Nolc1, short for Nucleolar and coiled-body phosphoprotein 1, is a nucleolar protein. It is responsible for nucleolus construction and rRNA synthesis, and also functions in chaperone shuttling between the nucleolus and cytoplasm. Nolc1 is involved in multiple cellular life activities such as ribosome biosynthesis, DNA replication, transcription regulation, RNA processing, cell cycle regulation, apoptosis, and cell regeneration [1].

Knockdown of Nolc1 suppresses prostate cancer cell proliferation by inhibiting AKT phosphorylation and β-catenin accumulation, suggesting its potential as a therapeutic target for prostate cancer [2]. Pten-Nolc1 fusion promotes cancers involving MET and EGFR signalings, indicating that this fusion gene is a driver for human cancers [3]. In epithelial ovarian cancer, circ-Nolc1 promotes tumorigenesis and progression by binding ESRP1 and modulating CDK1 and RhoA expression [4]. In endometrial cancer, Nolc1 is highly expressed in paclitaxel-resistant cells, and the SPOP/Nolc1/B4GALT1 signaling axis enhances paclitaxel resistance by inducing O-dysglycosylation [5]. In colorectal cancer, high expression of Nolc1 is an independent prognostic factor, and it enhances cell proliferation and migration [6]. In esophageal carcinoma, Nolc1 overexpression is associated with poor prognosis, and knockdown of Nolc1 inhibits the PI3K-AKT pathway to improve the prognosis [7].

In summary, Nolc1 plays crucial roles in various cellular processes and is significantly associated with multiple cancers, including prostate, epithelial ovarian, endometrial, colorectal, and esophageal cancers. Studies on Nolc1 using gene knockdown or fusion models help to understand its functions in cancer development, providing potential directions for cancer diagnosis and treatment.