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: 12Citation - Scopus: 12Sema6d Differentially Regulates Proliferation, Migration, and Invasion of Breast Cell Lines(American Chemical Society, 2022) Günyüz, Zehra Elif; Sahi İlhan, Ece; Küçükköse, Cansu; İpekgil, Doğaç; Tok, Güneş; Meşe, Gülistan; Özçivici, Engin; Yalçın Özuysal, ÖzdenSemaphorin 6D (SEMA6D), a member of the class 6 semaphorin family, is a membrane-associated protein that plays a key role in the development of cardiac and neural tissues. A growing body of evidence suggests that SEMA6D is also involved in tumorigenesis. In breast cancer, high SEMA6D levels are correlated with better survival rates. However, very little is known about the functional significance of SEMA6D in breast tumorigenesis. In the present study, we aimed to investigate the effects of SEMA6D expression on the normal breast cell line MCF10A and the breast cancer cell lines MCF7 and MDA MB 231. We demonstrated that SEMA6D expression increases the proliferation of MCF10A cells, whereas the opposite effect was observed in MCF7 cells. SEMA6D expression induced anchorage-independent growth in both cancer cell lines. Furthermore, migration of MCF10A and MCF7 cells and invasion of MDA MB 231 cells were elevated in response to SEMA6D overexpression. Accordingly, the genes related to epithelial-mesenchymal transition (EMT) were altered by SEMA6D expression in MCF10A and MCF7 cell lines. Finally, we provided evidence that SEMA6D levels were associated with the expression of the cell cycle, EMT, and Notch signaling pathway-related genes in breast cancer patients' data. We showed for the first time that SEMA6D overexpression has cell-specific effects on the proliferation, migration, and invasion of normal and cancer breast cell lines, which agrees with the gene expression data of clinical samples. This study lays the groundwork for future research into understanding the functional importance of SEMA6D in breast cancerConference Object Advantage of Co-Culture Strategy for Targeted Cancer Treatment and in Vitro Studies(Elsevier, 2021) Ulu, Gizem Tuğçe; Bayram, Nazende Nur; Dinçer İşoğlu, Sevil; Baran, YusufBreast cancer tissues include carcinoma cells and stromal cells, and intra-tumoral stroma that consists of different types of cells. For this point, cell-cell interaction and communication have a potential role in cancer progression. Mono-cell culture is used for cancer treatment approaches. However, cell-cell interaction and communication can not be evaluated on mono-culture cells. So, co-culture models provide low-cost screening to determine cell proliferation for drug application before moving forward to in vivo models. Also, determination of cell morphology in co culture system is critical to understand advantages.Article Citation - WoS: 8Citation - Scopus: 8The Role of Connexins in Breast Cancer: From Misregulated Cell Communication To Aberrant Intracellular Signaling(Taylor & Francis, 2022) Ünal, Yağmur Ceren; Yavuz, Büşra; Özçivici, Engin; Meşe Özçivici, GülistanIn spite of clinical advancements and improved diagnostic techniques, breast cancers are the leading cause of cancer-associated deaths in women worldwide. Although 70% of early breast cancers can be cured, there are no efficient therapies against metastatic breast cancers. Several factors including connexins and gap junctions play roles in breast tumorigenesis. Connexins are critical for cellular processes as a linkage between connexin mutations and hereditary disorders demonstrated their importance for tissue homeostasis. Further, alterations in their expression, localization and channel activities were observed in many cancers including breast cancer. Both channel-dependent and independent functions of connexins were reported in initiation and progression of cancers. Unlike initial reports suggesting tumor suppressor functions, connexins and gap junctions have stage, context and isoform dependent effects in breast cancers similar to other cancers. In this review, we tried to describe the current understanding of connexins in tumorigenesis specifically in breast cancers.Article Citation - WoS: 16Citation - Scopus: 18Connexin 32 