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Mitochondrial regulation of cell cycle progression through SLC25A43
University of Örebro, Sweden; Karolinska Institute, Sweden.
University of Örebro, Sweden.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Onkologiska kliniken US.
University of Örebro, Sweden.
2016 (Engelska)Ingår i: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 469, nr 4, s. 1090-1096Artikel i tidskrift (Refereegranskat) Published
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Abstract [en]

An increasing body of evidence is pointing towards mitochondrial regulation of the cell cycle. In a previous study of HER2-positive tumours we could demonstrate a common loss in the gene encoding for the mitochondrial transporter SLC25A43 and also a significant relation between SLC25A43 protein expression and S-phase fraction. Here, we investigated the consequence of suppressed SLC25A43 expression on cell cycle progression and proliferation in breast epithelial cells. In the present study, we suppressed SLC25A43 using siRNA in immortalised non-cancerous breast epithelial MCF10A cells and HER2-positive breast cancer cells BT-474. Viability, apoptosis, cell proliferation rate, cell cycle phase distribution, and nuclear Ki-67 and p21, were assessed by flow cytometry. Cell cycle related gene expressions were analysed using real-time PCR. We found that SLC25A43 knockdown in MCF10A cells significantly inhibited cell cycle progression during G(1)-to-S transition, thus significantly reducing the proliferation rate and fraction of Ki-67 positive MCF10A cells. In contrast, suppressed SLC25A43 expression in BT-474 cells resulted in a significantly increased proliferation rate together with an enhanced G(1)-to-S transition. This was reflected by an increased fraction of Ki-67 positive cells and reduced level of nuclear p21. In line with our previous results, we show a role for SLC25A43 as a regulator of cell cycle progression and proliferation through a putative mitochondrial checkpoint. These novel data further strengthen the connection between mitochondrial function and the cell cycle, both in non-malignant and in cancer cells. (C) 2015 Elsevier Inc. All rights reserved.

Ort, förlag, år, upplaga, sidor
ACADEMIC PRESS INC ELSEVIER SCIENCE , 2016. Vol. 469, nr 4, s. 1090-1096
Nyckelord [en]
SLC25A43; Mitochondrial checkpoint; Proliferation; Cell cycle regulation; Ki-67
Nationell ämneskategori
Klinisk medicin
Identifikatorer
URN: urn:nbn:se:liu:diva-125685DOI: 10.1016/j.bbrc.2015.12.088ISI: 000369353000046PubMedID: 26721434OAI: oai:DiVA.org:liu-125685DiVA, id: diva2:908207
Anmärkning

Funding Agencies|Lion Cancer Foundation Sweden; Research Committee at Orebro County Council; Swedish Research Council [K2011-54X-20639-04-6]

Tillgänglig från: 2016-03-01 Skapad: 2016-02-29 Senast uppdaterad: 2017-11-30

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Stål, Olle

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