RACK1 is required for adipogenesis

Am J Physiol Cell Physiol. 2016 Nov 1;311(5):C831-C836. doi: 10.1152/ajpcell.00224.2016. Epub 2016 Sep 21.

Abstract

Adipose tissue plays a critical role in metabolic diseases and the maintenance of energy homeostasis. RACK1 has been identified as an adaptor protein involved in multiple intracellular signal transduction pathways and diseases. However, whether it regulates adipogenesis remains unknown. Here, we reported that RACK1 is expressed in 3T3-L1 cells and murine white adipose tissue and that RACK1 knockdown by shRNA profoundly suppressed adipogenesis by reducing the expression of PPAR-γ and C/EBP-β. Depletion of RACK1 increased β-catenin protein levels and activated Wnt signaling. Furthermore, RACK1 knockdown also suppressed the PI3K-Akt-mTOR-S6K signaling pathway by reducing the PI3K p85α, pAkt T473, and S6K p70. Taken together, these results demonstrate that RACK1 is a novel factor required for adipocyte differentiation by emerging Wnt/β-catenin signaling and PI3K-Akt-mTOR-S6K signaling pathway(s).

Keywords: 3T3-L1; PI3K-Akt-mTOR-S6K; RACK1; Wnt; adipogenesis.

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / metabolism
  • Adipogenesis / physiology*
  • Adipose Tissue / metabolism
  • Animals
  • CCAAT-Enhancer-Binding Protein-beta / metabolism
  • Cell Differentiation / physiology
  • Cell Line
  • Mice
  • Neuropeptides / metabolism*
  • PPAR gamma / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Small Interfering / metabolism
  • Receptors for Activated C Kinase
  • TOR Serine-Threonine Kinases / metabolism
  • Wnt Signaling Pathway / physiology
  • beta Catenin / metabolism

Substances

  • CCAAT-Enhancer-Binding Protein-beta
  • Cebpb protein, mouse
  • Neuropeptides
  • PPAR gamma
  • RACK1 protein, mouse
  • RNA, Small Interfering
  • Receptors for Activated C Kinase
  • beta Catenin
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases