TY  - CONF
AU  - Petrović, Jelena
AU  - Pańczyszyn, Elżbieta
AU  - Corazzari, Marco
AU  - Banićević, Ivana
AU  - Milivojević, Milena
AU  - Bojić, Luka
AU  - Stevanović, Milena
AU  - Dragoj, Miodrag
AU  - Pešić, Milica
AU  - Janković, Radmila
AU  - Obradović, Bojana
AU  - Stojkovska, Jasmina
PY  - 2024
UR  - https://www.ache-pub.org.rs/index.php/HemInd/article/view/1264
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2364
AB  - The slow advance in anticancer drug development can be attributed to the limitations of conventional models, predominantly monolayer cell (2D) cultures and animal models, which inadequately recapitulate the complex nature of human malignant tumors. Three-dimensional (3D) in vitro models are invaluable tools in drug screening; however, creating a universal model for all cancer types poses challenges due to the diverse nature of cancers. The aim of this work was to develop a single, versatile model using alginate microfibers to accommodate cultivation of various cancer cells.
C3  - Hemijska industrija (Chemical Industry)
T1  - Adaptable alginate-based microfibers for 3D in vitro cultures of cancer cells: an anticancer drug testing model
EP  - 21
IS  - 1S
SP  - 21
VL  - 78
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2364
ER  - 

@conference{
author = "Petrović, Jelena and Pańczyszyn, Elżbieta and Corazzari, Marco and Banićević, Ivana and Milivojević, Milena and Bojić, Luka and Stevanović, Milena and Dragoj, Miodrag and Pešić, Milica and Janković, Radmila and Obradović, Bojana and Stojkovska, Jasmina",
year = "2024",
abstract = "The slow advance in anticancer drug development can be attributed to the limitations of conventional models, predominantly monolayer cell (2D) cultures and animal models, which inadequately recapitulate the complex nature of human malignant tumors. Three-dimensional (3D) in vitro models are invaluable tools in drug screening; however, creating a universal model for all cancer types poses challenges due to the diverse nature of cancers. The aim of this work was to develop a single, versatile model using alginate microfibers to accommodate cultivation of various cancer cells.",
journal = "Hemijska industrija (Chemical Industry)",
title = "Adaptable alginate-based microfibers for 3D in vitro cultures of cancer cells: an anticancer drug testing model",
pages = "21-21",
number = "1S",
volume = "78",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2364"
}

Petrović, J., Pańczyszyn, E., Corazzari, M., Banićević, I., Milivojević, M., Bojić, L., Stevanović, M., Dragoj, M., Pešić, M., Janković, R., Obradović, B.,& Stojkovska, J.. (2024). Adaptable alginate-based microfibers for 3D in vitro cultures of cancer cells: an anticancer drug testing model. in Hemijska industrija (Chemical Industry), 78(1S), 21-21.
https://hdl.handle.net/21.15107/rcub_imagine_2364

Petrović J, Pańczyszyn E, Corazzari M, Banićević I, Milivojević M, Bojić L, Stevanović M, Dragoj M, Pešić M, Janković R, Obradović B, Stojkovska J. Adaptable alginate-based microfibers for 3D in vitro cultures of cancer cells: an anticancer drug testing model. in Hemijska industrija (Chemical Industry). 2024;78(1S):21-21.
https://hdl.handle.net/21.15107/rcub_imagine_2364 .

Petrović, Jelena, Pańczyszyn, Elżbieta, Corazzari, Marco, Banićević, Ivana, Milivojević, Milena, Bojić, Luka, Stevanović, Milena, Dragoj, Miodrag, Pešić, Milica, Janković, Radmila, Obradović, Bojana, Stojkovska, Jasmina, "Adaptable alginate-based microfibers for 3D in vitro cultures of cancer cells: an anticancer drug testing model" in Hemijska industrija (Chemical Industry), 78, no. 1S (2024):21-21,
https://hdl.handle.net/21.15107/rcub_imagine_2364 .

