驱动前列腺癌发病和转移的分子机制仍然知之甚少。肌动蛋白,在肌动蛋白结合蛋白(ABP)的控制下,在塑造细胞骨架中起着至关重要的作用,这反过来支持正常细胞的形态学改变,以及肿瘤细胞的侵袭性扩散。先前的研究表明,各种类型的ABPs具有不同的功能,他们活动的任何中断都可能使个体易患前列腺癌。这些ABP通过一系列复杂的细胞内过程与前列腺癌的发生和发展密切相关。比如切断,链接,成核,诱导分支,装配,促进肌动蛋白丝伸长,终止伸长,促进肌动蛋白分子聚集。因此,这篇综述综合了与前列腺癌相关的几种ABPs的现有文献,包括cofilin,丝素A,和Fascin,目的是阐明ABP影响前列腺癌发展的分子机制并确定潜在的治疗靶标。最终,这项全面的检查旨在帮助了解和管理前列腺疾病。
The molecular mechanisms driving the onset and metastasis of prostate cancer remain poorly understood. Actin, under the control of actin-binding proteins (ABPs), plays a crucial role in shaping the cellular cytoskeleton, which in turn supports the morphological alterations in normal cells, as well as the invasive spread of tumor cells. Previous research indicates that ABPs of various types serve distinct functions, and any disruptions in their activities could predispose individuals to prostate cancer. These ABPs are intricately implicated in the initiation and advancement of prostate cancer through a complex array of intracellular processes, such as severing, linking, nucleating, inducing branching, assembling, facilitating actin filament elongation, terminating elongation, and promoting actin molecule aggregation. As such, this review synthesizes existing literature on several ABPs linked to prostate cancer, including cofilin, filamin A, and fascin, with the aim of shedding light on the molecular mechanisms through which ABPs influence prostate cancer development and identifying potential therapeutic targets. Ultimately, this comprehensive examination seeks to contribute to the understanding and management of prostate diseases.