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Recently, targeting cancer stem cells (CSCs) metabolism is becoming a promising therapeutic approach to improve cancer treatment outcomes. However, knowledge of the metabolic state of CSCs in small cell lung cancer is still lacking. In this study, we found that CSCs had significantly lower oxygen consumption rate and extracellular acidification rate than non-stem cancer cells. Meanwhile, this subpopulation of cells consumed less glucose, produced less lactate and maintained lower ATP levels. We also revealed that CSCs could produce more ATP through mitochondrial substrate-level phosphorylation during respiratory inhibition compared with non-stem cancer cells. Furthermore, they were more sensitive to suppression of oxidative phosphorylation. Therefore, oligomycin (inhibitor of oxidative phosphorylation) could severely impair sphere-forming and tumor-initiating abilities of CSCs. Our work suggests that CSCs represent metabolically inactive tumor subpopulations which sustain in a state showing low metabolic activity. However, mitochondrial substrate-level phosphorylation of CSCs may be more active than that of non-stem cancer cells. Moreover, CSCs showed preferential use of oxidative phosphorylation over glycolysis to meet their energy demand. These results extend our understanding of CSCs metabolism, potentially providing novel treatment strategies targeting metabolic pathways in small cell lung cancer.

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Long non-coding RNAs (lncRNAs) have been proven to play important roles in carcinogenesis and development of numerous cancers, but their biological functions in glioblastoma remain largely unknown. In this study, we found that HOXB-AS1 was highly expressed in human glioblastoma tissues and cell lines, and was associated with survival time of patients. Further analysis showed that knock-down of HOXB-AS1 inhibited cell proliferation via inducing S phase cell cycle arrest and suppressed migration and invasion ability of cells. Mechanism study revealed that HOXB-AS1 is mainly located in cytoplasm and functions as competing endogenous RNA via sponging of miR-885-3p. Moreover, inhibition of miR-885-3p antagonized the effects of HOXB-AS1 knock-down and promoted proliferation, migration and invasion of glioblastoma cells. Finally, we found that sponging of miR-885-3p by HOXB-AS1 could further affect the expression of HOXB2. Taken together, we demonstrate that HOXB-AS1/miR-885-3p/HOXB2 axis regulates proliferation, migration and invasion of glioblastoma cells and can serve as a potential biomarker for the malignancy.