{"id":{"repo_id":"nus","oai_identifier":"oai:scholarbank.nus.edu.sg:10635/47541"},"canonical_url":"https://search.dev.ndltd.org/etd/nus/oai:scholarbank.nus.edu.sg:10635/47541","repository":{"repo_id":"nus","name":"National University of Singapore","base_url":"https://scholarbank.nus.edu.sg/oai/request"},"display":{"title":"A NOVEL PRO-OXIDANT ROLE OF GELSOLIN IN CANCER CELL INVASION","abstract":"Although gelsolin is often implicated in cancer cell invasion, the mechanisms remain poorly understood. We have identified a new role of gelsolin in creating a pro-oxidant milieu thereby enhancing cancer cell invasion. Increased gelsolin expression in HCT116 results in heightened ROS levels, particularly the superoxides (O2-) as well as increased invasion; whereas silencing of gelsolin reduces O2- levels and invasion. Inhbition of O2- produciton using diphenyleneiodonium significanlty attenuates invasion in gelsolin-overexpresing HCT116 cells. Consistently, the invasive capacities of gelsolin-deficient cells were rescued by increasing the O2- levels in these cells. Furthermore we show that gelsolin overexpression suppresses the activity of the antioxidant Cu/Zn SOD, possibly by binding to it. The impairment of Cu/Zn SOD activity provides a mechanistic explanation for the elevated amount of intracellular O2- in gelsolin-overexpressing cells. Therefore, our findings demonstrate a new insight into the role of gelsolin in cancer cell invasion through upregulation of O2- levels.","abstract_html":"Although gelsolin is often implicated in cancer cell invasion, the mechanisms remain poorly understood. We have identified a new role of gelsolin in creating a pro-oxidant milieu thereby enhancing cancer cell invasion. Increased gelsolin expression in HCT116 results in heightened ROS levels, particularly the superoxides (O2-) as well as increased invasion; whereas silencing of gelsolin reduces O2- levels and invasion. Inhbition of O2- produciton using diphenyleneiodonium significanlty attenuates invasion in gelsolin-overexpresing HCT116 cells. Consistently, the invasive capacities of gelsolin-deficient cells were rescued by increasing the O2- levels in these cells. Furthermore we show that gelsolin overexpression suppresses the activity of the antioxidant Cu/Zn SOD, possibly by binding to it. The impairment of Cu/Zn SOD activity provides a mechanistic explanation for the elevated amount of intracellular O2- in gelsolin-overexpressing cells. Therefore, our findings demonstrate a new insight into the role of gelsolin in cancer cell invasion through upregulation of O2- levels.","abstract_has_math":false,"creators":["LALCHHANDAMI TOCHHAWNG"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-01-10","date_published":"2013-01-10","updated_at":"2026-07-24T03:33:34Z","subjects":["gelsolin, actin, superoxide dismutase, ROS, cancer, invasion,"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["LALCHHANDAMI TOCHHAWNG"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2013-01-10"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://scholarbank.nus.edu.sg/handle/10635/47541"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["gelsolin, actin, superoxide dismutase, ROS, cancer, invasion,"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://scholarbank.nus.edu.sg/bitstreams/ed32bcea-ef65-4bb1-a1a2-df047070b72d/download"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Although gelsolin is often implicated in cancer cell invasion, the mechanisms remain poorly understood. We have identified a new role of gelsolin in creating a pro-oxidant milieu thereby enhancing cancer cell invasion. Increased gelsolin expression in HCT116 results in heightened ROS levels, particularly the superoxides (O2-) as well as increased invasion; whereas silencing of gelsolin reduces O2- levels and invasion. Inhbition of O2- produciton using diphenyleneiodonium significanlty attenuates invasion in gelsolin-overexpresing HCT116 cells. Consistently, the invasive capacities of gelsolin-deficient cells were rescued by increasing the O2- levels in these cells. Furthermore we show that gelsolin overexpression suppresses the activity of the antioxidant Cu/Zn SOD, possibly by binding to it. The impairment of Cu/Zn SOD activity provides a mechanistic explanation for the elevated amount of intracellular O2- in gelsolin-overexpressing cells. 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Inhbition of O2- produciton using diphenyleneiodonium significanlty attenuates invasion in gelsolin-overexpresing HCT116 cells. Consistently, the invasive capacities of gelsolin-deficient cells were rescued by increasing the O2- levels in these cells. Furthermore we show that gelsolin overexpression suppresses the activity of the antioxidant Cu/Zn SOD, possibly by binding to it. The impairment of Cu/Zn SOD activity provides a mechanistic explanation for the elevated amount of intracellular O2- in gelsolin-overexpressing cells. 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