Unmasking PTEN's nuclear functions

Dai, Wei

doi:10.1080/15384101.2016.1241606

Cited by 1 publication

(1 citation statement)

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“…Multiple studies have confirmed that cytoplasmic PTEN is an antagonist of the PI3K/AKT pathway because of its lipid phosphatase activity against PIP3. Recently, growing evidence demonstrates that nuclear PTEN is important for maintaining genomic stability through critical roles in modulating DNA repair and cell-cycle arrest 37 . Although several components of the PI3K/AKT pathway also existed in the nucleus, such as PI3K, PIP3 and AKT, cytoplasmic but not nuclear pools of PIP3 have been discovered to be sensitive to the lipid phosphatase activity of PTEN 38 .…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA MIR22HG promotes osteogenic differentiation of bone marrow mesenchymal stem cells via PTEN/ AKT pathway

et al. 2020

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Osteoporosis is a prevalent metabolic bone disease characterized by low bone mineral density and degenerative disorders of bone tissues. Previous studies showed the abnormal osteogenic differentiation of endogenous bone marrow mesenchymal stem cells (BMSCs) contributes to the development of osteoporosis. However, the underlying mechanisms by which BMSCs undergo osteogenic differentiation remain largely unexplored. Recently, long non-coding RNAs have been discovered to play important roles in regulating BMSC osteogenesis. In this study, we first showed MIR22HG, which has been demonstrated to be involved in the progression of several cancer types, played an important role in regulating BMSC osteogenesis. We found the expression of MIR22HG was significantly decreased in mouse BMSCs from the osteoporotic mice and it was upregulated during the osteogenic differentiation of human BMSCs. Overexpression of MIR22HG in human BMSCs enhanced osteogenic differentiation, whereas MIR22HG knockdown inhibited osteogenic differentiation both in vitro and in vivo. Mechanistically, MIR22HG promoted osteogenic differentiation by downregulating phosphatase and tensin homolog (PTEN) and therefore activating AKT signaling. Moreover, we found MIR22HG overexpression promoted osteoclastogenesis of RAW264.7 cells, which indicated that MIR22HG played a significant role in bone metabolism and could be a therapeutic target for osteoporosis and other bone-related diseases.

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Section: Discussionmentioning

confidence: 99%