Abstract
Simple SummaryLong non-coding RNAs (lncRNAs) are a heterogenous group of transcripts that regulate various cellular functions. They are implicated in all hallmarks of cancer, including metabolic alterations. Through the modulation of expression of oncogenic or tumor-suppressive genes, alteration of various signaling pathways, protein stability, and upregulation of metabolic enzymes, lncRNAs enhance glucose uptake in cancer and, thus, favor cancer progression. These transcripts represent crucial regulators of cancer glucose metabolism and, as such, they are potential clinical biomarkers and therapeutic targets. This review aims to provide an overview of the lncRNAs involved in cancer glucose metabolism and summarizes their underlying molecular mechanisms.The rapid and uncontrolled proliferation of cancer cells is supported by metabolic reprogramming. Altered glucose metabolism supports cancer growth and progression. Compared with normal cells, cancer cells show increased glucose uptake, aerobic glycolysis and lactate production. Byproducts of adjusted glucose metabolism provide additional benefits supporting hallmark capabilities of cancer cells. Long non-coding RNAs (lncRNAs) are a heterogeneous group of transcripts of more than 200 nucleotides in length. They regulate numerous cellular processes, primarily through physical interaction with other molecules. Dysregulated lncRNAs are involved in all hallmarks of cancer including metabolic alterations. They may upregulate metabolic enzymes, modulate the expression of oncogenic or tumor-suppressive genes and disturb metabolic signaling pathways favoring cancer progression. Thus, lncRNAs are not only potential clinical biomarkers for cancer diagnostics and prediction but also possible therapeutic targets. This review summarizes the lncRNAs involved in cancer glucose metabolism and highlights their underlying molecular mechanisms.
Highlights
Cancers are characterized by uncontrolled and rapid cellular proliferation
The aim of this review is to provide an overview of the Long non-coding RNAs (lncRNAs) involved in cancer glucose metabolism
Another study proved that upregulated lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) in triple negative breast cancer is transcriptionally targeted by Yes-associated protein (YAP) and it is required for YAP-promoted glycolysis through GLI2-dependent Hedgehog signaling
Summary
Cancers are characterized by uncontrolled and rapid cellular proliferation. To satisfy the accompanying increased demand for energy, cancer cells have to reprogram their metabolism, especially glucose metabolism [1,2]. The effect of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on glucose metabolism is essential for its oncogenic activity in HCC It upregulates the metabolic transcription factor TCF7L2 via the mTORC1 pathway, which enhances the expression of glycolytic genes and downregulates enzymes involved in gluconeogenesis. TAIR alters cancer cell energy metabolism in pancreatic adenocarcinoma by the upregulation of HK2 This leads to the enhancement of tumor cell proliferation, glucose uptake, increased ATP and lactate production [61]. As already observed in HCC and esophageal cancers, lncRNA UCA1 promotes glycolysis in bladder cancer cells It regulates glycolysis by upregulating HK2 expression through mTOR and its downstream effector STAT3, which is a direct transcriptional activator for HK2 [81]. PCGEM1 binds directly to the target promoter of c-MYC where it functions as a coactivator and mediates enhanced c-MYC transcription [83]
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