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Introduction: NF-κB plays a pivotal role in the progression of cancers, including myosarcomas such as fibrosarcoma. Plants possess considerable potential for the provision of chemotherapeutic effects against cancer. The present study assessed, among others, the cytotoxicity, migration capacity and DNA damage induced by several natural compounds (berberine, curcumin, biochanin A, cucurbitacin E (CurE) and phenethyl caffeic acid (CAPE)) in cancer cells (WEHI-164) and normal muscle cells (L6). Methods: IC50 parameter was determined for all substances after 24-hour incubation. Molecular docking studies were performed to assess compound binding to cytoskeletal proteins. Neutral comet assay and immunocytochemical analysis were used to assess the intensity of apoptosis, and transmission electron microscopy was employed to validate these results at the ultrastructural level. Results and Discussion: The results showed that the tested compounds had a significantly increased cytotoxic effect on cancer cells compared to normal cells. Furthermore, molecular docking studies indicated that CAPE, biochanin A, and CurE could inhibit actin polymerization, suggesting their potential role in disrupting the cytoskeleton of cancer cells. Increased expression of caspase-3 and PARP-1 in WEHI-164 cells after treatment indicated the induction of apoptosis. Transmission electron microscopy confirmed the presence of cellular stress and vacuolation in cells treated with these compounds, with more pronounced effects observed in cancer cells compared to normal cells. The results indicate that natural NF-κB inhibitors may be capable of selectively targeting cancer cells, reducing their viability and inducing apoptosis while sparing normal cells. This selectivity is of great importance for the development of safer anticancer therapies. The results of this research support the hypothesis that these natural compounds may be effective anticancer agents, particularly in the treatment of fibrosarcoma. Further, in vivo studies and clinical trials are required to gain a full understanding of their mechanisms of action and potential synergies with existing chemotherapeutic agents. [ABSTRACT FROM AUTHOR]

Xenoestrogens (XEs) are a group of exogenous substances that may interfere with the functioning of the endocrine system. They may mimic the function of estrogens, and their sources are plants, water or dust, plastic, chemical agents, and some drugs. Thus, people are highly exposed to their actions. Together with the development of industry, the number of XEs in our environment increases. They interact directly with estrogen receptors, disrupting the transmission of cellular signals. It is proven that XEs exhibit clinical application in e.g., menopause hormone therapy, but some studies observed that intense exposure to XEs leads to the progression of various cancers. Moreover, these substances exhibit the ability to cross the placental barrier, therefore, prenatal exposure may disturb fetus development. Due to the wide range of effects resulting from the biological activity of these substances, there is a need for this knowledge to be systematized. This review aims to comprehensively assess the environmental sources of XEs and their role in increasing cancer risk, focusing on current evidence of their biological and pathological impacts. [ABSTRACT FROM AUTHOR]

Colon cancer (CC) management includes surgery, radio- and chemotherapy based on treatment with 5-fluorouracil (5-FU) or its derivatives. However, its application is limited to low-grade carcinomas. Thus, much research has been conducted to introduce new techniques and drugs to the therapy. CC mostly affects older people suffering from cardiac diseases, where iron compounds are commonly used. Ferric citrate and iron (III)–EDTA complexes have proven to be effective in colon cancer in vitro. This study aimed to determine the potency and action of iron-containing compounds in colon cancer treatment by chemo- and electrochemotherapy in both nano- and microsecond protocols. The viability of the cells was assessed after standalone iron (III) citrate and iron (III)–EDTA incubation. Both compounds were also assessed with 5-FU to determine the combination index. Additionally, frataxin expression was taken as the quantitative response to the exposition of iron compounds. Each of the substances exhibited a cytotoxic effect on the LoVo cell line. Electroporation with standalone drugs revealed the potency of 5-FU and iron(III)–EDTA in CC treatment. The combination of 5-FU with iron(III)–EDTA acted synergistically, increasing the viability of the cells in the nanosecond electrochemotherapy protocol. Iron(III)–EDTA decreased the frataxin expression, thus inducing ferroptosis. Iron(III) citrate induced the progression of cancer; therefore, it should not be considered as a potential therapeutic option. The relatively low stability of iron(III) citrate leads to the delivery of citrate anions to cancer cells, which could increase the Krebs cycle rate and promote progression. [ABSTRACT FROM AUTHOR]

Ketoprofen belongs to a group of widely used non-steroidal anti-inflammatory drugs (NSAIDs). It is found in several doses and various forms of medications. Therapeutic efficacy is related to the rate of release of the active substances, which depends on the formulation, the quality of the constituent substances, and solubility. In order to determine the efficacy of drug products containing ketoprofen available on the pharmaceutical market in Poland, studies comparing the release profiles of the active substance contained in specific formulations and doses, Ketokaps MAX, 50 mg, soft capsules, Ketonal Active, 50 mg, hard capsules, Ketokaps MED, 100 mg, soft capsules, Refastin, 100 mg, film-coated tablets and Ketonal Forte, 100 mg, film-coated tablets have been conducted. Drug release has been tested using FaSSGF and FaSSIF bioequivalent media in a type IV flow apparatus. The results indicate that the product Ketokaps MAX, 50 mg has a shorter release time of ketoprofen and a faster reached maximum concentration of the released active substance than the market product Ketonal Active, 50 mg. The same outcomes will be achieved by the product Ketokaps MED, 100 mg compared to the market products Refastin, 100 mg, and Ketonal Forte, 100 mg. In vitro studies confirm that the tested products differ noticeably in the kinetics of release of the active substance. Ketokaps MAX, 50 mg and Ketokaps MED, 100 mg achieve c max in a shorter time. [ABSTRACT FROM AUTHOR]