Hepatocyte Growth Factor/Scatter Factor (HGF/SF) stimulates migration of various cells and has been linked via Met tyrosine kinase signaling to transformation and the metastatic phenotype. HGF/SF-Met signaling also plays a role in malignancy. Migration of transformed MDCK-F cells depends on activation of a charybdotoxin (ChTX)-sensitive, volume-activated membrane K+ current. Patch-clamp electrophysiology and transwell migration assays were used to study the effects of HGF/SF on membrane K+ currents and cell migration in MDCK II cells. HGF/SF activated membrane K+ currents that increased over 24 hr, and these could be modulated by altering intracellular free calcium concentration [Ca2+]i. HGF/SF also significantly increased MDCK II cell migration. Specific Ca2+-activated K+ channel blockers, ChTX, iberiotoxin (IbTX), stichodactyla toxin (Stk) and clotrimazole (CLT) inhibited HGF/SF stimulation of membrane K+ currents and cell migration. This suggests that the activation of Ca2+-activated K+ channels is necessary for HGF/SF stimulation of MDCK II cell migration. Furthermore, HGF/SF induced ERK phosphorylation, and addition of the MEK inhibitor PD98059 inhibited ERK phosphorylation, as well as HGF/SF stimulation of Ca2+-activated K+ currents and cell migration in MDCK II cells. Taken together, HGF/SF induces phosphorylation of ERK, which plays a role in HGF/SF activation of Ca2+-activated K+ channels and enhancing cell migration in MDCK II cells.
","abstract_html":"<p>Hepatocyte Growth Factor/Scatter Factor (HGF/SF) stimulates migration of various cells and has been linked via Met tyrosine kinase signaling to transformation and the metastatic phenotype. HGF/SF-Met signaling also plays a role in malignancy. Migration of transformed MDCK-F cells depends on activation of a charybdotoxin (ChTX)-sensitive, volume-activated membrane K<sup>+</sup> current. Patch-clamp electrophysiology and transwell migration assays were used to study the effects of HGF/SF on membrane K<sup>+</sup> currents and cell migration in MDCK II cells. HGF/SF activated membrane K<sup>+</sup> currents that increased over 24 hr, and these could be modulated by altering intracellular free calcium concentration [Ca<sup>2+</sup>]i. HGF/SF also significantly increased MDCK II cell migration. Specific Ca<sup>2+</sup>-activated K<sup>+</sup> channel blockers, ChTX, iberiotoxin (IbTX), stichodactyla toxin (Stk) and clotrimazole (CLT) inhibited HGF/SF stimulation of membrane K<sup>+</sup> currents and cell migration. This suggests that the activation of Ca<sup>2+</sup>-activated K<sup>+</sup> channels is necessary for HGF/SF stimulation of MDCK II cell migration. Furthermore, HGF/SF induced ERK phosphorylation, and addition of the MEK inhibitor PD98059 inhibited ERK phosphorylation, as well as HGF/SF stimulation of Ca<sup>2+</sup>-activated K<sup>+</sup> currents and cell migration in MDCK II cells. Taken together, HGF/SF induces phosphorylation of ERK, which plays a role in HGF/SF activation of Ca<sup>2+</sup>-activated K<sup>+</sup> channels and enhancing cell migration in MDCK II cells.</p>","abstract_has_math":false,"creators":["Jin, Min"],"institution":null,"degree_name":"PhD (Doctor of Philosophy)","degree_level":"Dissertation - unrestricted","degree_discipline":"Biomedical Sciences","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2002,"date_issued":"2002-12-14T08:00:00Z","date_published":"2002-12-14T08:00:00Z","updated_at":"2026-07-24T02:19:21Z","subjects":["HGF/SF","Ca2+-activated K+ channel","MEK","ERK","Medical Sciences","Medicine and Health Sciences"],"languages":[],"rights":["Copyright by the authors."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dc.etsu.edu/etd/712","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Jin, Min"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2002-12-14T08:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation - unrestricted"]},{"key":"thesis:degree_name","label":"Degree Name","values":["PhD (Doctor of Philosophy)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["HGF/SF","Ca2+-activated K+ channel","MEK","ERK","Medical Sciences","Medicine and Health Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["Copyright by the authors."