Hyo-Jin Kim

Publications (2)15 Total impact

• Article: miR-221/222 targeting of trichorhinophalangeal 1 (TRPS1) promotes epithelial-to-mesenchymal transition in breast cancer.

  Susanna Stinson, Mark R Lackner, Alex T Adai, Nancy Yu, Hyo-Jin Kim, Carol O'Brien, Jill Spoerke, Suchit Jhunjhunwala, Zachary Boyd, Thomas Januario, Robert J Newman, Peng Yue, Richard Bourgon, Zora Modrusan, Howard M Stern, Søren Warming, Frederic J de Sauvage, Lukas Amler, Ru-Fang Yeh, David Dornan
  [show abstract] [hide abstract]
  ABSTRACT: Compared with the luminal subtype, the basal-like subtype of breast cancer has an aggressive clinical behavior, but the reasons for this difference between the two subtypes are poorly understood. We identified microRNAs (miRNAs) miR-221 and miR-222 (miR-221/222) as basal-like subtype-specific miRNAs that decrease expression of epithelial-specific genes and increase expression of mesenchymal-specific genes. In addition, expression of these miRNAs increased cell migration and invasion, which collectively are characteristics of the epithelial-to-mesenchymal transition (EMT). The basal-like transcription factor FOSL1 (also known as Fra-1) directly stimulated the transcription of miR-221/222, and the abundance of these miRNAs decreased with inhibition of MEK (mitogen-activated or extracellular signal-regulated protein kinase kinase), placing miR-221/222 downstream of the RAS pathway. The miR-221/222-mediated reduction in E-cadherin abundance depended on their targeting of the 3' untranslated region (3'UTR) of TRPS1 (trichorhinophalangeal syndrome type 1), which is a member of the GATA family of transcriptional repressors. TRPS1 inhibited EMT by directly repressing expression of ZEB2 (Zinc finger E-box-binding homeobox 2). Therefore, miR-221/222 may contribute to the aggressive clinical behavior of basal-like breast cancers.
  Science Signaling 08/2011; 4(186):pt5. · 7.50 Impact Factor
• Article: TRPS1 targeting by miR-221/222 promotes the epithelial-to-mesenchymal transition in breast cancer.

  Susanna Stinson, Mark R Lackner, Alex T Adai, Nancy Yu, Hyo-Jin Kim, Carol O'Brien, Jill Spoerke, Suchit Jhunjhunwala, Zachary Boyd, Thomas Januario, Robert J Newman, Peng Yue, Richard Bourgon, Zora Modrusan, Howard M Stern, Søren Warming, Frederic J de Sauvage, Lukas Amler, Ru-Fang Yeh, David Dornan
  [show abstract] [hide abstract]
  ABSTRACT: The basal-like subtype of breast cancer has an aggressive clinical behavior compared to that of the luminal subtype. We identified the microRNAs (miRNAs) miR-221 and miR-222 (miR-221/222) as basal-like subtype-specific miRNAs and showed that expression of miR-221/222 decreased expression of epithelial-specific genes and increased expression of mesenchymal-specific genes, and increased cell migration and invasion in a manner characteristic of the epithelial-to-mesenchymal transition (EMT). The transcription factor FOSL1 (also known as Fra-1), which is found in basal-like breast cancers but not in the luminal subtype, stimulated the transcription of miR-221/222, and the abundance of these miRNAs decreased with inhibition of the epidermal growth factor receptor (EGFR) or MEK (mitogen-activated or extracellular signal-regulated protein kinase kinase), placing miR-221/222 downstream of the RAS pathway. Furthermore, miR-221/222-mediated reduction in E-cadherin abundance depended on their targeting the 3' untranslated region of the GATA family transcriptional repressor TRPS1 (tricho-rhino-phalangeal syndrome type 1), which inhibited EMT by decreasing ZEB2 (zinc finger E-box-binding homeobox2) expression. We conclude that by promoting EMT, miR-221/222 may contribute to the more aggressive clinical behavior of basal-like breast cancers.
  Science Signaling 01/2011; 4(177):ra41. · 7.50 Impact Factor