The following is a summary of “Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer,” published in the March 2024 issue of Oncology by Karamali et al.
Breast cancer is profoundly influenced by endoplasmic reticulum (ER) stress, a pivotal factor impacting its initiation and progression. In response to the accumulation of misfolded or unfolded proteins, cells activate the unfolded protein response (UPR) to restore cellular equilibrium. Within the breast cancer milieu, the UPR is frequently instigated due to the challenging conditions prevailing within tumors. This response wields a dual impact on breast cancer dynamics: on one hand, it can bolster tumor growth by augmenting cell survival and fortifying resistance to programmed cell death in hostile microenvironments; conversely, prolonged and severe ER stress can incite cell death mechanisms, curtailing tumor advancement. Moreover, ER stress has been intricately linked to the regulatory mechanisms governing non-coding RNAs (ncRNAs) in breast cancer cells.
These ncRNAs, encompassing microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) emerge as key orchestrators in cancer development, modulating gene expression, and cellular processes. Enhanced comprehension of the interplay between ER stress and ncRNAs in breast cancer bears the potential to catalyze novel treatment paradigms. Targeting specific ncRNAs implicated in the ER stress response could perturb cancer cell survival and elicit programmed cell death. Additionally, directing attention towards UPR-associated proteins that interact with ncRNAs unveils promising therapeutic avenues. Thus, this review offers a succinct yet comprehensive exploration of the intricate interconnection between ER stress and ncRNAs in breast cancer, elucidating the nuanced effects of the UPR on cell fate while accentuating the pivotal regulatory roles played by ncRNAs in the progression of breast cancer.
Source: cancerci.biomedcentral.com/articles/10.1186/s12935-024-03296-3