Induces Pro-Tumorigenic Features in Mcf10a Normal Breast Cells and Mda-Mb Metastatic Breast Cancer Cells(Elsevier, 2020) Yalçın Özuysal, Özden; Adak, Aslı; Ünal, Yağmur Ceren; Yücel, Simge; Vural, Zehra; Turan, Fatma Başak; Meşe, GülistanConnexins (Cx), the basic subunit of gap junctions, play important roles in cell homeostasis, and their abnormal expression and function are associated with human hereditary diseases and cancers. In tumorigenesis, connexins were observed to have both anti-tumorigenic and pro-tumorigenic roles in a context- and stage-dependent manner. Initially, Cx26 and Cx43 were thought to be the only connexins involved in normal breast homeostasis and breast cancer. Later on, association of Cx32 expression with lymph node metastasis of breast cancer and subsequent demonstration of its expression in normal breast tissue suggested that Cx32 contributes to breast tissue homeostasis. Here, we aimed to determine the effects of Cx32 on normal breast cells, MCF10A, and on breast cancer cells, MDA-MB-231. Cx32 overexpression had profound effects on MCF10A cells, decreasing cell proliferation by increasing the doubling time of MCF10A. Furthermore, MCF10A cells acquired mesenchymal-like appearance upon Cx32 expression and had increased migration capacity and expression of both E-cadherin and vimentin. In contrast, Cx32 overexpression altered the EMT markers of MDA-MB-231 by increasing the expression of mesenchymal markers, such as slug and vimentin, and decreasing E-cadherin expression without affecting their proliferation and morphology. Our results indicate, for the first time in the literature, that Cx32 has tumor-promoting roles in MCF10A and MDA-MB-231 cells.Article Citation - WoS: 19Citation - Scopus: 19Irf6 Is Involved in the Regulation of Cell Proliferation and Transformation in Mcf10a Cells Downstream of Notch Signaling(Public Library of Science, 2015) Zengin, Talip; Ekinci, Burcu; Küçükköse, Cansu; Yalçın Özuysal, ÖzdenIRF6, a member of Interferon Regulatory Factors (IRF) family, is involved in orofacial and epidermal development. In breast cancer cell lines ectopic expression of IRF6 reduces cell numbers suggesting a role as negative regulator of cell cycle. IRF6 is a direct target of canonical Notch signaling in keratinocyte differentiation. Notch is involved in luminal cell fate determination and stem cell regulation in the normal breast and is implicated as an oncogene in breast cancer. Notch activation is sufficient to induce proliferation and transformation in non-tumorigenic breast epithelial cell line, MCF10A. ΔNp63, which is downregulated by Notch activation in the breast, regulates IRF6 expression in keratinocytes. In this report, we investigate Notch-IRF6 and ΔNp63-IRF6 interactions in MCF10A and MDA MB 231 cells. We observed that in these cells, IRF6 expression is partially regulated by canonical Notch signaling and ΔNp63 downregulation. Furthermore, we demonstrate that IRF6 abrogation impairs Notch-induced proliferation and transformation in MCF10A cells. Thus, we confirm the previous findings by showing a tissue independent regulation of IRF6 by Notch signaling, and extend them by proposing a context dependent role for IRF6, which acts as a positive regulator of proliferation and transformation in MCF10A cells downstream of Notch signaling.Letter Citation - WoS: 2Citation - Scopus: 3Rates of Myocardial Infarction and Coronary Artery Disease and Risk Factors in Patients Treated With Radiation Therapy for Early-Stage Breast Cancer(John Wiley and Sons Inc., 2007) Ural, Ali Uğur; Avcu, Ferit; Baran, YusufWe read the interesting article by Jagsi et al on the increased rates of coronary artery disease in patients treated with radiation therapy for early-stage breast cancer.1 In their study, those authors concluded that the findings support further assessment of clinical outcomes when newer techniques of chemotherapy planning are employed as well as investigation of the potential role of innovative techniques. However, there was no mention of the novel radiosensitizing and chemosensitizing effects of bisphosphonates (BPs), which inhibit tumor cell adhesion to bone, and tumor growth in breast cancer.