Overexpression of C10orf116 promotes proliferation, inhibits apoptosis and enhances glucose transport in 3T3-L1 adipocytes

Chen,Ling; Zhou,Xiao-Guang; Zhou,Xiao-Yu; Zhu,Chun; Ji,Chen-Bo; Shi,Chun-Mei; Qiu,Jie; Guo,Xi-Rong

doi:10.3892/mmr.2013.1351

Overexpression of C10orf116 promotes proliferation, inhibits apoptosis and enhances glucose transport in 3T3-L1 adipocytes

Authors:
- Ling Chen
- Xiao-Guang Zhou
- Xiao-Yu Zhou
- Chun Zhu
- Chen-Bo Ji
- Chun-Mei Shi
- Jie Qiu
- Xi-Rong Guo
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Affiliations: Department of Pediatrics, Nanjing Maternity and Child Health Hospital of Nanjing Medical University, Nanjing, Jiangsu 210004, P.R. China, Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China, Institute of Pediatrics of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China
Published online on: March 1, 2013 https://doi.org/10.3892/mmr.2013.1351
Pages: 1477-1481

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Abstract

Data from our previous study demonstrated that C10orf116 is an adipocyte lineage-specific nuclear factor, which regulates master adipogenesis transcription factors during early differentiation. However, the precise functional properties of this gene have yet to be identified and further investigation is required. In the present study, we report the effects of C10orf116 expression on cell proliferation and apoptosis in vitro and observed that the overexpression of C10orf116 stimulates proliferation and inhibits apoptosis in preadipocytes. Furthermore, we investigated the effects of C10orf116 on glucose uptake and demonstrated that the ectopic expression of C10orf116 significantly increases insulin-stimulated glucose uptake in adipocytes by increasing glucose transporter type 4 (GLUT4) expression levels. Collectively, these data further support the hypothesis that C10orf116 is important in regulating glucose transport in adipocytes as well as the number of preadipocytes. The results of the present study may also provide insights into the complex mechanisms involved in the development of obesity.

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