SwePub
Sök i LIBRIS databas

  Extended search

onr:"swepub:oai:DiVA.org:uu-461977"
 

Search: onr:"swepub:oai:DiVA.org:uu-461977" > TGF-beta-mediated e...

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist
  • Miyashita, NaoyaUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.,University of Tokyo (author)

TGF-beta-mediated epithelial-mesenchymal transition and tumor-promoting effects in CMT64 cells are reflected in the transcriptomic signature of human lung adenocarcinoma

  • Article/chapterEnglish2021

Publisher, publication year, extent ...

  • 2021-11-17
  • Springer Nature,2021
  • electronicrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-461977
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-461977URI
  • https://doi.org/10.1038/s41598-021-01799-xDOI
  • https://lup.lub.lu.se/record/5277ef74-bd06-452d-82ae-7fdc0a2c59f1URI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

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

Notes

  • Epithelial-mesenchymal transition (EMT) is a cellular process during which epithelial cells acquire mesenchymal phenotypes. Cancer cells undergo EMT to acquire malignant features and TGF-beta is a key regulator of EMT. Here, we demonstrate for the first time that TGF-beta could elicit EMT in a mouse lung adenocarcinoma cell line. TGF-beta signaling activation led to cell morphological changes corresponding to EMT and enhanced the expression of mesenchymal markers and EMT-associated transcription factors in CMT64 lung cancer cells. RNA-sequencing analyses revealed that TGF-beta increases expression of Tead transcription factors and an array of Tead2 target genes. TGF-beta stimulation also resulted in alternative splicing of several genes including Cd44, tight junction protein 1 (Tjp1), and Cortactin (Cttn). In parallel with EMT, TGF-beta enhanced cell growth of CMT64 cells and promoted tumor formation in a syngeneic transplantation model. Of clinical importance, the expression of TGF-beta-induced genes identified in CMT64 cells correlated with EMT gene signatures in human lung adenocarcinoma tissue samples. Furthermore, TGF-beta-induced gene enrichment was related to poor prognosis, underscoring the tumor-promoting role of TGF-beta signaling in lung adenocarcinoma. Our cellular and syngeneic transplantation model would provide a simple and useful experimental tool to study the significance of TGF-beta signaling and EMT.

Subject headings and genre

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

  • Enokido, TakayoshiUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.,University of Tokyo (author)
  • Horie, MasafumiOsaka Univ, Grad Sch Med, Dept Canc Genome Informat, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.,University of Tokyo (author)
  • Fukuda, KensukeUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.,University of Tokyo (author)
  • Urushiyama, HirokazuUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. (author)
  • Strell, CarinaUppsala University,Uppsala universitet,Klinisk och experimentell patologi,Patrick Micke(Swepub:uu)carst810 (author)
  • Brunnström, 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(Swepub:lu)med-hsb (author)
  • Micke, PatrickUppsala University,Uppsala universitet,Klinisk och experimentell patologi,Patrick Micke(Swepub:uu)patmi676 (author)
  • Saito, AkiraUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.,University of Tokyo (author)
  • Nagase, TakahideUniv Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.,University of Tokyo (author)
  • Univ Tokyo, Grad Sch Med, Dept Resp Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.University of Tokyo (creator_code:org_t)

Related titles

  • In:Scientific Reports: Springer Nature112045-2322

Internet link

Find in a library

To the university's database

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view