HULC: HULC, a long non-coding RNA (lncRNA), has been found to be dysregulated in digestive system tumors and may serve as a candidate oncogene for these tumors [PMC8908940]. High expression levels of HULC have been significantly correlated with poor survival prognosis in patients with digestive system tumors [PMC8908940]. HULC has also been shown to be overexpressed in digestive system tumors, promoting tumor development and poor tumor differentiation [PMC8908940]. The mechanism of HULC may vary among different types of digestive system tumors due to their complexity [PMC8908940]. HULC, particularly from serum and plasma, has the potential to be a new predictor of prognosis for patients with digestive system tumors [PMC8908940]. A meta-analysis was conducted to evaluate the association between HULC and the prognosis and clinicopathological features in patients with digestive system tumors, confirming the association between HULC expression levels and survival prognosis [PMC8908940]. Additionally, studies have shown that HULC is regulated by various factors such as IGF2BP1, miR-3200-5p, YB-1 protein, ERK pathway, and ATF4 [PMC9126659][PMC8990785][PMC10090411][PMC6025799][PMC2938198][PMC8997642][PMC5442347][ PMC6778481][ PMC9672467]. These findings provide insights into the potential therapeutic targets for liver cancer by targeting HULC-mediated pathways such as ferroptosis regulation and YB-1 phosphorylation [ PMC9126659] [ PMC8997642] . The RBP IGF2BP1 has been implicated in the degradation of HULC through CCR4-NOT complex recruitment [ PMC7215867] . Overall, these studies highlight the importance of understanding the role of HULC in digestive system tumors and its potential as a therapeutic target.