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Article: Epithelial-Mesenchymal Transition: A Fundamental Cellular and Microenvironmental Process in Benign and Malignant Prostate Pathologies.

Goncharov, Aviv Philip / Vashakidze, Nino / Kharaishvili, Gvantsa

2024 Volume 12, Issue 2

Abstract: Epithelial-mesenchymal transition (EMT) is a crucial and fundamental mechanism in many cellular processes, beginning with embryogenesis via tissue remodulation and wound healing, and plays a vital role in tumorigenesis and metastasis formation. EMT is a ... ...

Abstract	Epithelial-mesenchymal transition (EMT) is a crucial and fundamental mechanism in many cellular processes, beginning with embryogenesis via tissue remodulation and wound healing, and plays a vital role in tumorigenesis and metastasis formation. EMT is a complex process that involves many transcription factors and genes that enable the tumor cell to leave the primary location, invade the basement membrane, and send metastasis to other tissues. Moreover, it may help the tumor avoid the immune system and establish radioresistance and chemoresistance. It may also change the normal microenvironment, thus promoting other key factors for tumor survival, such as hypoxia-induced factor-1 (HIF-1) and promoting neoangiogenesis. In this review, we will focus mainly on the role of EMT in benign prostate disease and especially in the process of establishment of malignant prostate tumors, their invasiveness, and aggressive behavior. We will discuss relevant study methods for EMT evaluation and possible clinical implications. We will also introduce clinical trials conducted according to CONSORT 2010 that try to harness EMT properties in the form of circulating tumor cells to predict aggressive patterns of prostate cancer. This review will provide the most up-to-date information to establish a keen understanding of the cellular and microenvironmental processes for developing novel treatment lines by modifying or blocking the pathways.
Language	English
Publishing date	2024-02-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12020418
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Article ; Online: Skp2 and Slug Are Coexpressed in Aggressive Prostate Cancer and Inhibited by Neddylation Blockade.

Mickova, Alena / Kharaishvili, Gvantsa / Kurfurstova, Daniela / Gachechiladze, Mariam / Kral, Milan / Vacek, Ondrej / Pokryvkova, Barbora / Mistrik, Martin / Soucek, Karel / Bouchal, Jan

International journal of molecular sciences

2021 Volume 22, Issue 6

Abstract: Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men in Western countries, and there is still an urgent need for a better understanding of PCa progression to inspire new treatment strategies. Skp2 is a substrate-recruiting ... ...

