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  • Enokido, TakayoshiGraduate School of Medicine, University of Tokyo,Univ Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan. (author)

Distinct microRNA Signature and Suppression of ZFP36L1 Define ASCL1-Positive Lung Adenocarcinoma

  • Article/chapterEnglish2024

Publisher, publication year, extent ...

  • American Association For Cancer Research (AACR),2024
  • 12 s.

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:656a624a-7f1e-471b-8198-b8cad8b9f83f
  • https://lup.lub.lu.se/record/656a624a-7f1e-471b-8198-b8cad8b9f83fURI
  • https://doi.org/10.1158/1541-7786.MCR-23-0229DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-524635URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Achaete-scute family bHLH transcription factor 1 (ASCL1) is a master transcription factor involved in neuroendocrine differentiation. ASCL1 is expressed in approximately 10% of lung adenocarcinomas (LUAD) and exerts tumor-promoting effects. Here, we explored miRNA profiles in ASCL1-positive LUADs and identified several miRNAs closely associated with ASCL1 expression, including miR-375, miR-95–3p/miR-95–5p, miR-124–3p, and members of the miR-17~92 family. Similar to small cell lung cancer, Yes1 associated transcriptional regulator (YAP1), a representative miR-375 target gene, was suppressed in ASCL1-positive LUADs. ASCL1 knockdown followed by miRNA profiling in a cell culture model further revealed that ASCL1 positively regulates miR-124–3p and members of the miR-17~92 family. Integrative transcriptomic analyses identified ZFP36 ring finger protein like 1 (ZFP36L1) as a target gene of miR-124–3p, and IHC studies demonstrated that ASCL1-positive LUADs are associated with low ZFP36L1 protein levels. Cell culture studies showed that ectopic ZFP36L1 expression inhibits cell proliferation, survival, and cell-cycle progression. Moreover, ZFP36L1 negatively regulated several genes including E2F transcription factor 1 (E2F1) and snail family transcriptional repressor 1 (SNAI1). In conclusion, our study revealed that suppression of ZFP36L1 via ASCL1-regulated miR-124–3p could modulate gene expression, providing evidence that ASCL1-mediated regulation of miRNAs shapes molecular features of ASCL1-positive LUADs.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Horie, MasafumiKanazawa Univ, Grad Sch Med Sci, Dept Mol & Cellular Pathol, Kanazawa, Japan. (author)
  • Yoshino, SeikoNagoya University,Nagoya Univ, Ctr Neurol Dis & Canc, Grad Sch Med, Div Mol Oncol, Nagoya, Japan. (author)
  • Suzuki, Hiroshi I.Nagoya University,Nagoya Univ, Ctr Neurol Dis & Canc, Grad Sch Med, Div Mol Oncol, Nagoya, Japan.;Nagoya Univ, Inst Glyco Core Res iGCORE, Nagoya, Japan.;Nagoya Univ, Ctr One Med Innovat Translat Res COMIT, Nagoya, Japan. (author)
  • Matsuki, ReiGraduate School of Medicine, University of Tokyo,Univ Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan. (author)
  • Brunnstrom, HansLund University,Lunds universitet,Förbättrad diagnostik och prognostik vid lungcancer och metastaser till lunga,Forskargrupper vid Lunds universitet,LUCC: Lunds universitets cancercentrum,Övriga starka forskningsmiljöer,Patologi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Improved diagnostics and prognostics of lung cancer and metastases to the lungs,Lund University Research Groups,LUCC: Lund University Cancer Centre,Other Strong Research Environments,Pathology, Lund,Section V,Department of Clinical Sciences, Lund,Faculty of Medicine,Region Skåne,Lund Univ, Dept Clin Sci Lund, Lab Med Reg Skane, Pathol, Lund, Sweden.(Swepub:lu)med-hsb (author)
  • Micke, PatrickUppsala universitet,Uppsala University,Cancerimmunterapi(Swepub:uu)patmi676 (author)
  • Nagase, TakahideGraduate School of Medicine, University of Tokyo,Univ Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan. (author)
  • Saito, AkiraGraduate School of Medicine, University of Tokyo,Univ Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan. (author)
  • Miyashita, NaoyaGraduate School of Medicine, University of Tokyo,Duke University,Univ Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan.;Duke Univ, Sch Med, Dept Cell Biol, Durham, NC 27710 USA. (author)
  • Graduate School of Medicine, University of TokyoUniv Tokyo, Grad Sch Med, Dept Resp Med, Tokyo, Japan. (creator_code:org_t)

Related titles

  • In:Molecular Cancer Research: American Association For Cancer Research (AACR)22:1, s. 29-401541-77861557-3125

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