Cancer is the second leading cause of death in the world, and chemotherapy is one of the main methods of cancer treatment. However, the resistance of cancer cells to chemotherapeutic drugs has always been the main reason affecting the therapeutic effect. Synthetic lethality has emerged as a promising approach to augment the sensitivity of cancer cells to chemotherapy agents. Synthetic lethality (SL) refers to the specific cell death resulting from the simultaneous mutation of two non-lethal genes, which individually allow cell survival. This comprehensive review explores the classification of SL, screening methods, and research advancements in SL inhibitors, including Poly (ADP-ribose) polymerase (PARP) inhibitors, Ataxia telangiectasia and Rad3-related (ATR) inhibitors, WEE1 G2 checkpoint kinase (WEE1) inhibitors, and protein arginine methyltransferase 5 (PRMT5) inhibitors. Emphasizing their combined use with chemotherapy drugs, we aim to unveil more effective treatment strategies for cancer patients.

Dysregulated expression of specific non-coding RNAs (ncRNAs) has been strongly linked to tumorigenesis, cancer progression, and therapeutic resistance. These ncRNAs can act as either oncogenes or tumor suppressors, thereby serving as valuable diagnostic and prognostic markers. Numerous studies have implicated the participation of ncRNAs in the regulation of diverse signaling pathways, including the pivotal Wnt/β-catenin signaling pathway that is widely acknowledged for its pivotal role in embryogenesis, cellular proliferation, and tumor biology control. Recent emerging evidence has shed light on the capacity of ncRNAs to interact with key components of the Wnt/β-catenin signaling pathway, thereby modulating the expression of Wnt target genes in cancer cells. Notably, the activity of this pathway can reciprocally influence the expression levels of ncRNAs. However, comprehensive analysis investigating the specific ncRNAs associated with the Wnt/β-catenin signaling pathway and their intricate interactions in cancer remains elusive. Based on these noteworthy findings, this review aims to unravel the intricate associations between ncRNAs and the Wnt/β-catenin signaling pathway during cancer initiation, progression, and their potential implications for therapeutic interventions. Additionally, we provide a comprehensive overview of the characteristics of ncRNAs and the Wnt/β-catenin signaling pathway, accompanied by a thorough discussion of their functional roles in tumor biology. Targeting ncRNAs and molecules associated with the Wnt/β-catenin signaling pathway may emerge as a promising and effective therapeutic strategy in future cancer treatments.

Autophagy, a complex and highly regulated cellular process, is critical for the maintenance of cellular homeostasis by lysosomal degradation of cellular debris, intracellular pathogens, and dysfunctional organelles. It has become an interesting and attractive topic in cancer because of its dual role as a tumor suppressor and cell survival mechanism. As a highly conserved pathway, autophagy is strictly regulated by diverse non-coding RNAs (ncRNAs), ranging from short and flexible miRNAs to lncRNAs and even circRNAs, which largely contribute to autophagy regulatory networks via complex RNA interactions. The potential roles of RNA interactions during autophagy, especially in cancer procession and further anticancer treatment, will aid our understanding of related RNAs in autophagy in tumorigenesis and cancer treatment. Herein, we mainly summarized autophagy-related mRNAs and ncRNAs, also providing RNA–RNA interactions and their potential roles in cancer prognosis, which may deepen our understanding of the relationships between various RNAs during autophagy and provide new insights into autophagy-related therapeutic strategies in personalized medicine.

Background: The cell cycle, a critical and intricate biological process, comprises various phases, and its dysregulation plays a pivotal role in tumorigenesis and metastasis. The exploration of cell cycle-based molecular subtypes across pan-cancers, along with the application of synthetic lethality concepts, holds promise for advancing cancer therapies. Methods: A pan-cancer analysis was conducted to assess the cell cycle serves as a reliable signature for classifying molecular subtypes and to understand the potential clinical application of genes as potential drug targets based on synthetic lethality. Results: Molecular subtypes derived from cell cycle features in certain cancers, particularly kidney-related malignancies, exhibited distinct immune characteristics. Synthetic lethal interactions within the cell cycle pathway were common, with significant genetic interactions further identifying potential drug targets through the exploitation of genetic relationships with key driver genes. Additionally, miRNAs and lncRNAs may influence the cell cycle through miRNA:mRNA interactions and ceRNA networks, thereby enriching the genetic interaction landscape. Conclusions: These findings suggest that the cell cycle pathway could serve as a promising molecular subtype signature to enhance cancer prognostication and offer potential targets for anticancer drug development through synthetic lethality.