LGALS1 plays an anti-oncogenic role in cervical cancer by synthetically regulating transcriptome profile in HeLa cells

Long non-coding RNAs (lncRNAs) have been extensively studied as key regulators of cancer development in various cancers. *** is a newly identified lncRNA in recent years, and several studies have shown that *** may play oncogenic or anti-oncogenic roles in different cancers. Pan-cancer analysis showed that high *** expression was significantly associated with better prognosis. Nevertheless, the role of *** in the development of cervical cancer is unclear. In our study, we constructed a *** overexpression model in HeLa cell line. We found that *** overexpression significantly inhibited cell proliferation and induced apoptosis, and *** may be a novel anti-oncogenic factor in cervical cancer. Mechanistically, overexpression of *** could activate type I interferon signaling pathways and inhibits the expression of genes involved in DNA damage responses. Meanwhile, *** could regulate the expression of a large number of RNA binding protein genes thereby potentially affecting the alternative splicing of genes involved in cell proliferation or apoptosis regulation. We also established a ceRNA network to predict the regulatory effect of *** on gene expression through miRNA. Our study highlights the essential role of lncRNA *** in the development of cervical cancer and suggests the potential regulatory mechanisms. Overall design: We constructed a LGALS1 overexpression model in HeLa cell line, coupled with RNA-seq sequences, to comprehensively reveal the biological function of LGALS1 in HeLa cell and analyze the alterations of transcriptional profiles upon LGALS1 overexpression.