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Prostate cancer (PCa) represents the second most diagnosed tumor and the fifth most common cause of cancer death in men globally [1]. This disease ranges from indolent to aggressive tumors that may rapidly progress and metastasize to castration-resistant PCa (CRPC). Age, ethnicity, family history, and genetic defects are major factors that determine the aggressiveness and lethality of PCa [2]. This disease involves the aberrant activation and dysregulation of specific cellular pathways that contribute to its initiation, progression, and therapeutic resistance. Key molecular pathways implicated in prostate cancer include the androgen receptor (AR) pathway, the PI3K/Akt pathway, the MAPK pathway, the Wnt/β-catenin pathway, and the PTEN pathway [3,4]. These pathways regulate cell proliferation, apoptosis, migration, and invasion, among other critical cellular processes. Understanding the molecular basis of prostate cancer enables the development of targeted therapies that disrupt these pathways and effectively diminish tumor growth and progression [5].

Recent discoveries indicate that the complex crosstalk between the PI3K-AKT-mTOR pathway and multiple interacting cell signaling cascades can further promote prostate cancer progression. The PI3K-AKT-mTOR cascade interacts with multiple cooperative signal transduction cascades via a series of partially understood interactions and feedback loops to promote tumor growth (including MAPK, AR and WNT signaling). Hence, establishing the scope of this complex signaling program is fundamental for the identification of new and effective biomarkers and therapeutic approaches that will benefit patients with prostate cancer [6].

Bone metastasis in PCa is a highly frequent event that occurs in up to 90% of patients with advanced disease [7]. The bone microenvironment is a dynamic compartment that provides a milieu in which metastatic cancer cells can colonize and grow [8]. The "vicious cycle" hypothesis is an appropriate model with which to explain the process of cancer cells metastasizing to the bone [9]. Tumor cells in bone induce osteoclast-mediated bone resorption, while osteoclasts release bone-stored factors that stimulate tumor cell proliferation, establishing a vicious cycle [10]. Thus, various approaches that target the bone microenvironment, such as bone-targeting agents, are effective for managing bone metastases in PCa.

DNA damage in cells, including single-strand breaks (SSB) and double-strand breaks (DSB), can be induced by exposure to chemicals (such as chemotherapy), physical agents (such as radiotherapy), or endogenous reactive metabolites (such as reactive oxygen and nitrogen species). Effective DNA repair is essential for cellular survival. PARP is a family of enzymes involved in DNA repair and transcriptional regulation [11]. Activation of PARP1/2 is important for recruiting the key effectors of DNA repair [12]. Inhibition of PARP mediates synthetic lethality in PCa [2].

Tumors with defects in MMR genes or microsatellite instability (MSI) often have an enhanced antitumor immune response, displaying a higher density of tumor-infiltrating lymphocytes (TILs) [13]. Mutation of MMR genes in PCa is highly associated with increased expression of neoantigens and accumulation of TILs [14].

In addition to genomic changes, epigenetic alterations (such as histone modifications and DNA methylation) have been reported to be associated with PCa progression [15]. Aberrant histone modifications may upregulate oncogenes or reduce the expression of tumor suppressor genes. Importantly, histone methylation/acetylation and DNA methylation play a central role in controlling gene expression, thus promoting the progression and metastasis of PCa [16].

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Freya Freya is a technical support expert of enkilife, familiar with immunology and cell biology, and is committed to providing customers with high-quality product portfolio and technical support to help customers efficiently complete research.

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