Abstract	Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men in Western countries, and there is still an urgent need for a better understanding of PCa progression to inspire new treatment strategies. Skp2 is a substrate-recruiting component of the E3 ubiquitin ligase complex, whose activity is regulated through neddylation. Slug is a transcriptional repressor involved in the epithelial-to-mesenchymal transition, which may contribute to therapy resistance. Although Skp2 has previously been associated with a mesenchymal phenotype and prostate cancer progression, the relationship with Slug deserves further elucidation. We have previously shown that a high Gleason score (≥8) is associated with higher Skp2 and lower E-cadherin expression. In this study, significantly increased expression of Skp2, AR, and Slug, along with E-cadherin downregulation, was observed in primary prostate cancer in patients who already had lymph node metastases. Skp2 was slightly correlated with Slug and AR in the whole cohort (Rs 0.32 and 0.37, respectively), which was enhanced for both proteins in patients with high Gleason scores (Rs 0.56 and 0.53, respectively) and, in the case of Slug, also in patients with metastasis to lymph nodes (Rs 0.56). Coexpression of Skp2 and Slug was confirmed in prostate cancer tissues by multiplex immunohistochemistry and confocal microscopy. The same relationship between these two proteins was observed in three sets of prostate epithelial cell lines (PC3, DU145, and E2) and their mesenchymal counterparts. Chemical inhibition of Skp2, but not RNA interference, modestly decreased Slug protein in PC3 and its docetaxel-resistant subline PC3 DR12. Importantly, chemical inhibition of Skp2 by MLN4924 upregulated p27 and decreased Slug expression in PC3, PC3 DR12, and LAPC4 cells. Novel treatment strategies targeting Skp2 and Slug by the neddylation blockade may be promising in advanced prostate cancer, as recently documented for other aggressive solid tumors.
MeSH term(s)	Antigens, CD/genetics ; Antigens, CD/metabolism ; Antineoplastic Agents/pharmacology ; Cadherins/genetics ; Cadherins/metabolism ; Cell Line, Tumor ; Cell Survival/drug effects ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Cyclopentanes/pharmacology ; Docetaxel/pharmacology ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphatic Metastasis ; Male ; NEDD8 Protein/genetics ; NEDD8 Protein/metabolism ; Neoplasm Grading ; PC-3 Cells ; Prostate/metabolism ; Prostate/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Processing, Post-Translational ; Pyrimidines/pharmacology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors ; S-Phase Kinase-Associated Proteins/genetics ; S-Phase Kinase-Associated Proteins/metabolism ; Snail Family Transcription Factors/genetics ; Snail Family Transcription Factors/metabolism
Chemical Substances	Antigens, CD ; Antineoplastic Agents ; CDH1 protein, human ; Cadherins ; Cyclopentanes ; NEDD8 Protein ; NEDD8 protein, human ; Pyrimidines ; RNA, Small Interfering ; Receptors, Androgen ; S-Phase Kinase-Associated Proteins ; SKP2 protein, human ; SNAI1 protein, human ; Snail Family Transcription Factors ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Docetaxel (15H5577CQD) ; pevonedistat (S3AZD8D215)
Language	English
Publishing date	2021-03-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22062844
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Article ; Online: Skp2 and Slug Are Coexpressed in Aggressive Prostate Cancer and Inhibited by Neddylation Blockade

Alena Mickova / Gvantsa Kharaishvili / Daniela Kurfurstova / Mariam Gachechiladze / Milan Kral / Ondrej Vacek / Barbora Pokryvkova / Martin Mistrik / Karel Soucek / Jan Bouchal

International Journal of Molecular Sciences, Vol 22, Iss 2844, p

2021 Volume 2844

Abstract	Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men in Western countries, and there is still an urgent need for a better understanding of PCa progression to inspire new treatment strategies. Skp2 is a substrate-recruiting component of the E3 ubiquitin ligase complex, whose activity is regulated through neddylation. Slug is a transcriptional repressor involved in the epithelial-to-mesenchymal transition, which may contribute to therapy resistance. Although Skp2 has previously been associated with a mesenchymal phenotype and prostate cancer progression, the relationship with Slug deserves further elucidation. We have previously shown that a high Gleason score (≥8) is associated with higher Skp2 and lower E-cadherin expression. In this study, significantly increased expression of Skp2, AR, and Slug, along with E-cadherin downregulation, was observed in primary prostate cancer in patients who already had lymph node metastases. Skp2 was slightly correlated with Slug and AR in the whole cohort (Rs 0.32 and 0.37, respectively), which was enhanced for both proteins in patients with high Gleason scores (Rs 0.56 and 0.53, respectively) and, in the case of Slug, also in patients with metastasis to lymph nodes (Rs 0.56). Coexpression of Skp2 and Slug was confirmed in prostate cancer tissues by multiplex immunohistochemistry and confocal microscopy. The same relationship between these two proteins was observed in three sets of prostate epithelial cell lines (PC3, DU145, and E2) and their mesenchymal counterparts. Chemical inhibition of Skp2, but not RNA interference, modestly decreased Slug protein in PC3 and its docetaxel-resistant subline PC3 DR12. Importantly, chemical inhibition of Skp2 by MLN4924 upregulated p27 and decreased Slug expression in PC3, PC3 DR12, and LAPC4 cells. Novel treatment strategies targeting Skp2 and Slug by the neddylation blockade may be promising in advanced prostate cancer, as recently documented for other aggressive solid tumors.
Keywords	prostate cancer ; Skp2 (S-phase kinase-associated protein 2) ; Slug ; immunohistochemistry ; multiplex ; neddylation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Cancer-associated fibroblasts promote prostate tumor growth and progression through upregulation of cholesterol and steroid biosynthesis.