TY  - CONF
AU  - Obradović, Bojana
AU  - Stojkovska, Jasmina
AU  - Zvicer, Jovana
AU  - Milivojević, Milena
AU  - Janković, Radmila
AU  - Dragoj, Miodrag
AU  - Jančić, Ivan
PY  - 2024
UR  - https://www.ache-pub.org.rs/index.php/HemInd/article/view/1265
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2365
AB  - Development of novel, effective, and safe anti-tumor drugs is still a slow and cumbersome process, which is often attributed to weaknesses of current preclinical assays and low correlation of the preclinical in vitro and in vivo data with the results obtained in clinical trials. Consequently, there is a clear need for development of more reliable in vitro three dimensional (3D) tumor models, which will capture key features of the in vivo tumor cell microenvironment and provide drug testing results relevant for human patients. The aim of the project “Biomimetic tumor engineering to enhance drug discovery – BioengineeredTumor” funded by the Science Fund of the Republic of Serbia is to develop 2 novel, simple and robust 3D models for cultures of carcinoma and osteosarcoma cells by applying systematic and integrated methodology to comprehensively define the key model components. In specific, the aim is to use different human and animal cancer cell lines in conjunction with alginate-based biomaterials as artificial extracellular matrices imitating tumor environments and to cultivate the obtained constructs in perfusion bioreactors providing enhanced transport of nutrients, gases and biochemical signals to the cells as well as adequate levels of hydrodynamic shear stresses. Thus, the strategic goal is to establish an adaptable platform suited to the use by scientists without technical expertise for long-term in vitro studies of cancer cells for applications in anti-cancer drug discovery and validation, development of personalized medical treatments, and cancer research.
C3  - Hemijska industrija (Chemical Industry)
T1  - Biomimetic tumor engineering to enhance drug discovery - BioengineeredTumor
EP  - 22
IS  - 1S
SP  - 22
VL  - 78
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2365
ER  - 

@conference{
author = "Obradović, Bojana and Stojkovska, Jasmina and Zvicer, Jovana and Milivojević, Milena and Janković, Radmila and Dragoj, Miodrag and Jančić, Ivan",
year = "2024",
abstract = "Development of novel, effective, and safe anti-tumor drugs is still a slow and cumbersome process, which is often attributed to weaknesses of current preclinical assays and low correlation of the preclinical in vitro and in vivo data with the results obtained in clinical trials. Consequently, there is a clear need for development of more reliable in vitro three dimensional (3D) tumor models, which will capture key features of the in vivo tumor cell microenvironment and provide drug testing results relevant for human patients. The aim of the project “Biomimetic tumor engineering to enhance drug discovery – BioengineeredTumor” funded by the Science Fund of the Republic of Serbia is to develop 2 novel, simple and robust 3D models for cultures of carcinoma and osteosarcoma cells by applying systematic and integrated methodology to comprehensively define the key model components. In specific, the aim is to use different human and animal cancer cell lines in conjunction with alginate-based biomaterials as artificial extracellular matrices imitating tumor environments and to cultivate the obtained constructs in perfusion bioreactors providing enhanced transport of nutrients, gases and biochemical signals to the cells as well as adequate levels of hydrodynamic shear stresses. Thus, the strategic goal is to establish an adaptable platform suited to the use by scientists without technical expertise for long-term in vitro studies of cancer cells for applications in anti-cancer drug discovery and validation, development of personalized medical treatments, and cancer research.",
journal = "Hemijska industrija (Chemical Industry)",
title = "Biomimetic tumor engineering to enhance drug discovery - BioengineeredTumor",
pages = "22-22",
number = "1S",
volume = "78",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2365"
}

Obradović, B., Stojkovska, J., Zvicer, J., Milivojević, M., Janković, R., Dragoj, M.,& Jančić, I.. (2024). Biomimetic tumor engineering to enhance drug discovery - BioengineeredTumor. in Hemijska industrija (Chemical Industry), 78(1S), 22-22.
https://hdl.handle.net/21.15107/rcub_imagine_2365

Obradović B, Stojkovska J, Zvicer J, Milivojević M, Janković R, Dragoj M, Jančić I. Biomimetic tumor engineering to enhance drug discovery - BioengineeredTumor. in Hemijska industrija (Chemical Industry). 2024;78(1S):22-22.
https://hdl.handle.net/21.15107/rcub_imagine_2365 .

