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Fredriksson, Bengt-Arne
Publications (4 of 4) Show all publications
Jangamreddy, J., Ghavami, S., Grabarek, J., Kratz, G., Wiechec, E., Fredriksson, B.-A., . . . Łos, M. (2013). Salinomycin induces activation of autophagy, mitophagy and affects mitochondrial polarity: Differences between primary and cancer cells. Biochimica et Biophysica Acta. Molecular Cell Research, 1833(9), 2057-2069
Open this publication in new window or tab >>Salinomycin induces activation of autophagy, mitophagy and affects mitochondrial polarity: Differences between primary and cancer cells
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2013 (English)In: Biochimica et Biophysica Acta. Molecular Cell Research, ISSN 0167-4889, E-ISSN 1879-2596, Vol. 1833, no 9, p. 2057-2069Article in journal (Refereed) Published
Abstract [en]

The molecular mechanism of Salinomycin's toxicity is not fully understood. Various studies reported that Ca2 +, cytochrome c, and caspase activation play a role in Salinomycin-induced cytotoxicity. Furthermore, Salinomycin may target Wnt/β-catenin signaling pathway to promote differentiation and thus elimination of cancer stem cells. In this study, we show a massive autophagic response to Salinomycin (substantially stronger than to commonly used autophagic inducer Rapamycin) in prostrate-, breast cancer cells, and to lesser degree in human normal dermal fibroblasts. Interestingly, autophagy induced by Salinomycin is a cell protective mechanism in all tested cancer cell lines. Furthermore, Salinomycin induces mitophagy, mitoptosis and increased mitochondrial membrane potential (∆Ψ) in a subpopulation of cells. Salinomycin strongly, and in time-dependent manner decreases cellular ATP level. Contrastingly, human normal dermal fibroblasts treated with Salinomycin show some initial decrease in mitochondrial mass, however they are largely resistant to Salinomycin-triggered ATP-depletion. Our data provide new insight into the molecular mechanism of preferential toxicity of Salinomycin towards cancer cells, and suggest possible clinical application of Salinomycin in combination with autophagy inhibitors (i.e. clinically-used Chloroquine). Furthermore, we discuss preferential Salinomycins toxicity in the context of Warburg effect.

Keywords
cancer stem cells; mitofusin; mitophagy; mTOR; PGC1α; salinomycin
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:liu:diva-91756 (URN)10.1016/j.bbamcr.2013.04.011 (DOI)000321173900004 ()23639289 (PubMedID)
Available from: 2013-05-01 Created: 2013-05-01 Last updated: 2017-12-06
Gati, I., Danielsson, O., Gunnarsson, C., Vrethem, M., Häggqvist, B., Fredriksson, B.-A. & Landtblom, A.-M. (2012). Letter: Bent Spine Syndrome: A Phenotype of Dysferlinopathy or a Symptomatic DYSF Gene Mutation Carrier [Letter to the editor]. European Neurology, 67(5), 300-302
Open this publication in new window or tab >>Letter: Bent Spine Syndrome: A Phenotype of Dysferlinopathy or a Symptomatic DYSF Gene Mutation Carrier
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2012 (English)In: European Neurology, ISSN 0014-3022, E-ISSN 1421-9913, Vol. 67, no 5, p. 300-302Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Karger, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-77740 (URN)10.1159/000336265 (DOI)000303444900009 ()
Available from: 2012-05-28 Created: 2012-05-28 Last updated: 2017-12-07
Gati, I., Danielsson, O., Vrethem, M., Lindehammar, H., Lindvall, B., Häggqvist, B., . . . Landtblom, A.-M. (2011). SENSORY ATAXIC NEUROPATHY WITH DYSARTHRIA/DYSPHAGIA AND OPHTHALMOPLEGIA (SANDO) - CASE HISTORIES in EUROPEAN JOURNAL OF NEUROLOGY, vol 18, issue SI, pp 282-282. In: EUROPEAN JOURNAL OF NEUROLOGY (pp. 282-282). Wiley-Blackwell, 18(SI)
Open this publication in new window or tab >>SENSORY ATAXIC NEUROPATHY WITH DYSARTHRIA/DYSPHAGIA AND OPHTHALMOPLEGIA (SANDO) - CASE HISTORIES in EUROPEAN JOURNAL OF NEUROLOGY, vol 18, issue SI, pp 282-282
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2011 (English)In: EUROPEAN JOURNAL OF NEUROLOGY, Wiley-Blackwell , 2011, Vol. 18, no SI, p. 282-282Conference paper, Published paper (Refereed)
Abstract [en]

n/a

Place, publisher, year, edition, pages
Wiley-Blackwell, 2011
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-71080 (URN)000294806600516 ()
Available from: 2011-09-30 Created: 2011-09-30 Last updated: 2012-04-03
Yang, L., Olsson, B., Pfeifer, D., Jönsson, J.-I., Zhou, Z.-G., Jiang, X., . . . Sun, X.-F. (2010). Knockdown of peroxisome proliferator-activated receptor-beta induces less differentiation and enhances cell-fibronectin adhesion of colon cancer cells. ONCOGENE, 29(4), 516-526
Open this publication in new window or tab >>Knockdown of peroxisome proliferator-activated receptor-beta induces less differentiation and enhances cell-fibronectin adhesion of colon cancer cells
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2010 (English)In: ONCOGENE, ISSN 0950-9232, Vol. 29, no 4, p. 516-526Article in journal (Refereed) Published
Abstract [en]

The role of peroxisome proliferator-activated receptor-beta/delta (PPAR-beta/delta) in the pathogenesis of colon cancer remains highly controversial. This study specifically silenced the PPAR-beta expression in three colon cancer cell lines with different metastatic potentials. Although PPAR-beta knockdown resulted in more malignant morphological changes, bigger colony sizes and lower carcinoembryonic antigen (CEA) secretion, and enhanced the cell-fibronectin adhesion, cell invasion and migration were unaffected. These effects were stronger in poorly metastatic cell lines compared with highly metastatic ones. Simultaneously, PPAR-beta knockdown decreased the mRNAs encoding adipocyte differentiation-related protein and liver fatty acid binding protein, and increased the mRNA of ILK, whereas the mRNAs encoding integrin-beta 1 and angiopoietin-like 4 were unchanged. Using immunohistochemistry, we determined that the intensity of PPAR-beta expression was stronger in rectal cancers with better differentiation than in those with poor differentiation, and was stronger in early-stage tumors than in advanced ones. Together, these findings consistently indicate that PPAR-beta may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer. Interestingly, PPAR-beta seems to have a more important role in poorly metastatic cells than in highly metastatic ones.

Keywords
peroxisome proliferator-activated receptor, colon neoplasm, pathogenesis, RNA interference, differentiation
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-54059 (URN)10.1038/onc.2009.370 (DOI)000274084600005 ()
Available from: 2010-02-22 Created: 2010-02-22 Last updated: 2013-10-22
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