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dc.etsu.edu/context/etd/article/1869/viewcontent/JinM091302a.pdf","https://dc.etsu.edu/etd/712"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Hepatocyte Growth Factor/Scatter Factor (HGF/SF) stimulates migration of various cells and has been linked via Met tyrosine kinase signaling to transformation and the metastatic phenotype. HGF/SF-Met signaling also plays a role in malignancy. Migration of transformed MDCK-F cells depends on activation of a charybdotoxin (ChTX)-sensitive, volume-activated membrane K+ current. Patch-clamp electrophysiology and transwell migration assays were used to study the effects of HGF/SF on membrane K+ currents and cell migration in MDCK II cells. HGF/SF activated membrane K+ currents that increased over 24 hr, and these could be modulated by altering intracellular free calcium concentration [Ca2+]i. HGF/SF also significantly increased MDCK II cell migration. Specific Ca2+-activated K+ channel blockers, ChTX, iberiotoxin (IbTX), stichodactyla toxin (Stk) and clotrimazole (CLT) inhibited HGF/SF stimulation of membrane K+ currents and cell migration. This suggests that the activation of Ca2+-activated K+ channels is necessary for HGF/SF stimulation of MDCK II cell migration. Furthermore, HGF/SF induced ERK phosphorylation, and addition of the MEK inhibitor PD98059 inhibited ERK phosphorylation, as well as HGF/SF stimulation of Ca2+-activated K+ currents and cell migration in MDCK II cells. Taken together, HGF/SF induces phosphorylation of ERK, which plays a role in HGF/SF activation of Ca2+-activated K+ channels and enhancing cell migration in MDCK II cells.
"]},{"key":"dc:title","label":"Title","values":["Activation of Ca2+-activated K+ Channels and Cell Migration by Hepatocyte Growth Factor/Scatter Factor in Madin-Darby Canine Kidney Cells."]}]}],"canonical_facts":{"dc:creator":["Jin, Min"],"dc:date.issued":["2002-12-14T08:00:00Z"],"dc:description.abstract":["Hepatocyte Growth Factor/Scatter Factor (HGF/SF) stimulates migration of various cells and has been linked via Met tyrosine kinase signaling to transformation and the metastatic phenotype. HGF/SF-Met signaling also plays a role in malignancy. Migration of transformed MDCK-F cells depends on activation of a charybdotoxin (ChTX)-sensitive, volume-activated membrane K+ current. Patch-clamp electrophysiology and transwell migration assays were used to study the effects of HGF/SF on membrane K+ currents and cell migration in MDCK II cells. HGF/SF activated membrane K+ currents that increased over 24 hr, and these could be modulated by altering intracellular free calcium concentration [Ca2+]i. HGF/SF also significantly increased MDCK II cell migration. Specific Ca2+-activated K+ channel blockers, ChTX, iberiotoxin (IbTX), stichodactyla toxin (Stk) and clotrimazole (CLT) inhibited HGF/SF stimulation of membrane K+ currents and cell migration. This suggests that the activation of Ca2+-activated K+ channels is necessary for HGF/SF stimulation of MDCK II cell migration. Furthermore, HGF/SF induced ERK phosphorylation, and addition of the MEK inhibitor PD98059 inhibited ERK phosphorylation, as well as HGF/SF stimulation of Ca2+-activated K+ currents and cell migration in MDCK II cells. Taken together, HGF/SF induces phosphorylation of ERK, which plays a role in HGF/SF activation of Ca2+-activated K+ channels and enhancing cell migration in MDCK II cells.
"],"dc:identifier":["https://dc.etsu.edu/context/etd/article/1869/viewcontent/JinM091302a.pdf","https://dc.etsu.edu/etd/712"],"dc:rights":["Copyright by the authors."],"dc:subject":["HGF/SF","Ca2+-activated K+ channel","MEK","ERK","Medical Sciences","Medicine and Health Sciences"],"dc:title":["Activation of Ca2+-activated K+ Channels and Cell Migration by Hepatocyte Growth Factor/Scatter Factor in Madin-Darby Canine Kidney Cells."],"thesis:degree_discipline":["Biomedical Sciences"],"thesis:degree_level":["Dissertation - unrestricted"],"thesis:degree_name":["PhD (Doctor of Philosophy)"]},"updated_at":"2026-07-24T02:19:21Z"}