstract":["Bromocriptine, a D2 dopamine receptor (D2R) agonist, is used clinically as a treatment for pituitary tumors of a lactotroph origin. Many questions remain unanswered about the mechanism of this effect. The antiproliferative effect has not been demonstrated in DMS 53 cell line, a Small Cell Lung Cancer (SCLC). In this thesis, we have shown that treatment with NPA (N‑propylnorapomorphine), a dopamine receptor agonist inhibits ERK phosphorylation and proliferation in DMS 53 cells. NPA treatment causes significant increases in DUSP‑1 (MKP‑1), DUSP‑4 (MKP‑2) and DUSP5 mRNA. NPA treatment also correlates with increases in DUSP5 (hVHR3) protein visualized using Western Blot. These three genes were also induced by treatment with exogenous arachidonic acid (AA). In addition, the NPA mediated increases in these genes was inhibited by 5,8,11,14‑eicosatetraynoic acid (ETYA) an AA analog and inhibitor of downstream activity, suggesting NPA induction of these three genes is AA dependent. Ethanol treatment leads to inhibition of the NPA induction of DUSP4 and DUSP5, suggesting phosphatidic acid (PA) produced from Phospholipase D (PLD) is involved in this induction.
"],"dc:identifier":["https://dc.uthsc.edu/dissertations/149"],"dc:subject":["Arachidonic Acid","Dopamine","Dusp","ERK","MKP","Proliferation","Medical Cell Biology","Medical Sciences","Medicine and Health Sciences"],"dc:title":["D2R Dopamine Receptor Mediates Changes in Dual Specificity Phosphatase Expression in a Small Cell Lung Cancer Cell Line"],"thesis:degree_discipline":["Biomedical Sciences"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:00:11Z"}