Neuwirt, Hannes / Bouchal, Jan / Kharaishvili, Gvantsa / Ploner, Christian / Jöhrer, Karin / Pitterl, Florian / Weber, Anja / Klocker, Helmut / Eder, Iris E

Cell communication and signaling : CCS

2020 Volume 18, Issue 1, Page(s) 11

Abstract: Background: Androgen receptor targeted therapies have emerged as an effective tool to manage advanced prostate cancer (PCa). Nevertheless, frequent occurrence of therapy resistance represents a major challenge in the clinical management of patients, ... ...

Abstract	Background: Androgen receptor targeted therapies have emerged as an effective tool to manage advanced prostate cancer (PCa). Nevertheless, frequent occurrence of therapy resistance represents a major challenge in the clinical management of patients, also because the molecular mechanisms behind therapy resistance are not yet fully understood. In the present study, we therefore aimed to identify novel targets to intervene with therapy resistance using gene expression analysis of PCa co-culture spheroids where PCa cells are grown in the presence of cancer-associated fibroblasts (CAFs) and which have been previously shown to be a reliable model for antiandrogen resistance. Methods: Gene expression changes of co-culture spheroids (LNCaP and DuCaP seeded together with CAFs) were identified by Illumina microarray profiling. Real-time PCR, Western blotting, immunohistochemistry and cell viability assays in 2D and 3D culture were performed to validate the expression of selected targets in vitro and in vivo. Cytokine profiling was conducted to analyze CAF-conditioned medium. Results: Gene expression analysis of co-culture spheroids revealed that CAFs induced a significant upregulation of cholesterol and steroid biosynthesis pathways in PCa cells. Cytokine profiling revealed high amounts of pro-inflammatory, pro-migratory and pro-angiogenic factors in the CAF supernatant. In particular, two genes, 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2 (HMGCS2) and aldo-keto reductase family 1 member C3 (AKR1C3), were significantly upregulated in PCa cells upon co-culture with CAFs. Both enzymes were also significantly increased in human PCa compared to benign tissue with AKR1C3 expression even being associated with Gleason score and metastatic status. Inhibiting HMGCS2 and AKR1C3 resulted in significant growth retardation of co-culture spheroids as well as of various castration and enzalutamide resistant cell lines in 2D and 3D culture, underscoring their putative role in PCa. Importantly, dual targeting of cholesterol and steroid biosynthesis with simvastatin, a commonly prescribed cholesterol synthesis inhibitor, and an inhibitor against AKR1C3 had the strongest growth inhibitory effect. Conclusions: From our results we conclude that CAFs induce an upregulation of cholesterol and steroid biosynthesis in PCa cells, driving them into AR targeted therapy resistance. Blocking both pathways with simvastatin and an AKR1C3 inhibitor may therefore be a promising approach to overcome resistances to AR targeted therapies in PCa. Video abstract.
MeSH term(s)	Aged ; Benzamides/pharmacology ; Biosynthetic Pathways/genetics ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Cell Survival/drug effects ; Cell Survival/genetics ; Cholesterol/biosynthesis ; Culture Media, Conditioned/pharmacology ; Disease Progression ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Extracellular Matrix/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Middle Aged ; Models, Biological ; Molecular Sequence Annotation ; Nitriles/pharmacology ; Phenotype ; Phenylthiohydantoin/pharmacology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/metabolism ; Simvastatin/pharmacology ; Spheroids, Cellular/metabolism ; Spheroids, Cellular/pathology ; Up-Regulation
Chemical Substances	AR protein, human ; Benzamides ; Culture Media, Conditioned ; Nitriles ; Receptors, Androgen ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU) ; Cholesterol (97C5T2UQ7J) ; Simvastatin (AGG2FN16EV)
Language	English
Publishing date	2020-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1478-811X
ISSN (online)	1478-811X
DOI	10.1186/s12964-019-0505-5
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Article ; Online: Cancer-associated fibroblasts promote prostate tumor growth and progression through upregulation of cholesterol and steroid biosynthesis

