{"id":{"repo_id":"missouri","oai_identifier":"oai:mospace.umsystem.edu:10355/110319"},"canonical_url":"https://search.dev.ndltd.org/etd/missouri/oai:mospace.umsystem.edu:10355/110319","repository":{"repo_id":"missouri","name":"University of Missouri","base_url":"https://mospace.umsystem.edu/oai/request"},"display":{"title":"Evaluation of nanoscale delivery of miR 216 a/b, miR 217, and gemcitabine in pancreatic cancer cell lines","abstract":"Pancreatic cancer is one of the most lethal cancers, and mortality has remained largely unchanged despite advances in cancer diagnostics and therapeutics. MicroRNAs (miRNAs), a class of non-coding RNAs that regulate gene expression, have emerged as potential tools for early detection, prognosis, and therapeutic intervention in PDAC. Tumor-suppressive miRNAs such as miR-216a and miR-217 are typically downregulated in PDAC, and their restoration has been shown to inhibit tumor cell proliferation and promote apoptosis. A pentablock copolymer-based dual delivery nanoscale device (DDND) was developed co-delivers miRNA-216a/b, miRNA-/217 and gemcitabine. In vitro studies on human (Capan-1, MIAPaCa) and murine (KCT-3248) pancreatic cancer cell lines revealed that DDND treatment significantly reduced cell viability, increased apoptosis, and impaired cell migration and colony formation, compared to single-agent or polymer-alone treatments. To determine the underlying molecular mechanisms, Western blot analysis was conducted on lysates and supernatants from treated cells. Target proteins related to apoptosis, epithelial-to-mesenchymal transition, and oncogenic signaling pathways were evaluated. While some expected trends were observed, such as increased BAX expression in apoptotic cell supernatants and elevated E-cadherin in treated cells, many protein expression changes did not align with the hypothesized anti-tumor effects. Further refinement of western blot technique and the evaluation of additional target proteins is required to understand the mechanism through which the DDND treatment works.","abstract_html":"Pancreatic cancer is one of the most lethal cancers, and mortality has remained largely unchanged despite advances in cancer diagnostics and therapeutics. MicroRNAs (miRNAs), a class of non-coding RNAs that regulate gene expression, have emerged as potential tools for early detection, prognosis, and therapeutic intervention in PDAC. Tumor-suppressive miRNAs such as miR-216a and miR-217 are typically downregulated in PDAC, and their restoration has been shown to inhibit tumor cell proliferation and promote apoptosis. A pentablock copolymer-based dual delivery nanoscale device (DDND) was developed co-delivers miRNA-216a/b, miRNA-/217 and gemcitabine. In vitro studies on human (Capan-1, MIAPaCa) and murine (KCT-3248) pancreatic cancer cell lines revealed that DDND treatment significantly reduced cell viability, increased apoptosis, and impaired cell migration and colony formation, compared to single-agent or polymer-alone treatments. To determine the underlying molecular mechanisms, Western blot analysis was conducted on lysates and supernatants from treated cells. Target proteins related to apoptosis, epithelial-to-mesenchymal transition, and oncogenic signaling pathways were evaluated. While some expected trends were observed, such as increased BAX expression in apoptotic cell supernatants and elevated E-cadherin in treated cells, many protein expression changes did not align with the hypothesized anti-tumor effects. Further refinement of western blot technique and the evaluation of additional target proteins is required to understand the mechanism through which the DDND treatment works.","abstract_has_math":false,"creators":["Tran Hoang, Christine"],"institution":"University of Missouri--Columbia","degree_name":"M.S.","degree_level":"Masters","degree_discipline":"Biomedical Sciences","degree_department":null,"school":null,"contributors":[],"advisors":["Bryan, Jeffrey"],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025","date_published":"2025","updated_at":"2026-07-24T03:08:20Z","subjects":[],"languages":["eng","English"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.32469/10355/110319"],"render_values":[{"text":"https://doi.org/10.32469/10355/110319","href":"https://doi.org/10.32469/10355/110319","code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/10355/110319","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Bryan, Jeffrey"]},{"key":"dc:creator","label":"Author","values":["Tran Hoang, Christine"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2026-01-23T21:53:51Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2026-01-23T21:53:51Z"]},{"key":"dc:date.issued","label":"Date","values":["2025"]},{"key":"dc:publisher","label":"Institution","values":["University of Missouri--Columbia"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M.S."