AI Article Synopsis
- Period 2 (per2) is a key circadian clock gene whose dysregulation is linked to various human cancers and may indicate a worse prognosis.
- Researchers conducted experiments on MNNG/HOS human osteosarcoma cells by using small interfering RNA and plasmids to manipulate the levels of per2, observing their effects on cell growth, apoptosis, and migration.
- The study found that knocking down per2 increased cell growth and mobility while reducing cell death, whereas overexpressing per2 had the opposite effect, suggesting that targeting per2 could offer new treatment options for osteosarcoma.
Article Abstract
Period 2 (per2) is a core circadian clock gene. Dysregulation of the per2 gene has been identified in a number of types of human cancer and may be associated with a poor prognosis. To confirm the influence of per2 gene on MNNG/HOS human osteosarcoma cells, small interfering (si)RNA against per2 or plasmids containing per2 were transfected into MNNG/HOS cells, and the proliferation, apoptosis and migration were observed. The present study demonstrated that per2 knockdown significantly enhanced MNNG/HOS cell proliferation and migration and protected MNNG/HOS cells from apoptosis. Per2 overexpression inhibited MNNG/HOS cell proliferation and migration and promoted apoptosis. Furthermore, the protein expression of phosphorylated (p)-protein kinase B (Akt) and Bcl-2 were inhibited in per2-overexpressing cells, while the expression of p27, p21 and cleaved caspase-3 was promoted. In contrast, the expression of p-Akt and Bcl-2 was promoted in per2-knockdown cells, and p27, p21 and cleaved caspase-3 were decreased. This initial study may provide an alternative therapeutic strategy for the treatment of osteosarcoma.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036572 | PMC |
| http://dx.doi.org/10.3892/ol.2018.8952 | DOI Listing |
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