Obradović, Bojana, Stojkovska, Jasmina, Zvicer, Jovana, Milivojević, Milena, Janković, Radmila, Dragoj, Miodrag, Jančić, Ivan, "Biomimetic tumor engineering to enhance drug discovery - BioengineeredTumor" in Hemijska industrija (Chemical Industry), 78, no. 1S (2024):22-22,
https://hdl.handle.net/21.15107/rcub_imagine_2365 .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Dragoj, Miodrag
AU  - Ljujić, Mila
PY  - 2023
UR  - https://doi.org/10.1007/s00418-022-02172-3
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2243
AB  - Identification of the signature molecular profiles involved in therapy resistance is of vital importance in developing new strategies for treatments and disease monitoring. Protein alpha-1 antitrypsin (AAT, encoded by SERPINA1 gene) is an acute-phase protein, and its high expression has been linked with unfavorable clinical outcome in different types of cancer; however, data on its involvement in therapy resistance are still insufficient. We analyzed SERPINA1 mRNA expression in three different multidrug-resistant (MDR) cell lines—U87-TxR, NCI-H460/R, and DLD1-TxR—and in U87 cells grown in alginate microfibers as a 3D cellular model of glioblastoma. Expression of IL-6 as a major modulator of SERPINA1 was also analyzed. Additionally, AAT protein expression in MDR cells was analyzed by immunofluorescence. SERPINA1 gene expression and AAT protein expression were significantly upregulated in all the tested MDR cell lines compared with their sensitive counterparts. Moreover, SERPINA1 was significantly upregulated in 3D models of glioblastoma, previously found to have upregulated drug-resistance-related gene expression compared with 2D cells. With the exception of NCI-H460/R, in all cell lines as well as in a 3D model of U87 cells, increase in SERPINA1 expression correlated with the increase in IL-6 expression. Our results indicate that AAT could be utilized as a biomarker of therapy resistance in cancer; however, further studies are needed to elucidate the mechanisms driving AAT upregulation in therapy resistance and its biological significance in this process.
T2  - Histochemistry and Cell Biology
T1  - Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells
EP  - 437
IS  - 5
SP  - 431
VL  - 159
DO  - 10.1007/s00418-022-02172-3
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Jovanović Stojanov, Sofija and Dragoj, Miodrag and Ljujić, Mila",
year = "2023",
abstract = "Identification of the signature molecular profiles involved in therapy resistance is of vital importance in developing new strategies for treatments and disease monitoring. Protein alpha-1 antitrypsin (AAT, encoded by SERPINA1 gene) is an acute-phase protein, and its high expression has been linked with unfavorable clinical outcome in different types of cancer; however, data on its involvement in therapy resistance are still insufficient. We analyzed SERPINA1 mRNA expression in three different multidrug-resistant (MDR) cell lines—U87-TxR, NCI-H460/R, and DLD1-TxR—and in U87 cells grown in alginate microfibers as a 3D cellular model of glioblastoma. Expression of IL-6 as a major modulator of SERPINA1 was also analyzed. Additionally, AAT protein expression in MDR cells was analyzed by immunofluorescence. SERPINA1 gene expression and AAT protein expression were significantly upregulated in all the tested MDR cell lines compared with their sensitive counterparts. Moreover, SERPINA1 was significantly upregulated in 3D models of glioblastoma, previously found to have upregulated drug-resistance-related gene expression compared with 2D cells. With the exception of NCI-H460/R, in all cell lines as well as in a 3D model of U87 cells, increase in SERPINA1 expression correlated with the increase in IL-6 expression. Our results indicate that AAT could be utilized as a biomarker of therapy resistance in cancer; however, further studies are needed to elucidate the mechanisms driving AAT upregulation in therapy resistance and its biological significance in this process.",
journal = "Histochemistry and Cell Biology",
title = "Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells",
pages = "437-431",
number = "5",
volume = "159",
doi = "10.1007/s00418-022-02172-3"
}

