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Non-adherent culture method affects the proliferation and apoptosis of mesenchymal stem cells through inhibiting LINC00707 to promote RNF6-mediated QKI ubiquitination. | LitMetric

AI Article Synopsis

  • - Exploration of mesenchymal stem cell (MSC) growth at the molecular level reveals potential clinical applications, particularly involving long non-coding RNAs (lncRNAs) that impact MSC osteogenic differentiation.
  • - The study identified that LINC00707 is significantly reduced in non-adherent human MSCs (non-AC-hMSCs), and its overexpression enhances MSC proliferation and cell cycle progression while decreasing apoptosis; silencing LINC00707 has the opposite effect.
  • - LINC00707 interacts with the QKI protein and promotes its degradation via ubiquitination, with QKI overexpression reversing the effects of LINC00707 on MSC proliferation and apoptosis, highlighting its regulatory role in these processes.

Article Abstract

Exploration of the molecular mechanisms of mesenchymal stem cell (MSC) growth has significant clinical benefits. Long non-coding RNAs (lncRNAs) have been reported to play vital roles in the regulation of the osteogenic differentiation of MSCs. However, the mechanism by which lncRNA affects the proliferation and apoptosis of MSCs is unclear. In this study, sequencing analysis revealed that LINC00707 was significantly decreased in non-adherent human MSCs (non-AC-hMSCs) compared to adherent human MSCs. Moreover, LINC00707 overexpression promoted non-AChMSC proliferation, cell cycle progression from the G0/G1 phase to the S phase and inhibited apoptosis, whereas LINC00707 silencing had the opposite effect. Furthermore, LINC00707 interacted directly with the quaking (QKI) protein and enhanced the E3 ubiquitin-protein ligase ring finger protein 6 (RNF6)-mediated ubiquitination of the QKI protein. Additionally, the overexpression of QKI rescued the promotive effects on proliferation and inhibitory effects on apoptosis in non-AC-hMSCs induced by the ectopic expression of LINC00707. Thus, LINC00707 contributes to the proliferation and apoptosis in non-AChMSCs by regulating the ubiquitination and degradation of the QKI protein.

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http://dx.doi.org/10.1016/j.yexcr.2023.113877DOI Listing

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