Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer

• Published in: Cancer cell international Vol. 24; no. 1; p. 104
• Main Authors: Karamali, Negin, Daraei, Arshia, Rostamlou, Arman, Mahdavi, Roya, Akbari Jonoush, Zahra, Ghadiri, Nooshin, Mahmoudi, Zahra, Mardi, Amirhossein, Javidan, Moslem, Sohrabi, Sepideh, Baradaran, Behzad
• Format: Journal Article
• Language: English
• Published: England BioMed Central 11-03-2024; BMC
• Subjects: Apoptosis; Breast cancer; Cell cycle; Cell death; Cell fate; Cell growth; Cell survival; Endoplasmic reticulum; ER stress; Gene expression; Homeostasis; Kinases; Medical prognosis; Metabolism; Metastasis; MicroRNAs; miRNA; Motility; Non-coding RNA; Non-coding RNAs; Pathogenesis; Protein folding; Protein synthesis; Proteins; Review; Therapy; Tumors; UPR; ER stress; Non-coding RNAs; Therapy; Breast cancer; UPR
• ISSN: 1475-2867; 1475-2867
• DOI: 10.1186/s12935-024-03296-3

Breast cancer is significantly influenced by endoplasmic reticulum (ER) stress, impacting both its initiation and progression. When cells experience an accumulation of misfolded or unfolded proteins, they activate the unfolded protein response (UPR) to restore cellular balance. In breast cancer, the UPR is frequently triggered due to challenging conditions within tumors. The UPR has a dual impact on breast cancer. On one hand, it can contribute to tumor growth by enhancing cell survival and resistance to programmed cell death in unfavorable environments. On the other hand, prolonged and severe ER stress can trigger cell death mechanisms, limiting tumor progression. Furthermore, ER stress has been linked to the regulation of non-coding RNAs (ncRNAs) in breast cancer cells. These ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play essential roles in cancer development by influencing gene expression and cellular processes. An improved understanding of how ER stress and ncRNAs interact in breast cancer can potentially lead to new treatment approaches. Modifying specific ncRNAs involved in the ER stress response might interfere with cancer cell survival and induce cell death. Additionally, focusing on UPR-associated proteins that interact with ncRNAs could offer novel therapeutic possibilities. Therefore, this review provides a concise overview of the interconnection between ER stress and ncRNAs in breast cancer, elucidating the nuanced effects of the UPR on cell fate and emphasizing the regulatory roles of ncRNAs in breast cancer progression.