Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
Permanent URI for this collectionhttps://hdl.handle.net/11147/9
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Article Citation - WoS: 5Citation - Scopus: 5Angelica Sylvestris and Delphinium Staphisagria Extracts Induces Antiproliferation Through Caspase-Mediated Apoptosis on Human Cancer Cells(Instituto de Tecnologia do Parana, 2022) Akgün, Oğuzhan; Akgün, Halime; Şahin, Çağatay; Çelikler, Serap; Arı, FerdaAngelica sylvestris and Delphinium staphisagria are medicinal and aromatic herbs with a long history in medicine and food industry. In this study, we have investigated anti-cancer activity of Angelica sylvestris and Delphinium staphisagria extracts on various cell lines of lung (A549), breast (MCF-7), colon (HT-29), and cervix (HeLa) origin. Also, cytotoxicity was tested on human healthy bronchial epithelial (BEAS-2B) cells. In vitro experiments showed that plant extracts suppressed cell growth and proliferation at low concentrations by reducing cell viability on cancer cells in a time and concentration-dependent manner. It was observed that Angelica sylvestris was more effective in HT-29 and HeLa cells and Delphinium staphisagria in A549 and MCF-7 cells by suppressing cell proliferation and increasing cell death. Cell death mode (apoptosis/necrosis) was investigated via fluorescent imaging, caspase-cleaved cytokeratin 18, activated caspase-3, and cleaved-PARP (poly (ADP-ribose) polymerase). In order to evaluate the cell death mode by plant extracts apoptotic markers were investigated by fluorescence staining. Delphinium staphisagria extract (50-200 μg/mL) caused a decrease in cell density in A549 and MCF-7 cells compared to untreated controls. A similar situation was observed in HT-29 and HeLa cell lines when treated with ASE. As a result, Delphinium staphisagria extracts induced apoptosis in A549 and MCF-7, while Angelica sylvestris extracts induced apoptosis in HT-29 and HeLa cancer cellsArticle Citation - WoS: 5Citation - Scopus: 5Invadopodia: Proteolytic Feet of Cancer Cells(TUBITAK, 2014) Batı, Gizem; Pesen Okvur, DevrimThe leading cause of death in cancer patients is metastasis. Invasion is an integral part of metastasis and is carried out by proteolytic structures called invadopodia at the cellular level. In this introductory review, we start by evaluating the definition of invadopodia. While presenting the upstream signaling events involved, we integrate current models on invadopodia. In addition, we discuss the significance of invadopodia in 2D and 3D and in vivo. We finally point out technical challenges and conclude with open questions in the field. © TÜBİTAK.Article Citation - WoS: 8Citation - Scopus: 8Multidrug Resistance in Chronic Myeloid Leukemia(TÜBİTAK, 2014) Ünlü, Miray; Kiraz, Yağmur; Kacı, Fatma Necmiye; Özcan, Mehmet Ali; Baran, YusufChronic myeloid leukemia (CML) is characterized by the accumulation of Philadelphia chromosome-positive (Ph+) myeloid cells. Ph+ cells occur via a reciprocal translocation between the long arms of chromosomes 9 and 22 resulting in constitutively active Bcr-abl fusion protein. Tyrosine kinase inhibitors (TKIs) are used against the kinase activity of Bcr-abl fusion protein for the effective treatment of CML. However, the development of drug resistance, directed by different genetic mechanisms, is the major problem of clinical applications of TKIs. These mechanisms include mutations in the TKI binding site of Bcr-abl, overexpression of Bcr-abl, overexpression of ATP binding cassette transporters, aberrant ceramide metabolism, inhibition of apoptosis, and changes in expression levels of microRNAs. Recently, many studies have focused on understanding the molecular mechanisms of drug resistance in cancer while targeting therapies providing reversal of resistance. Cancer stem cells also have roles in tumor initiation, maintenance, progression, metastasis, and drug resistance. Uncovering the mechanisms of drug resistance can provide more efficient treatment of cancer since these findings may provide novel targets for a complete cure. In this review, we discuss recent findings on the mechanisms of multidrug resistance and its reversal in CML. © TÜBİTAK.Article Citation - WoS: 9Citation - Scopus: 10The Roles of Epigenetic Modifications of Proapoptotic Bid and Bim Genes in Imatinibresistant Chronic Myeloid Leukemia Cells(Taylor and Francis Ltd., 2013) Bozkurt, Süreyya; Özkan, Tülin; Özmen, Füsun; Baran, Yusuf; Sunguroglu, Asuman; Kansu, EminIn chronic myeloid leukemia (CML), epigenetic modifications such as promoter hypermethylation and inactive histone modification are known mechanisms of drug resistance. In our study, we investigated the roles of promoter hypermethylation of BIM and BID genes and H3K27me3 histone modification on imatinib resistance. We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells. While we determined the EZH2 and DNMT enzymes as bounded to the promoter of the BIM gene, we did not detect hypermethylation of this promoter. We also found the H3K27me3 histone modification promoter of BIM and BID genes in both cell lines. In conclusion, our results support the notion that DNA promoter methylation may be formed independently from EZH2-H3K27me3 and pro-apoptotic BIM and BID genes are not methyllated in the imatinib resistance of CML cells.