romoted migration and invasion of NSCLC cells in vitro, and enhanced lung metastasis formation in vivo Mechanistic investigations showed that MetaLnc9 interacted with the glycolytic kinase PGK1 and prevented its ubiquitination in NSCLC cells, leading to activation of the oncogenic AKT/mTOR signaling pathway. MetaLnc9 also interacted with P54nrb/NonO (NONO) to help mediate the activity of CRTC, a coactivator for the transcription factor CREB, reinforcing a positive feedback loop for metastasis. Taken together, our results establish MetaLnc9 as a driver of metastasis and a candidate therapeutic target for treating advanced NSCLC. Cancer Res; 77(21); 5782-94. ©2017 AACR.20:T46c,Metabolic switch from oxidative phosphorylation to aerobic glycolysis, which is also called the Warburg effect, is a hallmark of osteosarcoma (OS) and leads to the enhancement of cell chemoresistance, growth, metastasis, and invasion. Emerging evidence indicates that long non-coding RNA (lncRNA) plays a crucial role in the Warburg effect of cancer cells. Here, we report that lncRNA KCNQ1OT1 was upregulated in OS. Meanwhile, functional experiments demonstrated that the KCNQ1OT1 facilitated proliferation and suppressed apoptosis of OS cells. In addition, KCNQ1OT1 contributed to the Warburg effect by stimulating aldolase A (ALDOA) expression. Furthermore, using bioinformatics analysis, luciferase reporter, RNA immunoprecipitation, and RNA pull-down assay, we identified that KCNQ1OT1 functions as a competing endogenous RNA (ceRNA) by sponging miR-34c-5p, which inhibited ALDOA expression by directly targeting its 3'UTR. Taken together, these data identified a key role of KCNQ1OT1 in glucose metabolism reprogramming of OS. Targeting the KCNQ1OT1/miR-34c-5p/ALDOA axis may be a potential therapeutic target in OS treatment.21:T4fc,As the most common subtype of lung cancer, lung adenocarcinoma (LUAD) is the frequently occurred cancers in human. Therefore, thorough investigation is necessary for understanding the progression of LUAD. HMMR has functioned as a regulator in some cancers, whereas its biological role still needs to be investigated in LUAD. By bioinformatics analysis, we found that HMMR was highly expressed in LUAD tissues and associated with patients' poor prognosis. Further, qRT-PCR demonstrated that HMMR was up-regulated in LUAD tissues and cells. Loss-of-function assays manifested that HMMR knockdown refrained cell proliferation, migration and invasion and enhanced cell apoptosis in LUAD. Later, HMMR was identified as a target gene of miR-34a-5p, which expressed at a low level in LUAD cell and played an anti-oncogenic role in LUAD. Simultaneously, we discovered that miR-34a-5p could directly bind to HCG18. Subsequent assays revealed that HCG18 mediated HMMR expression by sequestering miR-34a-5p. At last, rescue assays proved the carcinogenic role of HCG18/miR-34a-5p/HMMR axis in LUAD cells growth. Importantly, HCG18 was found to facilitate tumor growth in LUAD. Conclusively, HCG18 acted an oncogene in LUAD and enhanced LUAD progression by targeting miR-34a-5p/HMMR axis.22:T50f,The Warburg effect (aerobic glycolysis) is a hallmark of cancer and is becoming a promising target for diagnosis and therapy. Phosphoglycerate kinase 1 (PGK1) is the first adenosine triphosphate (ATP)-generating glycolytic enzyme in the aerobic glycolysis pathway and plays an important role in cancer development and progression. However, how microRNAs (miRNAs) regulate PGK1-mediated aerobic glycolysis remains unknown. Here, we show that miR-16-1-3p inhibits PGK1 expression by directly targeting its 3'-untranslated region. Through inhibition of PGK1, miR-16-1-3p suppressed aerobic glycolysis by decreasing glucose uptake, lactate and ATP production, and extracellular acidification rate, and increasing oxygen consumption rate in breast cancer cells. Aerobic glycolysis regulated by the miR-16-1-3p/PGK1 axis is critical for modulating breast cancer cell proliferation, migration, invasion and metastasis in vitro and in vivo. In breast cancer pa

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