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Missouri--Columbia"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.32469/10355/110319"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/10355/110319"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Pancreatic cancer is one of the most lethal cancers, and mortality has remained largely unchanged despite advances in cancer diagnostics and therapeutics. MicroRNAs (miRNAs), a class of non-coding RNAs that regulate gene expression, have emerged as potential tools for early detection, prognosis, and therapeutic intervention in PDAC. Tumor-suppressive miRNAs such as miR-216a and miR-217 are typically downregulated in PDAC, and their restoration has been shown to inhibit tumor cell proliferation and promote apoptosis. A pentablock copolymer-based dual delivery nanoscale device (DDND) was developed co-delivers miRNA-216a/b, miRNA-/217 and gemcitabine. In vitro studies on human (Capan-1, MIAPaCa) and murine (KCT-3248) pancreatic cancer cell lines revealed that DDND treatment significantly reduced cell viability, increased apoptosis, and impaired cell migration and colony formation, compared to single-agent or polymer-alone treatments. To determine the underlying molecular mechanisms, Western blot analysis was conducted on lysates and supernatants from treated cells. Target proteins related to apoptosis, epithelial-to-mesenchymal transition, and oncogenic signaling pathways were evaluated. While some expected trends were observed, such as increased BAX expression in apoptotic cell supernatants and elevated E-cadherin in treated cells, many protein expression changes did not align with the hypothesized anti-tumor effects. Further refinement of western blot technique and the evaluation of additional target proteins is required to understand the mechanism through which the DDND treatment works."]},{"key":"dc:title","label":"Title","values":["Evaluation of nanoscale delivery of miR 216 a/b, miR 217, and gemcitabine in pancreatic cancer cell lines"]}]}],"canonical_facts":{"dc:contributor.advisor":["Bryan, Jeffrey"],"dc:creator":["Tran Hoang, Christine"],"dc:date.accessioned":["2026-01-23T21:53:51Z"],"dc:date.available":["2026-01-23T21:53:51Z"],"dc:date.issued":["2025"],"dc:description.abstract":["Pancreatic cancer is one of the most lethal cancers, and mortality has remained largely unchanged despite advances in cancer diagnostics and therapeutics. MicroRNAs (miRNAs), a class of non-coding RNAs that regulate gene expression, have emerged as potential tools for early detection, prognosis, and therapeutic intervention in PDAC. Tumor-suppressive miRNAs such as miR-216a and miR-217 are typically downregulated in PDAC, and their restoration has been shown to inhibit tumor cell proliferation and promote apoptosis. A pentablock copolymer-based dual delivery nanoscale device (DDND) was developed co-delivers miRNA-216a/b, miRNA-/217 and gemcitabine. In vitro studies on human (Capan-1, MIAPaCa) and murine (KCT-3248) pancreatic cancer cell lines revealed that DDND treatment significantly reduced cell viability, increased apoptosis, and impaired cell migration and colony formation, compared to single-agent or polymer-alone treatments. To determine the underlying molecular mechanisms, Western blot analysis was conducted on lysates and supernatants from treated cells. Target proteins related to apoptosis, epithelial-to-mesenchymal transition, and oncogenic signaling pathways were evaluated. While some expected trends were observed, such as increased BAX expression in apoptotic cell supernatants and elevated E-cadherin in treated cells, many protein expression changes did not align with the hypothesized anti-tumor effects. Further refinement of western blot technique and the evaluation of additional target proteins is required to understand the mechanism through which the DDND treatment works."],"dc:identifier.doi":["https://doi.org/10.32469/10355/110319"],"dc:identifier.uri":["https://hdl.handle.net/10355/110319"],"dc:language":["English"],"dc:language.iso":["eng"],"dc:publisher":["University of Missouri--Columbia"],"dc:title":["Evaluation of nanoscale delivery of miR 216 a/b, miR 217, and gemcitabine in pancreatic cancer cell lines"],"dc:type":["Thesis"],"thesis:degree_discipline":["Biomedical Sciences"],"thesis:degree_level":["Masters"],"thesis:degree_name":["M.S."],"thesis:institution_name":["University of Missouri--Columbia"]},"updated_at":"2026-07-24T03:08:20Z"}