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Wiechec, Emilia
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Publications (10 of 33) Show all publications
Banerjee, D., Cieslar-Pobuda, A., Zhu, G. H., Wiechec, E. & Patra, H. (2019). Adding nanotechnology to the metastasis treatment arsenal. TIPS - Trends in Pharmacological Sciences, 40(6), 403-418
Open this publication in new window or tab >>Adding nanotechnology to the metastasis treatment arsenal
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2019 (English)In: TIPS - Trends in Pharmacological Sciences, ISSN 0165-6147, E-ISSN 1873-3735, Vol. 40, no 6, p. 403-418Article, review/survey (Refereed) Published
Abstract [en]

Metastasis is a major cause of cancer-related mortality, accounting for 90% of cancer deaths. The explosive growth of cancer biology research has revealed new mechanistic network information and pathways that promote metastasis. Consequently, a large number of antitumor agents have been developed and tested for their antimetastatic efficacy. Despite their exciting cytotoxic effects on tumor cells in vitro and antitumor activities in preclinical studies in vivo, only a few have shown potent antimetastatic activities in clinical trials. In this review, we provide a brief overview of current antimetastatic strategies that show clinical efficacy and review nanotechnology-based approaches that are currently being incorporated into these therapies to mitigate challenges associated with treating cancer metastasis.

Place, publisher, year, edition, pages
Cambridge, Massachusets: Elsevier, 2019
Keywords
metastasis; nanotechnology; chemotherapy; combination therapy
National Category
Other Clinical Medicine Cancer and Oncology Pharmaceutical Sciences
Identifiers
urn:nbn:se:liu:diva-156845 (URN)10.1016/j.tips.2019.04.002 (DOI)000469437500007 ()31076247 (PubMedID)
Note

Funding agencies: EU H2020 Marie Sklodowska-Curie Individual Fellowship [706694]; Wolfson College (University of Cambridge, UK); MIIC Seed Grant from Linkoping University (LiU), Sweden

Available from: 2019-05-14 Created: 2019-05-14 Last updated: 2019-09-24
Hashemi, M., Karami, S., Sarabandi, S., Moazeni-Roodi, A., Malecki, A., Ghavami, S. & Wiechec, E. (2019). Association between PD-1 and PD-L1 polymorphisms and the risk of cancer: a meta analysis of case-control studies. Cancers, 11(8), Article ID 1150.
Open this publication in new window or tab >>Association between PD-1 and PD-L1 polymorphisms and the risk of cancer: a meta analysis of case-control studies
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2019 (English)In: Cancers, ISSN 2072-6694, Vol. 11, no 8, article id 1150Article in journal (Refereed) Published
Abstract [en]

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility. 

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
PD-1; PD-L1; apoptosis; cancer; meta-analysis; polymorphism
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-159931 (URN)10.3390/cancers11081150 (DOI)000484438000110 ()31405171 (PubMedID)
Note

Funding agencies: Institute of Physiotherapy and Health Sciences, The Jerzy Kukuczka Academy of Physical Education in Katowice; Research Manitoba New Investigators Operating Grant; CancerCare Manitoba Operating grant

Available from: 2019-08-28 Created: 2019-08-28 Last updated: 2019-09-30Bibliographically approved
Melissaridou, S., Wiechec, E., Magan, M., Jain, M. V., Chung, M. K., Farnebo, L. & Roberg, K. (2019). The effect of 2D and 3D cell cultures on treatment response, EMT profile and stem cell features in head and neck cancer.. Cancer Cell International, 19(16)
Open this publication in new window or tab >>The effect of 2D and 3D cell cultures on treatment response, EMT profile and stem cell features in head and neck cancer.
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2019 (English)In: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 19, no 16Article in journal (Refereed) Published
Abstract [en]

Background

Head and Neck Squamous Cell Carcinoma (HNSCC) tumors are often resistant to therapies. Therefore searching for predictive markers and new targets for treatment in clinically relevant in vitro tumor models is essential. Five HNSCC-derived cell lines were used to assess the effect of 3D culturing compared to 2D monolayers in terms of cell proliferation, response to anti-cancer therapy as well as expression of EMT and CSC genes.

Methods

The viability and proliferation capacity of HNSCC cells as well as induction of apoptosis in tumor spheroids cells after treatment was assessed by MTT assay, crystal violet- and TUNEL assay respectively. Expression of EMT and CSC markers was analyzed on mRNA (RT-qPCR) and protein (Western blot) level.

