Breast cancer is the most common type of cancer in women and the second cause of cancer-related death after lung cancer. Although the common methods used in the treatment of breast cancer are chemotherapy, radiotherapy and surgery, the search for alternative treatments continues. The leading alternative treatments are medicinal plants which actually inspire the production of many cancer drugs. In this study, the proliferative and metastatic effects of Carthamus tinctorius L., known for its many therapeutic properties, on metastatic breast cancer were investigated. Here, intending to evaluate the the content and actions of different extracts of safflower leaves extracts were prepared by extracting in water, alcohol and oil and analysed by FTIR. Their antioxidant effect was tested and then the extracts were applied to metastatic breast cancer cells. FTIR spectrums of all three extracts have revealed the presence of organic compounds. It is found that all extracts but mostly the oil extract has antioxidant property. MTT assay, wound healing assay and gene expression analysis were performed to assess the antiproliferative and anti metastatic effects of the extracts on breast cancer cells. It is found that, there is no significant antiproliferative effect of extracts on MDA-MB-231 cells except the alcohol extract. However, all safflower extracts, especially the oil extract, significantly reduced the metastatic potential of breast cancer cells. It is concluded that safflower contents are potent chemicals which inhibit the cellular mechanisms underlying the spreading of cancer cells and further analysis may lead to new initiatives in drug design research.

Koronavirüs hastalığı 2019 (COVID-19), şiddetli akut solunum sendromu koronavirüs 2'nin (SARS-CoV-2) neden olduğu özellikle akciğerde şiddetli doku hasarına neden olan, yoğun inflamatuvar yanıt oluşturan bulaşıcı bir hastalıktır. Yapılan çalışmalar, COVID-19 enfeksiyonu olan erkeklerin kadınlara göre daha şiddetli semptomlar gösterdiği, yaşlı popülasyonunda COVID-19'dan ölüm riskinin gençlere göre daha yüksek olduğu bildirilmiştir. Erkeklerde COVID-19’un kadınlara göre daha ciddi seyretmesi, cinsiyet hormonlarının bu duruma etkisinin olabileceğini düşündürmektedir. Kadın ve erkeklerde cinsiyet hormon seviyelerindeki farklılık immün yanıtları önemli derecede etkilemektedir. COVID-19 pandemisinin sağlık sistemleri ve küresel ekonomi üzerindeki etkileri göz önüne alındığında, yenilikçi tedavi stratejilerine ihtiyaç duyulmaktadır. Bu doğrultuda, cinsiyet hormon terapileri COVID-19 hastaları için umut verici terapötik stratejiler sağlayabilir. Bu derlemede, COVID-19 enfeksiyonu prognozunda etkili olabilecek cinsiyet hormonlarının immün sistemdeki etkileri ve tedavi stratejileri üzerine yapılan çalışmalar incelenmiştir. Cinsiyet hormonlarının immün sistem üzerindeki etkileri dikkate alınarak uygulanan hormon tedavilerinin klinisyenlere yol göstereceğini ve COVID-19 tedavi protokollerine katkı sağlayacağını düşünmekteyiz.

