Biology subjects

Yavuz, M.

Publications and source records attributed to Yavuz, M..

3 recordsLinked to original sources

bioRxiv2025

S4, a Selective Androgen Receptor Modulator, Suppresses Breast Cancer Progression via Cell Cycle Arrest, Apoptosis, and Metabolic Alterations

Breast cancer (BC) remains a leading cause of cancer-related mortality worldwide, highlighting the need for novel therapeutic strategies. Androgen receptor (AR) signaling has been implicated in BC progression, making it a potential target for treatment. Selective androgen receptor modulators (SARMs) have gained attention as alternatives to traditional hormone therapies. However, the effects of S4, a SARM, on BC have not been explored. This study investigates the impact of S4 on BC cell viability, proliferation, clonogenicity, migration, apoptosis, and cell cycle progression in MCF-7 and MDA-MB-231 cells. The results demonstrate that S4 significantly reduces BC cell viability in a dose-dependent manner, with IC50 values of 0.094 mM (MCF-7) and 0.067 mM (MDA-MB-231) after 24 hours. S4 suppresses clonogenicity and migration while promoting apoptosis and cell cycle arrest, with MCF-7 cells exhibiting S-phase arrest and MDA-MB-231 cells G0/G1-S arrest. Gene expression analysis reveals upregulation of tumor suppressor genes (CDKN1B and PUMA in MCF-7 cells, TP53, CDKN1A, and BAX in MDA-MB-231 cells, and GADD45A in both cells) and downregulation of oncogenes (ANKRD1, EDN1, CCND1 in MCF-7 cells, CXCL2 in MDA-MB-231 cells, CDK-6 and ATM in both cells), supporting the anti-carcinogenic effects of S4. Metabolomics profiling highlights significant alterations in phosphatidylcholine biosynthesis, catecholamine biosynthesis, and nucleotide metabolism, indicating a metabolic shift upon S4 treatment. These findings provide the first evidence of S4s potential as an anti-cancer agent in BC, suggesting that it exerts its effects by modulating gene expression and cellular metabolism. Further in-vivo studies are warranted to validate its therapeutic potential.

cancer biology↗

bioRxiv2021

Condition Medium of Glioblastoma Cell Lines Decreases the Viability of Glioblastoma Cells by Modulating Gene Expression Profile

Grade IV neoplasm of the central nervous system, GBM, is associated with poor prognosis and relatively short overall survival. Due to the current limitations in treatment methods, GBM is characterized as an incurable disease, and research to advance therapeutic options is required. Conditioned medium is commonly used in in-vitro studies complementary to animal experiments to simulate tumor microenvironment and has the potential to challenge and expand our current understanding of secretome effect on tumor characteristics. This study aimed to investigate the effects of conditioned mediums of GBM cell lines on each other. Conditioned mediums cellular and molecular effects were evaluated using commonly employed techniques such as MTT assay, colony formation assay, wound healing assay, EdU labeling-based flow cytometry, and qRT-PCR. Our study demonstrated that conditioned medium harvested from U87 or LN229 cells at 48th h exhibited an anti-growth activity on each other by changing the gene expression pattern. Furthermore, the conditioned medium of LN229 decreased the migration capacity of U87 cells, and the conditioned medium of U87 cells significantly suppressed the LN229 proliferation. We believe that this initial work provides new insights for a better understanding of GBM cell lines secretome roles and highlights the necessity of further studies to unveil the secretome content. HighlightsO_LIConditioned medium harvested from GBM cells at different time points displayed various effects. C_LIO_LIConditioned medium of GBM cell lines harvested at 48th h decreased the viability of each other. C_LIO_LIThe expression level of anti-and pro-proliferative genes is altered upon condition medium treatment. C_LI

cancer biology↗

bioRxiv2021

A comprehensive investigation of m6A regulators prognostic value and associated molecular pathways in breast invasive cancer

Breast invasive cancer (BIC) is one of the most commonly observed and the deadliest cancer among women. Despite the progress that has been made in improving breast cancer outcomes by the development of advanced treatment options, due to the heterogeneity and complexity of the disease, more studies are required to explore underlying molecular mechanisms of breast cancer which may provide useful insights to overcome the constraints related to current therapeutic options. The goal of this study was to reveal the crucial roles of m6A regulatory proteins in BIC development using various publicly available datasets and databases. We first conducted a comprehensive analysis to depict the mutation frequency and types for m6A regulatory genes in sub-types of BIC for the evaluation of the genetic alterations landscape of breast cancer. Changes in expression levels of m6A regulatory factors were identified as the key genetic alteration in BIC. Implementation of Kaplan-Meier tool to assess the predictive value of m6A pathway components in BIC validated the use of VIRMA, METTL14, RBM15B, EIF3B, YTHDF1, and YTHDF3 as prognostic biomarkers of breast cancer. We then examined the enriched gene ontology (GO) terms and KEGG pathways for the tumor samples with genetic alterations in the m6A pathway. Dysregulation of m6A regulatory factors in BIC was associated with cell division and survival-related pathways such as nuclear division and chromosome segregation via the upregulation of the genes functioning in these biological processes and the gained overactivity of these pathways may account for poor prognosis of the disease. The performed analyses highlighted m6A pathway genes as potential regulators of BIC growth and as a valuable set to be utilized as clinical biomarkers in BIC disease.

bioinformatics↗