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Understanding the molecular mechanisms of lung cancer metastasis is crucial for developing new treatment strategies. Cellular prion protein (PrPc), encoded by\n                      <jats:italic>PRNP<\/jats:italic>\n                      gene, was previously found to enhance lung cancer invasiveness. However, research on the post-transcriptional regulation of\n                      <jats:italic>PRNP<\/jats:italic>\n                      remains limited.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Dual-luciferase reporter assays identified miRNAs targeting the\n                      <jats:italic>PRNP<\/jats:italic>\n                      3'-UTR, and RNA immunoprecipitation (RIP) confirmed the interaction between miR-193b-3p and\n                      <jats:italic>PRNP<\/jats:italic>\n                      mRNA. Promoter deletions and chromatin immunoprecipitation (ChIP) assays established c-Jun as a transcriptional repressor of miR-193b-3p. Functional validation of the c-Jun-miR-193b-3p-PrPc axis was conducted using transwell assays, LNA-in situ hybridization, RT-PCR, Western blot, and immunohistochemistry. Subcutaneous mouse xenograft models assessed the anti-tumor effects of miR-193b-3p in vivo.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We demonstrated that miR-193b-3p downregulates PrPc expression by directly targeting the 3'-UTR of\n                      <jats:italic>PRNP<\/jats:italic>\n                      . Overexpression of miR-193b-3p significantly suppressed\n                      <jats:italic>PRNP<\/jats:italic>\n                      expression at both mRNA and protein levels, and reduced lung cancer cell migration, invasion and proliferation, which was reversed by PrPc overexpression. Conversely, miR-193b-3p silencing enhanced\n                      <jats:italic>PRNP<\/jats:italic>\n                      expression as well as those oncogenic properties, which were mitigated by\n                      <jats:italic>PRNP<\/jats:italic>\n                      knockdown. Spearman correlation analysis revealed a significant negative association between miR-193b-3p and PrPc expression in lung cancer tissues (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.017), and Kaplan\u2013Meier survival analysis demonstrated that high PrPc (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.039) or low miR-193b-3p (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.027) expression correlated with poorer overall survival. Intra-tumoral injection of the miR-193b-3p mimic in mouse xenograft models significantly reduced tumor volume. In addition, c-Jun was identified as a transcriptional repressor of miR-193b-3p. Functional studies revealed that c-Jun knockdown inhibited lung cancer cell migration, invasion, and proliferation, effects that were reversed by either PrPc overexpression or miR-193b-3p inhibitor treatment. A significant association between PrPc and c-Jun expression in lung cancer tissues (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004) was observed. High expression of PrPc and\/or c-Jun was found to be associated with poor overall survival of patients (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      This study is the first to uncover a novel regulatory pathway where c-Jun acts as a transcriptional repressor of miR-193b-3p, leading to\n                      <jats:italic>PRNP<\/jats:italic>\n                      upregulation, which promotes lung cancer migration and invasion. This previously unrecognized c-Jun-miR-193b-3p-PrPc axis also provides valuable insights for the potential development of new therapeutic strategies against lung cancer metastasis through RNA-targeting technology.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12929-025-01121-1","type":"journal-article","created":{"date-parts":[[2025,2,19]],"date-time":"2025-02-19T19:01:43Z","timestamp":1739991703000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["miR-193b-3p suppresses lung cancer cell migration and invasion through PRNP targeting"],"prefix":"10.1186","volume":"32","author":[{"given":"Hsiang-Ling","family":"Ho","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shin-Chih","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao-Wei","family":"Chiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Che-Wei","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Chen","family":"Yeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei-Yu","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5844-477X","authenticated-orcid":false,"given":"Teh-Ying","family":"Chou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,2,20]]},"reference":[{"issue":"1","key":"1121_CR1","doi-asserted-by":"publisher","first-page":"17","DOI":"10.3322\/caac.21763","volume":"73","author":"RL Siegel","year":"2023","unstructured":"Siegel RL, Miller KD, Wagle NS, Jemal A. 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