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@ARTICLE{Zhao:305553,
      author       = {B. Zhao and L. Wang and R. Fang$^*$ and X. Luo and L.
                      Zhang},
      title        = {{T}he {T}umor-{S}uppressive {R}ole of {SAT}2 in
                      {P}ancreatic {C}ancer: {I}nvolvement in
                      {PI}3{K}/{A}kt-{MAPK} {P}athways and {I}mmune {M}odulation.},
      journal      = {Current issues in molecular biology},
      volume       = {47},
      number       = {10},
      issn         = {1467-3037},
      address      = {Wymondham, Norfolk},
      publisher    = {[Verlag nicht ermittelbar]},
      reportid     = {DKFZ-2025-02223},
      pages        = {872},
      year         = {2025},
      abstract     = {Spermidine/spermine N1-Acetyltransferase 2 (SAT2),
                      belonging to the spermidine/spermine N1-Acetyltransferase
                      family, has been increasingly recognized for its potential
                      effects on tumor occurrence and development. Nonetheless,
                      little is known about its biological function and clinical
                      value for pancreatic cancer (PC). The present work focused
                      on investigating its expression pattern, prognostic value,
                      molecular mechanisms, and immune relevance in PC. SAT2
                      expression within PC samples and its prognostic significance
                      were analyzed by retrieving the relevant data from the TCGA,
                      CPTAC, and HPA databases. The biological function of SAT2
                      was investigated through GO and KEGG enrichment analyses.
                      The association of SAT2 with immune cell infiltration in
                      tumors was assessed by CIBERSORT. Additionally, in vitro
                      experiments were performed to examine how SAT2 expression
                      affected the PC cell proliferation, invasion, and migration
                      abilities. An in vivo xenograft tumor model was employed for
                      investigating how SAT2 expression affected the PC
                      cell-derived tumor growth. The expression of SAT2 within the
                      PC tissue exhibited a significant decrease in comparison
                      with a non-carcinoma sample. Such observation was validated
                      within PC cells. In addition, SAT2 expression showed a close
                      relation to both tumor growth (T stage) and prognosis. SAT2
                      primarily participates in pathways, including the PI3K/Akt
                      and MAPK pathways. Furthermore, we demonstrated a
                      significant association between SAT2 expression and immune
                      cell infiltration into tumors. The in vitro experiments
                      confirmed that elevated SAT2 expression significantly
                      suppressed PC cell viability, invasion, and migration
                      through modulating the PI3K/Akt and MAPK pathways. The in
                      vivo experimental results suggested the role of SAT2
                      overexpression in inhibiting xenograft tumor growth. Our
                      investigation confirms the role of SAT2 in PC development
                      through involvement in the PI3K/Akt and MAPK pathways. The
                      correlation between SAT2 expression levels, immune
                      infiltration, and checkpoint regulation provides valuable
                      insights for immunotherapy strategies targeting PC.},
      keywords     = {immune infiltration (Other) / invasion (Other) / migration
                      (Other) / pancreatic cancer (Other) / prognosis (Other) /
                      spermidine/spermine N1-Acetyltransferase 2 (Other)},
      cin          = {ED01},
      ddc          = {570},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41150820},
      pmc          = {pmc:PMC12562838},
      doi          = {10.3390/cimb47100872},
      url          = {https://inrepo02.dkfz.de/record/305553},
}