Cancer quiescence: non-coding RNAs in the spotlight

Cancer quiescence is defined as a dynamic and reversible slow-cycling or mitotically arrested cell state, serving as the hallmark of cancer dormancy.Cancer quiescence is a self-protecting mechanism that prevents tumor cell acute damage from therapy and microenvironment stress, allowing long-term survival, immune escape, and cancer progression and metastasis.p38/ERK, PI3K/AKT, and transforming growth factor beta (TGF-β) represent the main regulatory pathways of cancer quiescence through cyclin, cyclin dependent kinase (CDKs), and cyclin dependent kinase inhibitor (CDKI) manipulation.Non-coding RNAs (ncRNAs) have a profound impact on quiescence versus proliferation equilibrium, through targeting dormancy-associated modulators.ncRNAs hold a potential dynamic role in future cancer therapeutics, supporting personalized treatment decisions and modern precision medicine. Cancer quiescence reflects the ability of cancer cells to enter a reversible slow-cycling or mitotically dormant state and represents a powerful self-protecting mechanism preventing cancer cell ‘damage’ from hypoxic conditions, nutrient deprivation, immune surveillance, and (chemo)therapy. When stress conditions are restrained, and tumor microenvironment becomes beneficial, quiescent cancer cells re-enter cell cycle to facilitate tumor spread and cancer progression/metastasis. Recent studies have highlighted the dynamic role of regulatory non-coding RNAs (ncRNAs) in orchestrating cancer quiescence. The elucidation of regulatory ncRNA networks will shed light on the quiescence-proliferation equilibrium and, ultimately, pave the way for new treatment options. Herein, we have summarized the ever-growing role of ncRNAs upon cancer quiescence regulation and their impact on treatment resistance and modern cancer therapeutics. Cancer quiescence reflects the ability of cancer cells to enter a reversible slow-cycling or mitotically dormant state and represents a powerful self-protecting mechanism preventing cancer cell ‘damage’ from hypoxic conditions, nutrient deprivation, immune surveillance, and (chemo)therapy. When stress conditions are restrained, and tumor microenvironment becomes beneficial, quiescent cancer cells re-enter cell cycle to facilitate tumor spread and cancer progression/metastasis. Recent studies have highlighted the dynamic role of regulatory non-coding RNAs (ncRNAs) in orchestrating cancer quiescence. The elucidation of regulatory ncRNA networks will shed light on the quiescence-prol