Journal
ANTICANCER RESEARCH
Volume 37, Issue 1, Pages 81-85Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.11292
Keywords
Long non-coding RNA; PANDA; p18; transcription; osteosarcoma
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [26430127]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [26430127, 15K06994] Funding Source: KAKEN
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Background: A long noncoding RNA, p21-associated ncRNA DNA damage-activated (PANDA), associates with nuclear transcription factor Y subunit alpha (NF-YA) and inhibits its binding to promoters of apoptosis-related genes, thereby repressing apoptosis in normal human fibroblasts. Here, we show that PANDA is involved in regulating proliferation in the U2OS human osteosarcoma cell line. Materials and Methods: U2OS cells were transfected with siRNAs against PANDA 72 h later and they were subjected to reverse transcription-polymerase chain reaction (RT-PCR), quantitative RT-PCR and cell-cycle analysis. Results: PANDA was highly expressed in U2OS cells, and its expression was induced by DNA damage. Silencing PANDA caused arrest at the G(1) phase of the cell cycle, leading to inhibition of cell proliferation. Quantitative RT-PCR showed that silencing PANDA increased mRNA levels of the cyclin-dependent kinase inhibitor p18, which caused G(1) phase arrest. Conclusion: These results suggest that PANDA promotes G(1)-S transition by repressing p18 transcription, and thus promotes U2OS cell proliferation.
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