{"id":{"repo_id":"ku","oai_identifier":"oai:kuscholarworks.ku.edu:1808/37320"},"canonical_url":"https://search.dev.ndltd.org/etd/ku/oai:kuscholarworks.ku.edu:1808/37320","repository":{"repo_id":"ku","name":"University of Kansas","base_url":"https://kuscholarworks.ku.edu/server/oai/request"},"display":{"title":"Taxotere suppresses breast cancer growth through inducing lincRNA-p21 expression","abstract":"It has been reported that long non-coding RNA lincRNA-p21 is induced upon radiation and chemotherapy. This induction contributes to DNA-damage repair, cell death and cell cycle regulation. In this study, we focused on Taxotere (TXT) mediated chemotherapy of breast cancer cells and found that lincRNA-p21 is robotically induced upon TXT treatment. Secondly, we observed increased chemoresistance in three different breast cancer cell lines with lincRNA-p21 knockdown. Mechanistically, we found that lincRNA-p21 knockdown lead to decreased cell death during chemotherapy comparing to the negative control. In addition, our work showed that p21 is a downstream target of lincRNA-p21 in human breast cancer cells, and the loss of lincRNA-p21 caused p21 downregulation at both the RNA and protein levels.","abstract_html":"It has been reported that long non-coding RNA lincRNA-p21 is induced upon radiation and chemotherapy. This induction contributes to DNA-damage repair, cell death and cell cycle regulation. In this study, we focused on Taxotere (TXT) mediated chemotherapy of breast cancer cells and found that lincRNA-p21 is robotically induced upon TXT treatment. Secondly, we observed increased chemoresistance in three different breast cancer cell lines with lincRNA-p21 knockdown. Mechanistically, we found that lincRNA-p21 knockdown lead to decreased cell death during chemotherapy comparing to the negative control. In addition, our work showed that p21 is a downstream target of lincRNA-p21 in human breast cancer cells, and the loss of lincRNA-p21 caused p21 downregulation at both the RNA and protein levels.","abstract_has_math":false,"creators":["Guo, Yuxiao"],"institution":"University of Kansas","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Xu, Liang"],"committee_chairs":[],"committee_members":[],"year":2017,"date_issued":"2017-01-01","date_published":"2017-01-01","updated_at":"2026-07-24T02:46:29Z","subjects":["Biology","Breast Cancer","Long non-coding RNA","Taxotere"],"languages":["en"],"rights":["This item is protected by copyright and unless otherwise specified the copyright of this thesis/dissertation is held by the author."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["https://www.proquest.com/LegacyDocView/DISSNUM/10256469"],"render_values":[{"text":"https://www.proquest.com/LegacyDocView/DISSNUM/10256469","href":"https://www.proquest.com/LegacyDocView/DISSNUM/10256469","code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/1808/37320","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Xu, Liang"]},{"key":"dc:creator","label":"Author","values":["Guo, Yuxiao"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2026-04-14T19:43:39Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2026-04-14T19:43:39Z"]},{"key":"dc:date.issued","label":"Date","values":["2017-01-01"]},{"key":"dc:publisher","label":"Institution","values":["University of Kansas"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology","Breast Cancer","Long non-coding RNA","Taxotere"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["This item is protected by copyright and unless otherwise specified the copyright of this thesis/dissertation is held by the author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["https://www.proquest.com/LegacyDocView/DISSNUM/10256469"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/1808/37320"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["It has been reported that long non-coding RNA lincRNA-p21 is induced upon radiation and chemotherapy. This induction contributes to DNA-damage repair, cell death and cell cycle regulation. In this study, we focused on Taxotere (TXT) mediated chemotherapy of breast cancer cells and found that lincRNA-p21 is robotically induced upon TXT treatment. Secondly, we observed increased chemoresistance in three different breast cancer cell lines with lincRNA-p21 knockdown. Mechanistically, we found that lincRNA-p21 knockdown lead to decreased cell death during chemotherapy comparing to the negative control. In addition, our work showed that p21 is a downstream target of lincRNA-p21 in human breast cancer cells, and the loss of lincRNA-p21 caused p21 downregulation at both the RNA and protein levels."]},{"key":"dc:title","label":"Title","values":["Taxotere suppresses breast cancer growth through inducing lincRNA-p21 expression"]}]}],"canonical_facts":{"dc:contributor.advisor":["Xu, Liang"],"dc:creator":["Guo, Yuxiao"],"dc:date.accessioned":["2026-04-14T19:43:39Z"],"dc:date.available":["2026-04-14T19:43:39Z"],"dc:date.issued":["2017-01-01"],"dc:description.abstract":["It has been reported that long non-coding RNA lincRNA-p21 is induced upon radiation and chemotherapy. This induction contributes to DNA-damage repair, cell death and cell cycle regulation. In this study, we focused on Taxotere (TXT) mediated chemotherapy of breast cancer cells and found that lincRNA-p21 is robotically induced upon TXT treatment. Secondly, we observed increased chemoresistance in three different breast cancer cell lines with lincRNA-p21 knockdown. Mechanistically, we found that lincRNA-p21 knockdown lead to decreased cell death during chemotherapy comparing to the negative control. In addition, our work showed that p21 is a downstream target of lincRNA-p21 in human breast cancer cells, and the loss of lincRNA-p21 caused p21 downregulation at both the RNA and protein levels."],"dc:identifier.other":["https://www.proquest.com/LegacyDocView/DISSNUM/10256469"],"dc:identifier.uri":["https://hdl.handle.net/1808/37320"],"dc:language.iso":["en"],"dc:publisher":["University of Kansas"],"dc:rights":["This item is protected by copyright and unless otherwise specified the copyright of this thesis/dissertation is held by the author."],"dc:subject":["Biology","Breast Cancer","Long non-coding RNA","Taxotere"],"dc:title":["Taxotere suppresses breast cancer growth through inducing lincRNA-p21 expression"],"dc:type":["Thesis"]},"updated_at":"2026-07-24T02:46:29Z"}