Biology subjects

Kacar, S.

Publications and source records attributed to Kacar, S..

3 recordsLinked to original sources

bioRxiv2024

CHEMOKINE SIGNALING IN BREAST CANCER: FOCUS ON CC-MOTIF CHEMOKINE LIGANDS

Based on 2020 data from GLOBOCAN, breast cancer holds the highest incidence rate in the majority of countries (159 out of 185 countries) and is the leading cause of mortality in 110 countries Chemokines are 8-10 kDa proteins activating through transmembrane G-coupled receptors (GPCRs) with 24 CC-motif type known human cytokines and 10 respective receptors. Chemokines and chemokines receptors have the potential for new breast cancer therapeutics modalities. In the complex chemokine world, not only one chemokine can bind to multiple receptors but also one receptor can be activated by several chemokine ligands. The fact that immune cells possess the potential to express multiple receptors and also secrete a diverse number of chemokines further intensifies the intricate and challenging to grasp chemokines interaction with receptors and microenvironment. In addition, the implication of chemokines in the malignant activation of tumor cells makes them indispensable contributors to the cancer microenvironment and influences the fate of tumor cells and the overall survival of the patients. Therefore, herein, we aimed in this study at attracting the researchers attention to the particular function of all known CC-motif chemokines and to-date findings, their expressional changes in normal, tumor and tumor adjacent tissues, important key effects in breast cancer and more importantly, we analyzed the breast tumor samples expression data retrieved from TCGA, Xena UCSC as well as UALCAN database regarding to showing any potential to be a general, subclass-specific or stage-specific marker as well as effects of overall survival of the patients and their correlation with literature findings. Basically, we desire this study to be a sort of reference insights for effects of human CC-motif chemokines in breast cancer or provide ready-to-use source and insights for researchers with the graphs and analyzes from different databases.

cancer biology↗

bioRxiv2023

CURCUMIN HAS LOWER IC50 VALUES AGAINST A549 LUNG CANCER CELLS

In this study, we aimed to determine the toxic effect of curcumin on A549 lung cancer cells and to show how this effect is reflected in morphology. Firstly, the toxic doses of curcumin against A549 lung cancer cells were determined via MTT and neutral red cytotoxicity tests by using the doses of 6.25, 12.5, 25, 50, 100, 200 and 400 {micro}M. The morphological examination was performed using inverted microscope and light microscope with hematoxylin-eosin eosin.As a result, the IC50 dose of curcumin against A549 cells was 33 {micro}M according to MTT cytotoxicity test and 52 {micro}M according to the neutral red cytotoxicity test. When these doses were administered, the rounded and shrunken cells were visible in the inverted microscope, while apoptotic hallmarks such as nucleus condensation, renal nucleus structure and cellular shrinkage were detected in hematoxylin-eosin staining. In conclusion, the low IC50 values of curcumin for 24 hours indicate that curcumin is effective against A549 cells. It has the potential to be used either alone or in combination with other agents in cancer studies in case its low toxic effect on normal was assured.

pharmacology and toxicology↗

bioRxiv2023

The Prolonged Terminal Phase of Human Life Induces Survival Response in the Skin Transcriptome

Human death marks the end of organismal life under conditions such that the components of the human body continue to be alive. Such postmortem cellular survival depends on the nature (Hardy scale of slow-fast death) of human death. Slow and expected death typically results from terminal illnesses and includes a prolonged terminal phase of life. As such organismal death process unfolds, do cells of the human body adapt for postmortem cellular survival? Organs with low energy cost-of-living, such as the skin, are better suited for postmortem cellular survival. In this work, the effect of different durations of terminal phase of human life on postmortem changes in cellular gene expression was investigated using RNA sequencing data of 701 human skin samples from the Genotype-Tissue Expression (GTEx) database. Longer terminal phase (slow-death) was associated with a more robust induction of survival pathways (PI3K-Akt signaling) in postmortem skin. Such cellular survival response was associated with the upregulation of embryonic developmental transcription factors such as FOXO1, FOXO3, ATF4 and CEBPD. Upregulation of PI3K-Akt signaling was independent of sex or duration of death-related tissue ischemia. Analysis of single nucleus RNA-seq of post-mortem skin tissue specifically identified the dermal fibroblast compartment to be most resilient as marked by adaptive induction of PI3K-Akt signaling. In addition, slow death also induced angiogenic pathways in the dermal endothelial cell compartment of postmortem human skin. In contrast, specific pathways supporting functional properties of the skin as an organ were downregulated following slow death. Such pathways included melanogenesis and those representing the skin extracellular matrix (collagen expression and metabolism). Efforts to understand the significance of death as a biological variable (DABV) in influencing the transcriptomic composition of surviving component tissues has far-reaching implications including rigorous interpretation of experimental data collected from the dead and mechanisms involved in transplant-tissue obtained from dead donors.

genomics↗