Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 283, Issue -, Pages 84-90Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2018.01.019
Keywords
Hydroquinone; Apoptosis; Cell proliferation; miR-7-5p; PARP-1; BRCA1
Funding
- National Natural Science Foundation of China [81273116, 81430079]
- Guangdong Provincial Natural Science Foundation [S2013010015153]
- Characteristics of Innovative Projects of Colleges and Universities of Guangdong [2015KTSCX052]
- Science and Technology Program of Zhanjiang Bureau of Science and Technology, China [2013B01082]
- Science Foundation of Guangdong Medical University [M2013004]
- Guangdong Provincial Medical Science and Technology Program [A2016037]
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Hydroquinone (HQ), one of the major metabolic products of benzene, is a carcinogen, which induces apoptosis and inhibit proliferation in lymphoma cells. microRNA-7-5p (miR-7-5p), a tumor suppressor, participates in various biological processes including cell proliferation and apoptosis regulation by repressing expression of specific oncogenic target genes. To explore whether miR-7-5p is involved in HQ-induced cell proliferation and apoptosis, we assessed the effect of miR-7-5p overexpression on induction of apoptosis analyzed by FACSCalibur flow cytometer in transfection of TK6 cells with miR-7-5p mimic (TK6-miR-7-5p). We observed an increased apoptosis by 25.43% and decreased proliferation by 28.30% in TK6-miR-7-5p cells compared to those negative control cells (TK6-shNC) in response to HQ treatment. Furthermore, HQ might active the apoptotic pathway via partly downregulation the expression of BRCA1 and PARP-1, followed by p53 activation, in TK6-miR-7-5p cells. In contrast, attenuated p53 and BRCA1 expression was observed in shPARP-1 cells than in NC cells after HQ treatment. Therefore, we conclude that HQ may activate apoptotic signals via inhibiting the tumor suppressive effects of miR-7-5p, which may be mediated partly by upregulating the expression of PARP-1 and BRCA1 in control cells. The increase of miR-7-5p expression further intensified downregulation of PARP-1 and BRCA1 in TK6-miR-7-5p cells, resulting in an increase of apoptosis and proliferation inhibited.
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