Metal nanoparticles play an outstanding role in the field of wound healing due to their excellent properties, and the significance of iron, one of the most widely used metals globally, cannot be overlooked. The purpose of this review is to determine the importance of iron nanoparticles in wound-healing dressings. Prolonged, poorly healing wounds may induce infections; wound infections are a major cause of chronic wound formation. The primary components of iron nanoparticles are iron oxide nanoparticles, which promote wound healing by being antibacterial, releasing metal ions, and overcoming bacterial resistance. The diameter of iron oxide nanoparticles typically ranges between 1 and 100 nm. Magnetic nanoparticles with a diameter of less than 30 nm are superparamagnetic and are referred to as superparamagnetic iron oxide nanoparticles. This subset of iron oxide nanoparticles can use an external magnetic field for novel functions such as magnetization and functionalization. Iron nanoparticles can serve clinical purposes not only to enhance wound healing through the aforementioned means but also to ameliorate anemia and glucose irregularities, capitalizing on iron’s properties. Iron nanoparticles positively impact the healing process of chronic wounds, potentially extending beyond wound management.

Integrins are heterodimers composed of non-covalently associated alpha and beta subunits that mediate the dynamic linkage between extracellular adhesion molecules and the intracellular actin cytoskeleton. Integrins are present in various tissues and organs and are involved in different physiological and pathological molecular responses in vivo. Wound healing is an important process in the recovery from traumatic diseases and consists of three overlapping phases: inflammation, proliferation, and remodeling. Integrin regulation acts throughout the wound healing process to promote wound healing. Prolonged inflammation may lead to failure of wound healing, such as wound chronicity. One of the main causes of chronic wound formation is bacterial colonization of the wound. In this review, we review the role of integrins in the regulation of wound healing processes such as angiogenesis and re-epithelialization, as well as the role of integrins in mediating bacterial infections during wound chronicity, and the challenges and prospects of integrins as therapeutic targets for infected wound healing.

Gastric cancer ranks as one of the most prevalent cancers worldwide. While the incidence of gastric cancer in Western countries has notably diminished over the past century, it continues to be a leading cause of cancer‑related mortality on a global scale. The majority of gastric cancers in humans are attributed to chronic Helicobacter pylori infection and the progression of gastric cancer is often preceded by gastritis, atrophy, metaplasia and dysplasia. However, the precise mechanisms underlying the development of gastric cancer remain ambiguous, including the formation of gastric polyps and precancerous lesions. In humans, two types of precancerous metaplasia have been identified in relation to gastric malignancies: Intestinal metaplasia and spasmolytic polypeptide‑expressing metaplasia (SPEM). The role of SPEM in the induction of gastric cancer has gained recent attention and its link with early‑stage human gastric cancer is increasingly evident. To gain insight into SPEM, the present study reviewed the role and research progress of SPEM in gastric cancer.

As a newly discovered cancer-related molecule, we explored the unreported mechanism of LINC01615 intervention in colon cancer. LINC01615 expression in clinical samples and cells were detected. Effects of LINC01615 silencing/overexpression on the malignant development of colon cancer cells were analyzed through cell function experiments. Changes at the level of molecular biology were detected by quantitative real-time polymerase chain reaction and Western blot. Bioinformatics analysis and dual luciferase reporter assay were involved in the display and verification of targeted binding sequences. The rescue tests and correlation analysis examined the relationship among LINC01615, miR-3653-3p and zinc finger E-box binding homeobox 2 (ZEB2) in colon cancer cells. The xenograft experiment and immunohistochemistry were performed to verify these results. TCGA suggested that LINC01615 was high-expressed in colon cancer, as verified in clinical and cell samples, and patients with LINC01615 overexpression suffered from a poor prognosis. Silent LINC01615 blocked the malignant development of colon cancer cells through regulating related genes expressions, while overexpressed LINC01615 had the opposite effect. LINC01615, which was targeted by miR-3653-3p, partially offset the inhibitory effect of miR-3653-3p on colon cancer cells. The downstream target gene ZEB2 of miR-3653-3p was high-expressed in colon cancer. MiR-3653-3p was negatively correlated with LINC01615 or ZEB2, while LINC01615 was positively correlated with ZEB2. Therefore, LINC01615 induced ZEB2 up-regulation, while miR-3653-3p reduced ZEB2 level. The results of in vivo studies were consistent with cell experiments. LINC01615 competitively binds with miR-3653-3p to regulate ZEB2 and promote canceration of colon cancer cells.