Results

We showed that HNSCC cells from different tumors formed spheroids that differed in size and density in regard to EMT-associated protein expression and culturing time. In all spheroids, an up regulation of CDH1, NANOG and SOX2 was observed in comparison to 2D but changes in the expression of EGFR and EMT markers varied among the cell lines. Moreover, most HNSCC cells grown in 3D showed decreased sensitivity to cisplatin and cetuximab (anti-EGFR) treatment.

Conclusions

Taken together, our study points at notable differences between these two cellular systems in terms of EMT-associated gene expression profile and drug response. As the 3D cell cultures imitate the in vivo behaviour of neoplastic cells within the tumor, our study suggest that 3D culture model is superior to 2D monolayers in the search for new therapeutic targets.

Place, publisher, year, edition, pages
BioMed Central, 2019
Keywords
Cancer stem cells; Drug response; Epithelial–mesenchymal transition; Head and Neck Squamous Cell Carcinoma; Spheroids
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-153947 (URN)10.1186/s12935-019-0733-1 (DOI)000455593400001 ()30651721 (PubMedID)2-s2.0-85059943217 (Scopus ID)
Note

Funding agencies: Korea-Sweden Joint Research Programme; Swedish Cancer Society [2017/301]; County Council of Ostergotland; Research Funds of Linkoping University Hospital; Cancer Foundation of Ostergotland

Available from: 2019-01-21 Created: 2019-01-21 Last updated: 2019-03-29Bibliographically approved
Wiechec, E., Tiefenböck Hansson, K., Alexandersson, L., Jönsson, J.-I. & Roberg, K. (2017). Hypoxia Mediates Differential Response to Anti-EGFR Therapy in HNSCC Cells.. International Journal of Molecular Sciences, 18(5)
Open this publication in new window or tab >>Hypoxia Mediates Differential Response to Anti-EGFR Therapy in HNSCC Cells.
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2017 (English)In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 18, no 5Article in journal (Refereed) Published
Abstract [en]

Despite advances in the head and neck squamous cell carcinoma (HNSCC) treatment modalities, drug resistance and cancer recurrence are often reported. Hypoxia signaling through hypoxia-inducible factor 1 (HIF-1) promotes angiogenesis and metastasis by inducing epithelial-mesenchymal-transition (EMT). The aim of this study was to evaluate the impact of hypoxia on response to therapy as well as EMT and expression of stem cell markers in HNSCC cells. Five HNSCC cell lines (UT-SCC-2, UT-SCC-14, LK0412, LK0827, and LK0923) were selected for this study. The treatment sensitivity for radiation, cisplatin, cetuximab, and dasatinib was assessed by crystal violet assay. Gene expression of EMT and cancer stem cell (CSC) markers as well as protein level of EGFR signaling molecules were analyzed by qPCR and western blotting, respectively. Unlike UT-SCC-14 and LK0827, the LK0412 cell line became significantly more sensitive to cetuximab in hypoxic conditions. This cetuximab sensitivity was efficiently reversed after suppression of HIF-1α with siRNA. Additionally, hypoxia-induced EMT and expression of stem cell markers in HNSCC cells was partially revoked by treatment with cetuximab or knockdown of HIF-1α. In summary, our study shows that hypoxia might have a positive influence on the anti-EGFR therapy effectiveness in HNSCC. However, due to heterogeneity of HNSCC lesions, targeting HIF-1α may not be sufficient to mediate such a response. Further studies identifying a trait of hypoxia-specific response to cetuximab in HNSCC are advisable.

Place, publisher, year, edition, pages
M D P I AG, 2017
Keywords
HIF-1α; cancer stem cells (CSC); cetuximab; cisplatin; epithelial-mesenchymal transition (EMT); head and neck tumors; hypoxia; radiotherapy
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-137276 (URN)10.3390/ijms18050943 (DOI)000404113900050 ()28468237 (PubMedID)2-s2.0-85018414799 (Scopus ID)
Note

Funding agenceis: County Council of Ostergotland; Research Funds of Linkoping University Hospital; Cancer Foundation of Ostergotland; Swedish Cancer Society; Swedish Research Council

Available from: 2017-05-09 Created: 2017-05-09 Last updated: 2018-05-02Bibliographically approved
Alizadeh, J., Zeki, A. A., Mirzaei, N., Tewary, S., Rezaei Moghadam, A., Glogowska, A., . . . Ghavami, S. (2017). Mevalonate Cascade Inhibition by Simvastatin Induces the Intrinsic Apoptosis Pathway via Depletion of Isoprenoids in Tumor Cells. Scientific Reports, 7, Article ID 44841.
Open this publication in new window or tab >>Mevalonate Cascade Inhibition by Simvastatin Induces the Intrinsic Apoptosis Pathway via Depletion of Isoprenoids in Tumor Cells
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2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 44841Article in journal (Refereed) Published
Abstract [en]

