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  • Okita, YukariUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)

The transcription factor MAFK induces EMT and malignant progression of triple-negative breast cancer cells through its target GPNMB

  • Artikel/kapitelEngelska2017

Förlag, utgivningsår, omfång ...

  • AMER ASSOC ADVANCEMENT SCIENCE,2017
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-321838
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-321838URI
  • https://doi.org/10.1126/scisignal.aak9397DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Triple-negative breast cancer (TNBC) is particularly aggressive and difficult to treat. For example, the transforming growth factor-beta (TGF-beta) pathway is implicated in TNBC progression and metastasis, but its opposing role in tumor suppression in healthy tissues and early-stage lesions makes it a challenging target. Therefore, additional molecular characterization of TNBC may lead to improved patient prognosis by informing the development and optimum use of targeted therapies. We found that musculoaponeurotic fibrosarcoma (MAF) oncogene family protein K (MAFK), a member of the small MAF family of transcription factors that are induced by the TGF-beta pathway, was abundant in human TNBC and aggressive mouse mammary tumor cell lines. MAFK promoted tumorigenic growth and metastasis by 4T1 cells when implanted subcutaneously in mice. Overexpression of MAFK in mouse breast epithelial NMuMG cells induced epithelial-mesenchymal transition (EMT) phenotypes and promoted tumor formation and invasion in mice. MAFK induced the expression of the gene encoding the transmembrane glycoprotein nmb(GPNMB). Similar to MAFK, GPNMB overexpression in NMuMG cells induced EMT, tumor formation, and invasion, in mice, whereas knockdown of MAFK in tumor cells before implantation suppressed tumor growth and progression. MAFK and GPNMB expression correlated with poor prognosis in TNBC patients. These findings suggest that MAFK and its target gene GPNMB play important roles in the malignant progression of TNBC cells, offering potentially new therapeutic targets for TNBC patients.

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Kimura, MinoriUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Xie, RudyUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Chen, ChenUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Shen, Larina Tzu-WeiUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Kojima, YurikaUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Suzuki, HiroyukiUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Muratani, MasafumiUniv Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Genome Biol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Saitoh, MasaoUniv Yamanashi, Grad Sch Med & Engn, Dept Biochem, Chuo Ku, 1110 Shimokato, Yamanashi 4093898, Japan. (författare)
  • Semba, KentaroWaseda Univ, Sch Adv Sci & Engn, Dept Life Sci & Med Biosci, Shinjuku Ku, 2-2Wakamatsu Cho, Tokyo 1628480, Japan. (författare)
  • Heldin, Carl-Henrik,1952-Uppsala universitet,Ludwiginstitutet för cancerforskning,Science for Life Laboratory, SciLifeLab(Swepub:uu)carlheld (författare)
  • Kato, MitsuyasuUniv Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (författare)
  • Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Expt Pathol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.Univ Tsukuba, Fac Med, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.;Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Genome Biol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Science Signaling: AMER ASSOC ADVANCEMENT SCIENCE10:4741945-08771937-9145

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