Hannes Neuwirt / Jan Bouchal / Gvantsa Kharaishvili / Christian Ploner / Karin Jöhrer / Florian Pitterl / Anja Weber / Helmut Klocker / Iris E. Eder

Cell Communication and Signaling, Vol 18, Iss 1, Pp 1-

2020 Volume 18

Abstract: Abstract Background Androgen receptor targeted therapies have emerged as an effective tool to manage advanced prostate cancer (PCa). Nevertheless, frequent occurrence of therapy resistance represents a major challenge in the clinical management of ... ...

Abstract	Abstract Background Androgen receptor targeted therapies have emerged as an effective tool to manage advanced prostate cancer (PCa). Nevertheless, frequent occurrence of therapy resistance represents a major challenge in the clinical management of patients, also because the molecular mechanisms behind therapy resistance are not yet fully understood. In the present study, we therefore aimed to identify novel targets to intervene with therapy resistance using gene expression analysis of PCa co-culture spheroids where PCa cells are grown in the presence of cancer-associated fibroblasts (CAFs) and which have been previously shown to be a reliable model for antiandrogen resistance. Methods Gene expression changes of co-culture spheroids (LNCaP and DuCaP seeded together with CAFs) were identified by Illumina microarray profiling. Real-time PCR, Western blotting, immunohistochemistry and cell viability assays in 2D and 3D culture were performed to validate the expression of selected targets in vitro and in vivo. Cytokine profiling was conducted to analyze CAF-conditioned medium. Results Gene expression analysis of co-culture spheroids revealed that CAFs induced a significant upregulation of cholesterol and steroid biosynthesis pathways in PCa cells. Cytokine profiling revealed high amounts of pro-inflammatory, pro-migratory and pro-angiogenic factors in the CAF supernatant. In particular, two genes, 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2 (HMGCS2) and aldo-keto reductase family 1 member C3 (AKR1C3), were significantly upregulated in PCa cells upon co-culture with CAFs. Both enzymes were also significantly increased in human PCa compared to benign tissue with AKR1C3 expression even being associated with Gleason score and metastatic status. Inhibiting HMGCS2 and AKR1C3 resulted in significant growth retardation of co-culture spheroids as well as of various castration and enzalutamide resistant cell lines in 2D and 3D culture, underscoring their putative role in PCa. Importantly, dual targeting of cholesterol and ...
Keywords	Prostate cancer ; Castration resistance ; Antiandrogens ; HMGCS2 ; AKR1C3 ; Simvastatin ; Medicine ; R ; Cytology ; QH573-671
Subject code	616
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Glycoprotein asporin as a novel player in tumour microenvironment and cancer progression.

Simkova, Dana / Kharaishvili, Gvantsa / Slabakova, Eva / Murray, Paul G / Bouchal, Jan

Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia

2016 Volume 160, Issue 4, Page(s) 467–473

Abstract: Background: Small leucine rich proteoglycans (SLRPs), major non-collagen components of the extracellular matrix (ECM), have multiple biological roles with diverse effects. Asporin, a member of the SLRPs class I, competes with other molecules in binding ... ...

