CXCL3: A key player in tumor microenvironment and inflammatory diseases.

CXCL3 (C-X-C Motif Chemokine 3), a member of the C-X-C chemokine subfamily, operates as a potent chemoattractant for neutrophils, thereby orchestrating the recruitment and migration of leukocytes alongside eliciting an inflammatory response. Recent inquiries have shed light on the pivotal roles of CXCL3 in the context of carcinogenesis. In the tumor microenvironment, CXCL3 emanating from both tumor and stromal cells intricately modulates cellular behaviors through autocrine and paracrine actions, primarily via interaction with its receptor CXCR2. Activation of signaling cascades such as ERK/MAPK, AKT, and JAK2/STAT3 underscores CXCL3's propensity to favor tumorigenic processes. However, CXCL3 exhibits dualistic behaviors, as evidenced by its capacity to exert anti-tumor effects under specific conditions. Additionally, the involvement of CXCL3 extends to inflammatory disorders like eclampsia, obesity, and asthma. This review encapsulates the structural attributes, biological functionalities, and molecular underpinnings of CXCL3 across both tumorigenesis and inflammatory diseases.

Insights into the complex interactions between Rab22a and extracellular vesicles in cancers.

INTRODUCTION: Oncogenic Ras-related GTP-binding proteins, referred to as Rabs, are characterized by their intricate interactions with upstream, downstream molecules, and notably, extracellular vesicles (EVs). While the expansive family of Rabs and their associated signaling pathways have been exhaustively dissected, Rab22a emerges as an entity of outstanding interest, owing to its potent influence in many biological processes and its conspicuous correlation with cancer metastasis and migration. A burgeoning interest in the interactions between Rab22a and EVs in the field of oncology underscores the necessity for more in-depth reviews and scholarly discourses. METHODS: We performed a review based on published original and review articles related to Rab22a, tumor, microRNA, exosome, microvesicles, EVs, CD147, lysosome, degradation, endosomal recycling, etc. from PubMed, Web of Science and Google Scholar databases. RESULTS AND CONCLUSIONS: We summarize the regulatory processes governing the expression of Rab22a and the mutants of Rab22a. Notably, the present understanding of complex interactions between Rab22a and EVs are highlighted, encompassing both the impact of Rab22a on the genesis of EVs and the role of EVs that are affected by Rab22a mutants in propelling tumor advancement. The dynamic interaction between Rab22a and EVs plays a significant role in the progression of tumors, and it can provide novel insights into the pathogenesis of cancers and the development of new therapeutic targets.

Research progress on the premature ovarian failure caused by cisplatin therapy.

Cisplatin is a common anticancer drug able to kill tumor cells, but it causes adverse reactions in the kidney, digestive tract, and other systems. The antitumor effects of cisplatin are mainly due to its ability to bind to the DNA in tumor cells to prevent replication, thereby reducing RNA and protein syntheses, leading to cell damage and death. Cisplatin has a wide range of applications; it can be used to treat cervical, thyroid, ovarian, and other cancers. Cisplatin has a beneficial therapeutic effect, but its therapeutic selectivity is poor. In addition to eliminating diseased target cells, cisplatin can damage normal cells; in women of reproductive age being treated for cancer, cisplatin can lead to ovarian function impairment, premature ovarian failure (POF), and/or infertility. Therefore, reducing the adverse effects of cisplatin on ovarian function is an important topic in clinical research. In this paper, we explore the research progress on the POF caused by cisplatin treatment.

Crucial roles of Rab22a in endosomal cargo recycling.

Endosomal cargo recycling lies at the heart of subcellular trafficking processes under the management of several Ras-related GTP-binding proteins (Rabs) which are coordinated by their upstream regulators and require their downstream effectors to display their functions. In this regard, several Rabs have been well-reviewed except Rab22a. Rab22a is a crucial regulator of vesicle trafficking, early endosome and recycling endosome formation. Notably, recent studies demonstrated the immunological roles of Rab22a, which are closely associated with cancers, infection and autoimmune disorders. This review provides an overview of the regulators and effectors of Rab22a. Also, we highlight the current knowledge of the role of Rab22a in endosomal cargo recycling, including the biogenesis of recycling tubules with the help of a complex with Rab22a at its core, and how different internalized cargo chooses different recycling routes thanks to the cooperation of Rab22a, its effectors and its regulators. Of note, contradictions and speculation related to endosomal cargo recycling that Rab22a brings impacts on are also discussed. Finally, this review endeavors to briefly introduce the various events impacted by Rab22a, particularly focusing on the commandeered Rab22a-associated endosomal maturation and endosomal cargo recycling, in addition to the extensively investigated oncogenic role of Rab22a.

FGF4 Promotes Skin Wound Repair through p38 MAPK and GSK3ß-Mediated Stabilization of Slug.

Cutaneous wound healing is an orderly and intricate process that restores the barrier function and integrity of injured skin. Re-epithelialization, which involves the proliferation and migration of keratinocytes to cover the denuded surface, is essential for successful wound closure. There are many members of the FGF family, of which the paracrine-acting FGF1 and FGF7 subfamily members have been identified as positive regulators of wound repair. However, the role and underlying mechanisms of some other paracrine FGFs in wound repair still remain obscure. In this report, we found that paracrine FGF4 localized predominantly to the epidermal keratinocytes and was markedly upregulated at the wound edges in response to re-epithelialization in human and mouse wound models. Blockade of FGF4 resulted in delayed re-epithelialization of human ex vivo skin wounds, whereas recombinant FGF4 treatment promoted re-epithelialization and wound repair. Mechanistically, recombinant FGF4 promotes p38 MAPK‒GSK3ß‒mediated stabilization of Slug by reducing its ubiquitination, which triggers epithelial-to-mesenchymal transition and promotes the migration and proliferation of keratinocytes and thus wound re-epithelialization. Our findings uncover FGF4 as an important regulator of wound healing, highlighting a promising therapeutic avenue for skin injury.