The long noncoding RNA urothelial carcinoma‐associated 1 (UCA1) has been reported to sustain the proliferation of acute myeloid leukemia (AML) cells through downregulating cell cycle regulators p27kip1. Yet, the foundational mechanism of UCA1 in AML pathologies remains unclear. Herein, we found an escalation of UCA1 expression and suppression of miR‐204 expression in pediatric AML patients and cells. UCA1 silencing suppressed cell proliferative abilities, promoted apoptotic rates, decreased Ki67, and increased cleaved caspase‐3 in AML cells. Moreover, UCA1 sponged miR‐204 and suppressed its expression. UCA1 overexpression inversed the miR‐204 suppressed proliferation and promoted apoptosis. UCA1 also boosted the expression of SIRT1, a miR‐204 target, via the sponging interaction. Furthermore, miR‐204 inhibited inducible nitric oxide synthase and cyclooxygenase‐2 expression, while UCA1 overexpression inversed the inhibitory effects in AML cells. Our findings concluded that UCA1 downregulation repressed cell proliferation and promoted apoptosis through inactivating SIRT1 signals by upregulating miR‐204 in pediatric AML.

LncRNAs are known to regulate a plethora of key events of cellular processes; however, little is known about the function of lncRNAs in autophagy. Here in the current study, we report lncRNA-IGFBP4 which has previously been known to regulate the proliferation and reprogramming of cancer cells, but its role in autophagy is not yet known. We found that serum starvation provokes autophagy-induced downregulation of lncRNA-IGFBP4 levels. Next, we determined that c-Myc can negatively regulate lncRNA-IGFBP4 in HeLa cells. Phenotypically, we found that upon depletion of lncRNA-IGFBP4, the HeLa cells undergo autophagy through ULK1/Beclin1 signaling. Furthermore, through TCGA data analysis, we found lncRNA-IGFB4 overexpressed in most cancers including cervical cancer. Based on these findings, we conclude that c-Myc maintains cellular homeostasis through negatively regulating lncRNA-IGFBP4 in cervical cancer cells.