Divac Rankov, A., Jovanović Stojanov, S., Dragoj, M.,& Ljujić, M.. (2023). Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells. in Histochemistry and Cell Biology, 159(5), 431-437.
https://doi.org/10.1007/s00418-022-02172-3

Divac Rankov A, Jovanović Stojanov S, Dragoj M, Ljujić M. Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells. in Histochemistry and Cell Biology. 2023;159(5):431-437.
doi:10.1007/s00418-022-02172-3 .

Divac Rankov, Aleksandra, Jovanović Stojanov, Sofija, Dragoj, Miodrag, Ljujić, Mila, "Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells" in Histochemistry and Cell Biology, 159, no. 5 (2023):431-437,
https://doi.org/10.1007/s00418-022-02172-3 . .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Kostić, Ana
AU  - Ljujić, Mila
AU  - Lupšić, Ema
AU  - Dragoj, Miodrag
AU  - Jovanović, Mirna
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1736
AB  - Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora.
AB  - Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306
T1  - Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306
SP  - 330
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1736
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Kostić, Ana and Ljujić, Mila and Lupšić, Ema and Dragoj, Miodrag and Jovanović, Mirna and Pešić, Milica and Dinić, Jelena",
year = "2022",
abstract = "Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora., Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306, Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306",
pages = "330",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1736"
}

Jovanović Stojanov, S., Kostić, A., Ljujić, M., Lupšić, E., Dragoj, M., Jovanović, M., Pešić, M.,& Dinić, J.. (2022). Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 330.
https://hdl.handle.net/21.15107/rcub_imagine_1736

Jovanović Stojanov S, Kostić A, Ljujić M, Lupšić E, Dragoj M, Jovanović M, Pešić M, Dinić J. Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije. 2022;:330.
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

Jovanović Stojanov, Sofija, Kostić, Ana, Ljujić, Mila, Lupšić, Ema, Dragoj, Miodrag, Jovanović, Mirna, Pešić, Milica, Dinić, Jelena, "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306" in Treći kongres biologa Srbije (2022):330,
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

TY  - JOUR
AU  - Jovanović, Mirna
AU  - Stanković, Tijana
AU  - Stojković Burić, Sonja
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Ljujić, Mila
AU  - Pesić, Milica
AU  - Dragoj, Miodrag
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1526
AB  - Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.
PB  - MDPI, Basel
T2  - Life-Basel
T1  - Decreased TSPAN14 Expression Contributes to NSCLC Progression
IS  - 9
VL  - 12
DO  - 10.3390/life12091291
ER  - 

@article{
author = "Jovanović, Mirna and Stanković, Tijana and Stojković Burić, Sonja and Banković, Jasna and Dinić, Jelena and Ljujić, Mila and Pesić, Milica and Dragoj, Miodrag",
year = "2022",
abstract = "Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.",
publisher = "MDPI, Basel",
journal = "Life-Basel",
title = "Decreased TSPAN14 Expression Contributes to NSCLC Progression",
number = "9",
volume = "12",
doi = "10.3390/life12091291"
}

Jovanović, M., Stanković, T., Stojković Burić, S., Banković, J., Dinić, J., Ljujić, M., Pesić, M.,& Dragoj, M.. (2022). Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel
MDPI, Basel., 12(9).
https://doi.org/10.3390/life12091291

Jovanović M, Stanković T, Stojković Burić S, Banković J, Dinić J, Ljujić M, Pesić M, Dragoj M. Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel. 2022;12(9).
doi:10.3390/life12091291 .

Jovanović, Mirna, Stanković, Tijana, Stojković Burić, Sonja, Banković, Jasna, Dinić, Jelena, Ljujić, Mila, Pesić, Milica, Dragoj, Miodrag, "Decreased TSPAN14 Expression Contributes to NSCLC Progression" in Life-Basel, 12, no. 9 (2022),
https://doi.org/10.3390/life12091291 . .