Abstract	Background: Small leucine rich proteoglycans (SLRPs), major non-collagen components of the extracellular matrix (ECM), have multiple biological roles with diverse effects. Asporin, a member of the SLRPs class I, competes with other molecules in binding to collagen and affects its mineralization. Its role in cancer is only now being elucidated. Methods: The PubMed online database was used to search relevant reviews and original articles. Furthermore, altered asporin expression was analysed in publicly available genome-wide expression data at the Gene Expression Omnibus database. Results: Polymorphisms in the N-terminal polyaspartate domain, which binds calcium, are associated with osteoarthritis and prostate cancer. Asporin also promotes the progression of scirrhous gastric cancer where it is required for coordinated invasion by cancer associated fibroblasts and cancer cells. Besides the enhanced expression of asporin observed in multiple cancer types, such as breast, prostate, gastric, pancreas and colon cancer, tumour suppressive effects of asporin were described in triple-negative breast cancer. We also discuss a number of factors modulating asporin expression in different cell types relevant for alterations toing the tumour microenvironment. Conclusion: The apparent contradicting tumour promoting and suppressive effects of asporin require further investigation. Deciphering the role of asporin and other SLRPs in tumour-stroma interactions is needed for a better understanding of cancer progression and potentially also for novel tumour microenvironment based therapies.
MeSH term(s)	Adipose Tissue/physiology ; Disease Progression ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Extracellular Matrix Proteins/physiology ; Female ; Humans ; Male ; MicroRNAs/physiology ; Neoplasms/etiology ; Neoplasms/genetics ; Polymorphism, Genetic/genetics ; Tumor Microenvironment/genetics ; Tumor Microenvironment/physiology
Chemical Substances	ASPN protein, human ; Extracellular Matrix Proteins ; MicroRNAs
Language	English
Publishing date	2016-12
Publishing country	Czech Republic
Document type	Journal Article ; Review
ZDB-ID	17196-7
ISSN	1804-7521 ; 1213-8118 ; 0231-5599 ; 0862-481X
ISSN (online)	1804-7521
ISSN	1213-8118 ; 0231-5599 ; 0862-481X
DOI	10.5507/bp.2016.037
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Article ; Online: High Skp2 expression is associated with a mesenchymal phenotype and increased tumorigenic potential of prostate cancer cells.

Šimečková, Šárka / Kahounová, Zuzana / Fedr, Radek / Remšík, Ján / Slabáková, Eva / Suchánková, Tereza / Procházková, Jiřina / Bouchal, Jan / Kharaishvili, Gvantsa / Král, Milan / Beneš, Petr / Souček, Karel

Scientific reports

2019 Volume 9, Issue 1, Page(s) 5695

Abstract: Skp2 is a crucial component of ... ...

Abstract	Skp2 is a crucial component of SCF
MeSH term(s)	Animals ; CD24 Antigen/genetics ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Hyaluronan Receptors/genetics ; Male ; Mice ; Mice, Nude ; Neoplasm Grading ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/physiology ; PC-3 Cells ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/physiopathology ; S-Phase Kinase-Associated Proteins/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	CD24 Antigen ; CD24 protein, human ; CD44 protein, human ; Hyaluronan Receptors ; S-Phase Kinase-Associated Proteins ; SKP2 protein, human
Language	English
Publishing date	2019-04-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-42131-y
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Article ; Online: Glycoprotein asporin as a novel player in tumour microenvironment and cancer progression

Dana Simkova / Gvantsa Kharaishvili / Eva Slabakova / Paul G. Murray / Jan Bouchal

Biomedical Papers, Vol 160, Iss 4, Pp 467-

2016 Volume 473

Abstract	Background: Small leucine rich proteoglycans (SLRPs), major non-collagen components of the extracellular matrix (ECM), have multiple biological roles with diverse effects. Asporin, a member of the SLRPs class I, competes with other molecules in binding to collagen and affects its mineralization. Its role in cancer is only now being elucidated. Methods: The PubMed online database was used to search relevant reviews and original articles. Furthermore, altered asporin expression was analysed in publicly available genome-wide expression data at the Gene Expression Omnibus database. Results: Polymorphisms in the N-terminal polyaspartate domain, which binds calcium, are associated with osteoarthritis and prostate cancer. Asporin also promotes the progression of scirrhous gastric cancer where it is required for coordinated invasion by cancer associated fibroblasts and cancer cells. Besides the enhanced expression of asporin observed in multiple cancer types, such as breast, prostate, gastric, pancreas and colon cancer, tumour suppressive effects of asporin were described in triple-negative breast cancer. We also discuss a number of factors modulating asporin expression in different cell types relevant for alterations toing the tumour microenvironment. Conclusion: The apparent contradicting tumour promoting and suppressive effects of asporin require further investigation. Deciphering the role of asporin and other SLRPs in tumour-stroma interactions is needed for a better understanding of cancer progression and potentially also for novel tumour microenvironment based therapies.
Keywords	asporin ; polymorphism ; cancer ; gastric ; breast ; prostate ; adipose tissue ; mirnas ; Medicine ; R
Subject code	616 ; 610
Language	English
Publishing date	2016-12-01T00:00:00Z
Publisher	Palacký University Olomouc, Faculty of Medicine and Dentistry
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Sphingosine kinase-1 predicts overall survival outcomes in non-small cell lung cancer patients treated with carboplatin and navelbine.

