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@ARTICLE{Sumer:298213,
      author       = {O. E. Sumer$^*$ and K. Schelzig$^*$ and J. Jung$^*$ and X.
                      Li$^*$ and J. Moros$^*$ and L. Schwarzmüller$^*$ and E.
                      Sen$^*$ and S. Karolus$^*$ and A. Wörner$^*$ and V. R. de
                      Melo Costa$^*$ and N. B. Nataraj and E.-I. Vlachavas$^*$ and
                      C. Gerhäuser$^*$ and K. Müller-Decker$^*$ and D. Helm$^*$
                      and Y. Yarden and B. E. Michels$^*$ and C. Körner$^*$},
      title        = {{S}elective arm-usage of pre-mi{R}-1307 dysregulates
                      angiogenesis and affects breast cancer aggressiveness.},
      journal      = {BMC biology},
      volume       = {23},
      number       = {1},
      issn         = {1741-7007},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2025-00220},
      pages        = {25},
      year         = {2025},
      note         = {#EA:B050#LA:B050#},
      abstract     = {Breast cancer is the leading cause of cancer-related
                      mortality in women. Deregulation of miRNAs is frequently
                      observed in breast cancer and affects tumor biology. A
                      pre-miRNA, such as pre-miR-1307, gives rise to several
                      mature miRNA molecules with distinct functions. However, the
                      impact of global deregulation of pre-miR-1307 and its
                      individual mature miRNAs in breast cancer has not been
                      investigated in breast cancer, yet.Here, we found
                      significant upregulation of three mature miRNA species
                      derived from pre-miR-1307 in human breast cancer tissue.
                      Surprisingly, the overexpression of pre-miR-1307 in breast
                      cancer cell lines resulted in reduced xenograft growth and
                      impaired angiogenesis. Mechanistically, overexpression of
                      miR-1307-5p altered the secretome of breast cancer cells and
                      reduced endothelial cell sprouting. Consistently, expression
                      of miR-1307-5p was inversely correlated with endothelial
                      cell fractions in human breast tumors pointing at an
                      anti-angiogenic role of miR-1307-5p. Importantly, the arm
                      usage of miR-1307 and other miRNAs was highly correlated,
                      which suggests an undefined common regulatory mechanism.In
                      summary, miR-1307-5p reduces angiogenesis in breast cancer,
                      thereby antagonizing the oncogenic effects of miR-1307-3p.
                      Our results emphasize the importance of future research on
                      the regulation of miRNA arm selection in cancer. The
                      underlying mechanisms might inspire new therapeutic
                      strategies aimed at shifting the balance towards
                      tumor-suppressive miRNA species.},
      keywords     = {MicroRNAs: genetics / MicroRNAs: metabolism / Breast
                      Neoplasms: genetics / Breast Neoplasms: pathology / Humans /
                      Female / Neovascularization, Pathologic: genetics / Animals
                      / Cell Line, Tumor / Mice / Gene Expression Regulation,
                      Neoplastic / Angiogenesis / Angiogenesis (Other) / Breast
                      cancer (Other) / IsomiRs (Other) / Metastasis (Other) /
                      Selective arm-usage of miRNA (Other) / miR-1307 (Other) /
                      miRNA arm switch (Other) / miRNAs (Other) / MicroRNAs (NLM
                      Chemicals) / MIRN1307 microRNA, human (NLM Chemicals)},
      cin          = {B050 / B370 / W420 / W120},
      ddc          = {610},
      cid          = {I:(DE-He78)B050-20160331 / I:(DE-He78)B370-20160331 /
                      I:(DE-He78)W420-20160331 / I:(DE-He78)W120-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39849498},
      pmc          = {pmc:PMC11756181},
      doi          = {10.1186/s12915-025-02133-x},
      url          = {https://inrepo02.dkfz.de/record/298213},
}