The mevalonate (MEV) cascade is responsible for cholesterol biosynthesis and the formation of the intermediate metabolites geranylgeranylpyrophosphate (GGPP) and farnesylpyrophosphate (FPP) used in the prenylation of proteins. Here we show that the MEV cascade inhibitor simvastatin induced significant cell death in a wide range of human tumor cell lines, including glioblastoma, astrocytoma, neuroblastoma, lung adenocarcinoma, and breast cancer. Simvastatin induced apoptotic cell death via the intrinsic apoptotic pathway. In all cancer cell types tested, simvastatin-induced cell death was not rescued by cholesterol, but was dependent on GGPP-and FPP-depletion. We confirmed that simvastatin caused the translocation of the small Rho GTPases RhoA, Cdc42, and Rac1/2/3 from cell membranes to the cytosol in U251 (glioblastoma), A549 (lung adenocarcinoma) and MDA-MB231( breast cancer). Simvastatin-induced Rho-GTP loading significantly increased in U251 cells which were reversed with MEV, FPP, GGPP. In contrast, simvastatin did not change Rho-GTP loading in A549 and MDA-MB-231. Inhibition of geranylgeranyltransferase I by GGTi-298, but not farnesyltransferase by FTi-277, induced significant cell death in U251, A549, and MDA-MB-231. These results indicate that MEV cascade inhibition by simvastatin induced the intrinsic apoptosis pathway via inhibition of Rho family prenylation and depletion of GGPP, in a variety of different human cancer cell lines.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2017
National Category
Cell Biology
Identifiers
urn:nbn:se:liu:diva-136580 (URN)10.1038/srep44841 (DOI)000397441300001 ()28344327 (PubMedID)
Note

Funding Agencies|University of Manitoba; URGP; Health Science Foundation Operating; Manitoba Medical Service Foundation; Divisional start-up funds; MITACS Globalink program in Canada; Graduate Enhancement of Tri-council Stipends (GETS) program at the University of Manitoba; NSERC; Research Manitoba; Canadian Research Society (CRS); Department of Surgery Research Fund; Health Science Foundation Centre (Winnipeg); Heart and Stroke Foundation of Canada; Canada Research Chair in Molecular Cardiolipin Metabolism; [1K08HL114882-01A1]

Available from: 2017-04-21 Created: 2017-04-21 Last updated: 2018-05-03
Skonieczna, M., Cieslar-Pobuda, A., Saenko, Y., Foksinski, M., Olinski, R., Rzeszowska-Wolny, J. & Wiechec, E. (2017). The impact of DIDS-induced inhibition of voltage-dependent anion channels (VDAC) on cellular response of lymphoblastoid cells to ionizing radiation.. Medicinal chemistry, 13(5), 477-483
Open this publication in new window or tab >>The impact of DIDS-induced inhibition of voltage-dependent anion channels (VDAC) on cellular response of lymphoblastoid cells to ionizing radiation.
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2017 (English)In: Medicinal chemistry, ISSN 1573-4064, Vol. 13, no 5, p. 477-483Article in journal (Refereed) Published
Abstract [en]

Background: The voltage-dependent ion channels (VDAC) play an essential role in the cross talk between mitochondria and the rest of the cell. Their implication in cell life and cell death has been studied extensively in recent years. In this work we studied the impact of mitochondrial membrane voltage-dependent anion channels (VDACs) on cell survival and response to X-ionizing radiation (IR) of human lymphoblastoid K562 cells. Methods: The inhibition of VDACs was achieved by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) inhibitor and in vitro experiments including clonogenity assay, UV-visible spectrophotometry, comet assay and FACS analysis were implemented. Results: Inhibition of VDAC led to augmentation of IR-induced apoptosis and ROS production. Additionally, DIDS affected repair of IR-induced DNA strand breaks and was in line with both induction of apoptosis and caspase activity. The IR-induced NO production was potently reduced by inhibition of VDAC. Conclusion: Our results suggest that VDAC control cellular response to ionizing radiation through modulation of the ROS- and NO-dependent signaling pathways. Inhibition of VDAC with DIDS induced apoptosis in irradiated K562 lymphoblastoid cells points at DIDS, as a promising agent to enhance the effectiveness of radiotherapy.