Gachechiladze, Mariam / Tichý, Tomáš / Kolek, Vítězslav / Grygárková, Ivona / Klein, Jiří / Mgebrishvili, Giorgi / Kharaishvili, Gvantsa / Janíková, Mária / Smičková, Petra / Cierna, Lucia / Pitson, Stuart / Maddelein, Marie-Lise / Cuvillier, Olivier / Škarda, Jozef

Oncology letters

2019 Volume 18, Issue 2, Page(s) 1259–1266

Abstract: Sphingosine 1-phosphate (S1P) is a bioactive lipid metabolite associated with cancer cell proliferation, survival, migration and regulation of tumor angiogenesis in various cellular and animal models. Sphingosine kinase-1 (SphK1) and S1P lyase are the ... ...

Abstract	Sphingosine 1-phosphate (S1P) is a bioactive lipid metabolite associated with cancer cell proliferation, survival, migration and regulation of tumor angiogenesis in various cellular and animal models. Sphingosine kinase-1 (SphK1) and S1P lyase are the main enzymes that respectively control the synthesis and degradation of S1P. The present study analyzed the prognostic and predictive value of SphK1 and S1P lyase expression in patients with non-small cell lung cancer (NSCLC), treated with either surgery alone or in combination with adjuvant carboplatin and navelbine. Formalin-fixed, paraffin-embedded tissue samples from 176 patients with NSCLC were stained immunohistochemically using antibodies against SphK1 and S1P lyase, and their expression was correlated with all available clinicopathological factors. Increased expression of SphK1 was significantly associated with shorter overall and disease free survival in patients treated with adjuvant platinum-based chemotherapy. No prognostic relevance for S1P lyase expression was observed. Collectively, the results suggest that the immunohistochemical detection of SphK1 may be a promising predictive marker in NSCLC patients treated with adjuvant platinum-based chemotherapy.
Language	English
Publishing date	2019-06-07
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2019.10447
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Article: The role of cancer-associated fibroblasts, solid stress and other microenvironmental factors in tumor progression and therapy resistance.

Kharaishvili, Gvantsa / Simkova, Dana / Bouchalova, Katerina / Gachechiladze, Mariam / Narsia, Nato / Bouchal, Jan

Cancer cell international

2014 Volume 14, Page(s) 41

Abstract: Tumors are not merely masses of neoplastic cells but complex tissues composed of cellular and noncellular elements. This review provides recent data on the main components of a dynamic system, such as carcinoma associated fibroblasts that change the ... ...

Abstract	Tumors are not merely masses of neoplastic cells but complex tissues composed of cellular and noncellular elements. This review provides recent data on the main components of a dynamic system, such as carcinoma associated fibroblasts that change the extracellular matrix (ECM) topology, induce stemness and promote metastasis-initiating cells. Altered production and characteristics of collagen, hyaluronan and other ECM proteins induce increased matrix stiffness. Stiffness along with tumor growth-induced solid stress and increased interstitial fluid pressure contribute to tumor progression and therapy resistance. Second, the role of immune cells, cytokines and chemokines is outlined. We discuss other noncellular characteristics of the tumor microenvironment such as hypoxia and extracellular pH in relation to neoangiogenesis. Overall, full understanding of the events driving the interactions between tumor cells and their environment is of crucial importance in overcoming treatment resistance and improving patient outcome.
Language	English
Publishing date	2014-05-16
Publishing country	England
Document type	Journal Article ; Review
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/1475-2867-14-41
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