% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Zhu:293309,
      author       = {Y. Zhu and S. N. Kim and Z.-R. Chen and R. Will$^*$ and
                      R.-D. Zhong and P. Dammann and U. Sure},
      title        = {{PDCD}10 {I}s a {K}ey {P}layer in {TMZ}-{R}esistance and
                      {T}umor {C}ell {R}egrowth: {I}nsights into {I}ts
                      {U}nderlying {M}echanism in {G}lioblastoma {C}ells.},
      journal      = {Cells},
      volume       = {13},
      number       = {17},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2024-01867},
      pages        = {1442},
      year         = {2024},
      abstract     = {Overcoming temozolomide (TMZ)-resistance is a major
                      challenge in glioblastoma therapy. Therefore, identifying
                      the key molecular player in chemo-resistance becomes urgent.
                      We previously reported the downregulation of PDCD10 in
                      primary glioblastoma patients and its tumor suppressor-like
                      function in glioblastoma cells. Here, we demonstrate that
                      the loss of PDCD10 causes a significant TMZ-resistance
                      during treatment and promotes a rapid regrowth of tumor
                      cells after treatment. PDCD10 knockdown upregulated MGMT, a
                      key enzyme mediating chemo-resistance in glioblastoma,
                      accompanied by increased expression of DNA mismatch repair
                      genes, and enabled tumor cells to evade TMZ-induced
                      cell-cycle arrest. These findings were confirmed in
                      independent models of PDCD10 overexpressing cells.
                      Furthermore, PDCD10 downregulation led to the
                      dedifferentiation of glioblastoma cells, as evidenced by
                      increased clonogenic growth, the upregulation of
                      glioblastoma stem cell (GSC) markers, and enhanced
                      neurosphere formation capacity. GSCs derived from PDCD10
                      knockdown cells displayed stronger TMZ-resistance and
                      regrowth potency, compared to their parental counterparts,
                      indicating that PDCD10-induced stemness may independently
                      contribute to tumor malignancy. These data provide evidence
                      for a dual role of PDCD10 in tumor suppression by
                      controlling both chemo-resistance and dedifferentiation, and
                      highlight PDCD10 as a potential prognostic marker and target
                      for combination therapy with TMZ in glioblastoma.},
      keywords     = {Humans / Glioblastoma: pathology / Glioblastoma: genetics /
                      Glioblastoma: metabolism / Glioblastoma: drug therapy /
                      Temozolomide: pharmacology / Drug Resistance, Neoplasm:
                      genetics / Drug Resistance, Neoplasm: drug effects / Cell
                      Line, Tumor / Apoptosis Regulatory Proteins: metabolism /
                      Apoptosis Regulatory Proteins: genetics / Gene Expression
                      Regulation, Neoplastic: drug effects / Neoplastic Stem
                      Cells: metabolism / Neoplastic Stem Cells: pathology /
                      Neoplastic Stem Cells: drug effects / Brain Neoplasms:
                      pathology / Brain Neoplasms: genetics / Brain Neoplasms:
                      metabolism / Brain Neoplasms: drug therapy / Membrane
                      Proteins: metabolism / Membrane Proteins: genetics /
                      Proto-Oncogene Proteins: metabolism / Proto-Oncogene
                      Proteins: genetics / Cell Proliferation: drug effects / DNA
                      Modification Methylases: metabolism / DNA Modification
                      Methylases: genetics / Tumor Suppressor Proteins: metabolism
                      / Tumor Suppressor Proteins: genetics / DNA Repair Enzymes:
                      metabolism / DNA Repair Enzymes: genetics / MGMT and MMR
                      genes (Other) / acquired TMZ-resistance (Other) /
                      glioblastoma (GBM) (Other) / programmed cell death 10
                      (PDCD10) (Other) / stemness (Other) / Temozolomide (NLM
                      Chemicals) / Apoptosis Regulatory Proteins (NLM Chemicals) /
                      PDCD10 protein, human (NLM Chemicals) / Membrane Proteins
                      (NLM Chemicals) / Proto-Oncogene Proteins (NLM Chemicals) /
                      DNA Modification Methylases (NLM Chemicals) / MGMT protein,
                      human (NLM Chemicals) / Tumor Suppressor Proteins (NLM
                      Chemicals) / DNA Repair Enzymes (NLM Chemicals)},
      cin          = {W111},
      ddc          = {570},
      cid          = {I:(DE-He78)W111-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39273014},
      pmc          = {pmc:PMC11394141},
      doi          = {10.3390/cells13171442},
      url          = {https://inrepo02.dkfz.de/record/293309},
}