Place, publisher, year, edition, pages
Bentham Science Publishers Ltd., 2017
Keywords
4, 4′-diisothiocyanostilbene-2, 2′-disulfonic acid (DIDS); voltage-dependent anion channel (VDAC); reactive oxygen species (ROS), ionizing radiation, cell death, DNA strand breaks.
National Category
Health Sciences
Identifiers
urn:nbn:se:liu:diva-137275 (URN)10.2174/1573406413666170421102353 (DOI)000405545000008 ()28427245 (PubMedID)
Note

Funding agencies: National Science Center [DEC-2012/07/B/NZ1/00008, NCN 2015/19/B/ST7/02984]; Innovative Economy Operational Programme (POIG) [02.01.00-00-166/08, POIG. 02.03.01-00040/13]

Available from: 2017-05-09 Created: 2017-05-09 Last updated: 2017-08-17Bibliographically approved
Iranpour, M., Moghadam, A. R., Yazdi, M., Ande, S. R., Alizadeh, J., Wiechec, E., . . . Ghavami, S. (2016). Apoptosis, autophagy and unfolded proteinresponse pathways in Arbovirus replicationand pathogenesis. Expert Reviews in Molecular Medicine, 18(e1), 21
Open this publication in new window or tab >>Apoptosis, autophagy and unfolded proteinresponse pathways in Arbovirus replicationand pathogenesis
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2016 (English)In: Expert Reviews in Molecular Medicine, ISSN 1462-3994, E-ISSN 1462-3994, Vol. 18, no e1, p. 21-Article, review/survey (Refereed) Published
Abstract [en]

Arboviruses are pathogens that widely affect the health of people in different communities around the world. Recently, a few successful approaches toward production of effective vaccines against some of these pathogens have been developed, but treatment and prevention of the resulting diseases remain a major health and research concern. The arbovirus infection and replication processes are complex, and many factors are involved in their regulation. Apoptosis, autophagy and the unfolded protein response (UPR) are three mechanisms that are involved in pathogenesis of many viruses. In this review, we focus on the importance of these pathways in the arbovirus replication and infection processes. We provide a brief introduction on how apoptosis, autophagy and the UPR are initiated and regulated, and then discuss the involvement of these pathways in regulation of arbovirus pathogenesis.

Place, publisher, year, edition, pages
Cambridge University Press: , 2016
Keywords
apoptosis; cell death, viral infection;
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:liu:diva-124168 (URN)10.1017/erm.2015.19 (DOI)000368708700001 ()26781343 (PubMedID)
Note

Funding agencies: University of Manitoba; Manitoba Medical Service Foundation; Canadian Institutes of Health Research [MT-11630]

Available from: 2016-01-20 Created: 2016-01-20 Last updated: 2018-01-10
Yeganeh, B., Moghadam, A. R., Alizadeh, J., Wiechec, E., Alavian, S. M., Hashemi, M., . . . Ghavami, S. (2015). Hepatitis B and C virus-induced hepatitis: apoptosis, autophagy and unfolded protein response.. World Journal of Gastroenterology, 21(47), 13225-13239
Open this publication in new window or tab >>Hepatitis B and C virus-induced hepatitis: apoptosis, autophagy and unfolded protein response.
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2015 (English)In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 21, no 47, p. 13225-13239Article in journal (Refereed) Published
Abstract [en]

AIM: To investigate the co-incidence of apoptosis, autophagy, and unfolded protein response (UPR) in hepatitis B (HBV) and C (HCV) infected hepatocytes.

METHODS: We performed immunofluorescence confocal microscopy on 10 liver biopsies from HBV and HCV patients and tissue microarrays of HBV positive liver samples. We used specific antibodies for LC3β, cleaved caspase-3, BIP (GRP78), and XBP1 to detect autophagy, apoptosis and UPR, respectively. Anti-HCV NS3 and anti-HBs antibodies were also used to confirm infection. We performed triple blind counting of events to determine the co-incidence of autophagy (LC3β punctuate), apoptosis (cleaved caspase-3), and unfolded protein response (GRP78) with HBV and HCV infection in hepatocytes. All statistical analyses were performed using SPSS software for Windows (Version 16 SPSS Inc, Chicago, IL, United States). P-values < 0.05 were considered statistically significant. Statistical analyses were performed with Mann-Whitney test to compare incidence rates for autophagy, apoptosis, and UPR in HBV- and HCV-infected cells and adjacent non-infected cells.

RESULTS: Our results showed that infection of hepatocytes with either HBV and HCV induces significant increase (P < 0.001) in apoptosis (cleavage of caspase-3), autophagy (LC3β punctate), and UPR (increase in GRP78 expression) in the HCV- and HBV-infected cells, as compared to non-infected cells of the same biopsy sections. Our tissue microarray immunohistochemical expression analysis of LC3β in HBVNeg and HBVPos revealed that majority of HBV-infected hepatocytes display strong positive staining for LC3β. Interestingly, although XBP splicing in HBV-infected cells was significantly higher (P < 0.05), our analyses show a slight increase of XBP splicing was in HCV-infected cells (P > 0.05). Furthermore, our evaluation of patients with HBV and HCV infection based on stage and grade of the liver diseases revealed no correlation between these pathological findings and induction of apoptosis, autophagy, and UPR.

