liu.seSök publikationer i DiVA
Ändra sökning
Länk till posten
Permanent länk

Direktlänk
BETA
Fredriksson, Bengt-Arne
Publikationer (4 of 4) Visa alla publikationer
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
Öppna denna publikation i ny flik eller fönster >>Salinomycin induces activation of autophagy, mitophagy and affects mitochondrial polarity: Differences between primary and cancer cells
Visa övriga...
2013 (Engelska)Ingår i: Biochimica et Biophysica Acta. Molecular Cell Research, ISSN 0167-4889, E-ISSN 1879-2596, Vol. 1833, nr 9, s. 2057-2069Artikel i tidskrift (Refereegranskat) 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.

Nyckelord
cancer stem cells; mitofusin; mitophagy; mTOR; PGC1α; salinomycin
Nationell ämneskategori
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)
Identifikatorer
urn:nbn:se:liu:diva-91756 (URN)10.1016/j.bbamcr.2013.04.011 (DOI)000321173900004 ()23639289 (PubMedID)
Tillgänglig från: 2013-05-01 Skapad: 2013-05-01 Senast uppdaterad: 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
Öppna denna publikation i ny flik eller fönster >>Letter: Bent Spine Syndrome: A Phenotype of Dysferlinopathy or a Symptomatic DYSF Gene Mutation Carrier
Visa övriga...
2012 (Engelska)Ingår i: European Neurology, ISSN 0014-3022, E-ISSN 1421-9913, Vol. 67, nr 5, s. 300-302Artikel i tidskrift, Letter (Övrigt vetenskapligt) Published
Abstract [en]

n/a

Ort, förlag, år, upplaga, sidor
Karger, 2012
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-77740 (URN)10.1159/000336265 (DOI)000303444900009 ()
Tillgänglig från: 2012-05-28 Skapad: 2012-05-28 Senast uppdaterad: 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)
Öppna denna publikation i ny flik eller fönster >>SENSORY ATAXIC NEUROPATHY WITH DYSARTHRIA/DYSPHAGIA AND OPHTHALMOPLEGIA (SANDO) - CASE HISTORIES in EUROPEAN JOURNAL OF NEUROLOGY, vol 18, issue SI, pp 282-282
Visa övriga...
2011 (Engelska)Ingår i: EUROPEAN JOURNAL OF NEUROLOGY, Wiley-Blackwell , 2011, Vol. 18, nr SI, s. 282-282Konferensbidrag, Publicerat paper (Refereegranskat)
Abstract [en]

n/a

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2011
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-71080 (URN)000294806600516 ()
Tillgänglig från: 2011-09-30 Skapad: 2011-09-30 Senast uppdaterad: 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
Öppna denna publikation i ny flik eller fönster >>Knockdown of peroxisome proliferator-activated receptor-beta induces less differentiation and enhances cell-fibronectin adhesion of colon cancer cells
Visa övriga...
2010 (Engelska)Ingår i: ONCOGENE, ISSN 0950-9232, Vol. 29, nr 4, s. 516-526Artikel i tidskrift (Refereegranskat) 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.

Nyckelord
peroxisome proliferator-activated receptor, colon neoplasm, pathogenesis, RNA interference, differentiation
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-54059 (URN)10.1038/onc.2009.370 (DOI)000274084600005 ()
Tillgänglig från: 2010-02-22 Skapad: 2010-02-22 Senast uppdaterad: 2013-10-22
Organisationer

Sök vidare i DiVA

Visa alla publikationer