Systematic Survey of the Regulatory Networks of the Long Noncoding RNA BANCR in Cervical Cancer Cells

Abstract

Long noncoding RNAs (lncRNAs) are increasingly recognized as functional regulators of human cancers. BRAF-activated noncoding RNA (BANCR), an oncogenic lncRNA, has a carcinogenic effect on many types of cancers. However, the clinical significance and molecular mechanisms of BANCR in cervical cancer are still unclear. Here, we generated BANCR knockout cell lines via CRISPR/Cas9 editing and revealed that BANCR plays roles in the apoptosis, proliferation, and migration of HeLa cells. A quantitative proteomics strategy was employed to globally identify BANCR-regulated proteins in HeLa cells. In total, we identified 569 differentially expressed proteins (DEPs) upon knockout of BANCR in HeLa cells. Bioinformatic analysis revealed that these DEPs were involved in diverse cellular pathways. Functional studies revealed that BANCR exerts its effects on the proliferation and apoptosis of HeLa cells through the regulation of cAMP-responsive element binding protein 1 (CREB1) expression. Mechanistically, BANCR could inhibit the expression of miR-582-5p, and CREB1 is a direct target of miR-582-5p; therefore, BANCR may exert its function by regulating CREB1 expression via targeting miR-582-5p in cervical cancer cells. Collectively, this study established a proteome-wide BANCR regulatory network, which provides novel insight into the molecular pathogenesis of cervical cancer and can serve as a basis for the development of targeted therapies.

Interaction of BANCR in the relationship between Hashimoto’s thyroiditis and papillary thyroid carcinoma expression patterns and possible molecular mechanisms

“…BANCR is a 693 bp transcript located on chromosome 9 and has been implicated in a variety of biological processes, such as cell proliferation, migration, and invasion. However, the exact role of BANCR in cancer remains a subject of debate and further investigation 6–9 . In addition to its involvement in cancer, BANCR has also been implicated in autoimmune disorders such as HT.…”

“…However, the exact role of BANCR in cancer remains a subject of debate and further investigation. [6][7][8][9] In addition to its involvement in cancer, BANCR has also been implicated in autoimmune disorders such as HT. It has been observed that individuals with HT have an elevated risk of developing PTC compared to the general population.…”

LINC00586 Represses ASXL1 Expression Thus Inducing Epithelial-To-Mesenchymal Transition of Colorectal Cancer Cells Through LSD1-Mediated H3K4me2 Demethylation

“…A previous study clarified that LINC00586 induces the migration of CRC cells and promotes the process of EMT ( Guo et al, 2014 ). Of note, researchers performed quantitative proteomics strategy to globally identify LINC00586-regulated proteins in HeLa cells and found 569 differentially expressed proteins (DEPs) in HeLa cells upon knockout of BANCR ( Wang et al, 2022 ). Nevertheless, the detailed molecular mechanism underlying LINC00586 waits to be further elucidated.…”

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

“…CAMP‐response element‐binding protein 1 (Creb1) encodes a transcription factor that binds as a homodimer to the cAMP‐responsive element. The phosphorylated status of Creb1 can induce gene transcription to respond to hormonal stimulation of the cAMP pathway 20 . In ischemia‐related studies, Creb1 correlated with the ischemic injury and ischemia–reperfusion injury process in various tissues.…”

“…The phosphorylated status of Creb1 can induce gene transcription to respond to hormonal stimulation of the cAMP pathway. 20 In ischemia‐related studies, Creb1 correlated with the ischemic injury and ischemia–reperfusion injury process in various tissues. For example, in the mouse hindlimb muscle ischemic tissue, JNK3 deletion is involved in the upregulated vascular remodeling response during peripheral ischemia through the activation of Creb1, leading to the upregulation of various growth factors in the ischemic muscles.…”