CONCLUSION: The results of this study indicate that HCV and HBV infection activates apoptosis, autophagy and UPR, but slightly differently by each virus. Further studies are warranted to elucidate the interconnections between these pathways in relation to pathology of HCV and HBV in the liver tissue.

Place, publisher, year, edition, pages
Pleasanton, CA, United States: Baishideng Publishing Group, 2015
Keywords
cell fate; cell death; hepatocyte; viral infection;
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-123870 (URN)10.3748/wjg.v21.i47.13225 (DOI)000366889600003 ()
Note

Funding agencies: University of Manitoba Start-up funds; Manitoba Medical Service Foundation

Available from: 2016-01-12 Created: 2016-01-12 Last updated: 2017-11-30Bibliographically approved
Bose, T., Cieślar-Pobuda, A. & Wiechec, E. (2015). Role of ion channels in regulating Ca2+ homeostasis during the interplay between immune and cancer cells.. Cell Death and Disease, 19(6), Article ID e1648.
Open this publication in new window or tab >>Role of ion channels in regulating Ca2+ homeostasis during the interplay between immune and cancer cells.
2015 (English)In: Cell Death and Disease, ISSN 2041-4889, E-ISSN 2041-4889, Vol. 19, no 6, article id e1648Article, review/survey (Refereed) Published
Abstract [en]

Ion channels are abundantly expressed in both excitable and non-excitable cells, thereby regulating the Ca2+ influx and downstream signaling pathways of physiological processes. The immune system is specialized in the process of cancer cell recognition and elimination, and is regulated by different ion channels. In comparison with the immune cells, ion channels behave differently in cancer cells by making the tumor cells more hyperpolarized and influence cancer cell proliferation and metastasis. Therefore, ion channels comprise an important therapeutic target in anti-cancer treatment. In this review, we discuss the implication of ion channels in regulation of Ca2+ homeostasis during the crosstalk between immune and cancer cell as well as their role in cancer progression.

Keywords
ion channels, cancer, Ca2+-influx, cytotoxic T cells, natural killer cells, anti-cancer immunity
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-115101 (URN)10.1038/cddis.2015.23 (DOI)000350575800022 ()25695601 (PubMedID)
Available from: 2015-03-08 Created: 2015-03-08 Last updated: 2017-12-04Bibliographically approved
Cieślar-Pobuda, A., Vilas Jain, M., Kratz, G., Rzeszowska-Wolny, J., Ghavami, S. & Wiechec, E. (2015). The expression pattern of PFKFB3 enzyme distinguishes between induced-pluripotent stem cells and cancer stem cells.. OncoTarget, 6(30), 29753--29770
Open this publication in new window or tab >>The expression pattern of PFKFB3 enzyme distinguishes between induced-pluripotent stem cells and cancer stem cells.
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2015 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 6, no 30, p. 29753--29770Article in journal (Refereed) Published
Abstract [en]

Induced pluripotent stem cells (iPS) have become crucial in medicine and biology. Several studies indicate their phenotypic similarities with cancer stem cells (CSCs) and a propensity to form tumors. Thus it is desirable to identify a trait which differentiates iPS populations and CSCs. Searching for such a feature, in this work we compare the restriction (R) point-governed regulation of cell cycle progression in different cell types (iPS, cancer, CSC and normal cells) based on the expression profile of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase3 (PFKFB3) and phosphofructokinase (PFK1). Our study reveals that PFKFB3 and PFK1 expression allows discrimination between iPS and CSCs. Moreover, cancer and iPS cells, when cultured under hypoxic conditions, alter their expression level of PFKFB3 and PFK1 to resemble those in CSCs. We also observed cell type-related differences in response to inhibition of PFKFB3. This possibility to distinguish CSC from iPS cells or non-stem cancer cells by PFKB3 and PFK1 expression improves the outlook for clinical application of stem cell-based therapies and for more precise detection of CSCs.

Place, publisher, year, edition, pages
Albany, NY, USA: Impact Journals LLC, 2015
Keywords
PFKFB3; R-point; cancer stem cells; induced pluripotent stem cells
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-121349 (URN)10.18632/oncotarget.4995 (DOI)000363183200098 ()26337471 (PubMedID)
Available from: 2015-09-14 Created: 2015-09-14 Last updated: 2018-01-11Bibliographically approved
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