Researchers are amazed at the multitude of biological effects of 3′,4′,5,7-tetrahydroxyflavone, more commonly known as luteolin, as it simultaneously has antioxidant and pro-oxidant, as well as antimicrobial, anti-inflammatory, and cancer-preventive, properties. The anticancer properties of luteolin constitute a mosaic of pathways due to which this flavonoid influences cancer cells. Not only is it able to induce apoptosis and inhibit cancer cell proliferation, but it also suppresses angiogenesis and metastasis. Moreover, luteolin succeeds in cancer cell sensitization to therapeutically induced cytotoxicity. Nevertheless, apart from its promising role in chemoprevention, luteolin exhibits numerous potential utilizations in patients with conditions other than neoplasms, which include inflammatory skin diseases, diabetes mellitus, and COVID-19. This review aims to present the multidimensionality of the luteolin’s impact on both neoplastic and nonneoplastic diseases. When it comes to neoplasms, we intend to describe the complexity of the molecular mechanisms that underlay luteolin’s anticancer effectiveness, as well as to prove the usefulness of integrating this flavonoid in cancer therapy via the analysis of recent research on breast, colon, and lung cancer. Regarding nonneoplastic diseases, this review aims to emphasize the importance of researching the potential of luteolin in areas such as diabetology, virology, and dermatology as it summarizes the most important discoveries in those fields regarding its application.

Heat shock proteins (Hsps) are involved in one of the adaptive mechanisms protecting cells against environmental and metabolic stress. Moreover, the large role of these proteins in the carcinogenesis process, as well as in chemoresistance, was noticed. This review aims to draw attention to the possibilities of using Hsps in developing new cancer therapy methods, as well as to indicate directions for future research on this topic. In order to discuss this matter, a thorough review of the latest scientific literature was carried out, taking into account the importance of selected proteins from the Hsp family, including Hsp27, Hsp40, Hsp60, Hsp70, Hsp90 and Hsp110. One of the more characteristic features of all Hsps is that they play a multifaceted role in cancer progression, which makes them an obvious target for modern anticancer therapy. Some researchers emphasize the importance of directly inhibiting the action of these proteins. In turn, others point to their possible use in the design of cancer vaccines, which would work by inducing an immune response in various types of cancer. Due to these possibilities, it is believed that the use of Hsps may contribute to the progress of oncoimmunology, and thus help in the development of modern anticancer therapies, which would be characterized by higher effectiveness and lower toxicity to the patients.

Interleukin-5 functions as a B-cell differentiation factor, but more importantly, in the context of this review, it plays a variety of roles in eosinophil biology, including eosinophil differentiation and maturation in the bone marrow, and facilitates eosinophil migration to tissue sites, usually in the context of an allergic reaction. Given the availability of selective anti-IL-5 drugs such as mepolizumab and reslizumab, as well as the IL-5 receptor antagonist benralizumab, it is worth investigating whether they could be used in some cases of allergic disease. Asthma has a well-documented involvement of IL-5 in its pathophysiology and has clear benefits in the case of anti-IL-5 therapy; therefore, current knowledge is presented to provide a reference point for the study of less-described diseases such as atopic dermatitis, chronic rhinosinusitis, chronic spontaneous urticaria, and its association with both IL-5 and anti-IL-5 treatment options. We then review the current literature on these diseases, explain where appropriate potential reasons why anti-IL-5 treatments are ineffective, and then point out possible future directions for further research.

Exosomes and microvesicles bear great potential to broaden therapeutic options in the clinical context. They differ in genesis, size, cargo, and composition despite their similarities. They were identified as participating in various processes such as angiogenesis, cell migration, and intracellular communication. Additionally, they are characterized by their natural biocompatibility. Therefore, researchers concluded that they could serve as a novel curative method capable of achieving unprecedented results. Indeed, in experiments, they proved remarkably efficient in enhancing wound regeneration and mitigating inflammation. Despite immense advancements in research on exosomes and microvesicles, the time for their large-scale application is yet to come. This article aims to gather and analyze current knowledge on those promising particles, their characteristics, and their potential clinical implementations.

Asthma is a complex chronic respiratory disease characterized by airway hyperresponsiveness, inflammation, and obstruction. Many genes have been identified as associated with asthma but none with such substantial significance as the ADAM33 gene due to its role in airway remodeling and bronchial hyperresponsiveness. This review summarizes the current knowledge on the genetic and functional aspects of ADAM33 in asthma pathogenesis. We highlight its genetic variants associated with asthma susceptibility and severity, as well as the functional effects of ADAM33 on airway remodeling, smooth muscle cell proliferation, and its interplay with environmental factors. Additionally, we discuss the potential clinical implications of ADAM33 as a therapeutic target for asthma management.

Several molecular pathways are likely involved in the regulation of cancer stem cells (CSCs) via Ras-associated C3 botulinum toxin substrate 2, RAC2, and pituitary tumor-transforming gene 1 product, PTTG1, given their roles in cellular signaling, survival, proliferation, and metastasis. RAC2 is a member of the Rho GTPase family and plays a crucial role in actin cytoskeleton dynamics, reactive oxygen species production, and cell migration, contributing to epithelial–mesenchymal transition (EMT), immune evasion, and therapy resistance. PTTG1, also known as human securin, regulates key processes such as cell cycle progression, apoptosis suppression, and EMT, promoting metastasis and enhancing cancer cell survival. This article aims to describe the molecular pathways involved in the proliferation, invasiveness, and drug response of cancer cells through RAC2 and PTTG1, aiming to clarify their respective roles in neoplastic process dependencies. Both proteins are involved in critical signaling pathways, including PI3K/AKT, TGF-β, and NF-κB, which facilitate tumor progression by modulating CSC properties, angiogenesis, and immune response. This review highlights the molecular mechanisms by which RAC2 and PTTG1 influence tumorigenesis and describes their potential and efficacy as prognostic biomarkers and therapeutic targets in managing various neoplasms.