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Immune response regulates implanted biomaterial−tissue integration and tissue regeneration, in which macrophages play a key role due to their plasticity and polarization. Chirality, an inherent property of carbon‐based life, can also exist in biomaterials such as gold monolayer. Constructing chiral nanostructured surfaces of implants can imitate the chirality of extracellular environment in a biomimetic manner, but the manipulation and mechanism of chiral nanotopography on macrophages remain poorly understood. Here, highly ordered gold nanoparticle arrays with 300 or 900 nm spacing are fabricated and modified with L‐ or D‐chirality. The D‐nanoarrays can promote M2 polarization and related cytokine secretion of macrophages, thus facilitating the reduction of inflammatory reaction and promoting tissue healing and regeneration. The mechanistic analysis further suggests that D‐nanoarrays proceeded these regulations through enhancing the expression of integrin αv/α8/β3‐p‐FAK pathway in macrophages, which may be largely attributed to its higher stereo‐affinity for fibronectin as revealed by quantitative experiments and molecular dynamics simulations. Overall, this study demonstrates that biomimetic chiral nanotopography can promote biomaterial−tissue integration by manipulating macrophage phenotype, bringing a novel strategy for immunomodulation. [ABSTRACT FROM AUTHOR]

Endometrial cancer (EC), a widely occurring cancer in the uterus, is among the top four most frequent malignancies in women. To improve approaches for combating this disease, it is essential to gain a more comprehensive comprehension of the intricate causes of EC. Accumulating evidence highlight the essential role of long non‐coding RNA (LncRNA) in EC progression, while its biological and mechanical function has not been fully revealed. In this study, a LncRNA microarray analysis was performed using four pairs of paclitaxel (PTX) resistant EC cells, FGD5‐AS1 was identified as a significantly upregulated gene. Biologically, it was found that FGD5‐AS1 enhances chemoresistance of EC cells to PTX treatment and blocking immune escape via PD‐1/PD‐L1 checkpoint. Furthermore, FGD5‐AS1 exerted an oncogene role in EC cells via promoting cell proliferation and migration. Mechanically, METTL3 could upregulate FGD5‐AS1 expression via N6‐methyladenosine (m6A) modification. The biological roles of METTL3 were exerted via modulating FGD5‐AS1 expression in EC. Collectively, our research has shed light on the involvement of the METTL3/FGD5‐AS1 axis in the development of PTX resistance in EC. This finding offers a new avenue for further exploration of the underlying mechanisms of chemoresistance in EC and provides valuable insights for the development of potential therapeutic targets in the treatment of EC. [ABSTRACT FROM AUTHOR]