Background: One of the main reasons for the unsuccessful treatment of pancreatic cancer is the intense desmoplastic pancreatic microenvironment. In the literature, the effects of mesenchymal stem cells (MSCs) and their inflammatory phenotypes on cancer cells have been a subject of controversy. Therefore, it is crucial to elucidate the underlying mechanisms of this interaction, especially in the context of pancreatic cancer. We aimed to investigate the effects of naive, TLR4‐activated, and TLR4‐inhibited phenotypes of adipose‐derived MSCs (ADMSC) on pancreatic ductal cell line (Panc‐1).Methods and Materials: Adipose‐derived MSCs were induced into a proinflammatory phenotype using a 0.5 μg/mL dose of TLR4 agonist, while an anti‐inflammatory phenotype was generated in ADMSCs using a 25 μg/mL dose of TLR4 antagonist. We observed that the proliferation of Panc‐1 cells was inhibited when naive ADMSCs:Panc‐1(10:1) and proinflammatory ADMSCs:Panc‐1(10:1) were directly cocultured.Results: In indirect coculture, both naive and proinflammatory ADMSCs exhibited a significant 10‐fold increase in their inhibitory effect on the proliferation and colony forming capacity of Panc‐1 cells, with the added benefit of inducing apoptosis. In our study, both naive and proinflammatory ADMSCs were found to regulate the expression of genes associated with metastasis (MMP2, KDR, MMP9, TIMP1, IGF2R, and COL1A1) and EMT (CDH1, VIM, ZEB1, and CLDN1) in Panc‐1 cells. Remarkably, both naive and proinflammatory ADMSCs demonstrated antitumor effects on Panc‐1 cells. However, it was observed that anti‐inflammatory ADMSCs showed tumor‐promoting effects instead. Furthermore, we observed a reciprocal influence between ADMSCs and Panc‐1 cells on each other's proinflammatory cytokine expressions, suggesting a dynamic interplay within the tumor microenvironment.Conclusions: These findings underscore the significance of both the naive state and different inflammatory phenotypes of MSCs in the microenvironment and represent a pivotal step toward the development of novel therapeutic approaches for pancreatic cancer. Understanding the intricate interactions between MSCs and cancer cells may open new avenues for targeted interventions in cancer therapy.

Objectives: Lung cancer remains a predominant cancer type with high incidence and low survival rates. Key challenges in its treatment include impaired cellular mechanisms, notably resistance to apoptosis and altered immune responses. A critical aspect in this context is the heightened TLR4-mediated signaling, known to promote cell survival, metastasis, and resistance to cell death, particularly impacting immune microenvironment regulation. This study focuses on evaluating the impact of TLR4 signaling activation on potential therapeutic strategies. Methods: Our research utilizes cannabidiol (CBD), a compound already employed in mitigating chemotherapy side effects in lung adenocarcinoma, recognized for its antitumor properties including antiproliferative, antimetastatic, and apoptosis-inducing effects. However, the effectiveness of CBD in lung cancer cells with elevated TLR4 signaling remains uncertain. Results: Our findings reveal that the combination of CBD and TLR4 agonist affects cell viability, proliferation, cell cycle progression, apoptosis, and gene expression related to immune response and extracellular matrix regulation. In lung adenocarcinoma cells with activated TLR4, CBD shows an increased IC ₅₀ value, reflecting reduced antiproliferative capacity. Furthermore, its efficacy in arresting the cell cycle and inducing apoptosis is also compromised. The influence on immune response and extracellular matrix regulation is also altered in TLR4-activated cells. Conclusions: These results indicate that TLR4 activation significantly diminishes the antitumor efficacy of CBD. This highlights the importance of considering TLR4 signaling activation in future research on therapeutic agents like CBD for cancer treatment.

Introduction: Toll-like receptor 4 (TLR4) is a receptor that traditionally plays an important role in immunomodulation (regulation of the immune system) and the initiation of proinflammatory responses. TLR4 is used in the body to recognize molecular patterns of pathogens or damaged cells from outside. However, in recent years, it has also become clear that TLR4 can affect the immune system and the function of stem cells, especially mesenchymal stem cells. Therefore, understanding how TLR4 signaling works at the cellular and molecular level and using this knowledge in regenerative medicine could be potentially useful, especially in the treatment of adipose- derived mesenchymal stem cells (ADMSCs). How these cells can use TLR4 signaling when used to increase their regenerative potential and repair tissues is an area of research. Aims: This study aims to elucidate the multifaceted role of TLR4-mediated signaling in ADMSCs. Methods: Employing a comprehensive set of assays, including MTT for cell viability, flow cytometry for surface marker expression, and gene expression analysis, we demonstrate that TLR4 activation significantly modulates key aspects of ADMSC biology. Specifically, TLR4 signaling was found to regulate ADMSCs proliferation, surface marker expression, and regenerative capacity in a dose- and time-dependent manner. Furthermore, TLR4 activation conferred cytoprotective effects against Doxorubicin (DOX)-induced cellular apoptosis. Results: These findings suggest that TLR4 signaling could be used to enhance the regenerative abilities of ADMSCs and enable ADMSC-based therapies to be used more effectively for tissue engineering and therapeutic purposes. Conclusion: However, it is important to note that research in this area needs more details and clinical studies.