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Background: Abnormal glucose metabolism is one of the malignant characteristics of tumors. LncRNA plays an important role in the process of aerobic glycolysis of tumors. Aims: To investigate the expression of LncRNA MEG3 in gastric cancer and its correlation with glycolysis. Methods: RT-qPCR was used to detect the mRNA expression of MEG3 in gastric cancer and paracancerous tissue. Immunohistochemical EnVision method was used to detect the protein expressions of PKM2, LDHA, mTOR, HIF-1α in gastric cancer and paracancerous tissue. Relationship between expressions of above-mentioned indices and clinicopathological features of gastric cancer were analyzed. The correlation between MEG3 and glycolysis level of gastric cancer was analyzed by Spearman correlation analysis, and its possible mechanism was explored. Results: The expression of MEG3 in gastric cancer tissue was significantly lower than that in paracancerous tissue (P< 0.05), and was correlated with lymph node metastasis (P<0.05). The positivity rates of expression of PKM2, LDHA, mTOR and HIF-1α in gastric cancer tissue were significantly higher than those in paracancerous tissue, and were correlated with the depth of tumor invasion, lymph node metastasis and pTNM stage (P<0.05). Spearman correlation analysis showed that the expression of MEG3 was negatively correlated with the expressions of PKM2, LDHA, mTOR and HIF-1α (r=-0.346，r= -0.306，r=-0.389, r=-0.338; P<0.05). The expression of MEG3 in HIF-1α
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Objective:Calcium/calmodulin-dependent kinase kinase (CAMKK2) is activated in prostate cancer (PCa). The aim of our study is to identify the effects of preadipocyte and CAMKK2 on the PCa cell invasion.Methods:The coculture system between PCa cells and preadipocyte cells (3T3L1) was established and then Transwell assay was used to determine the invasive effect after coculture. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to investigate the CAMKK2 expression in the coculture system.Results:The 3T3L1 cells promoted the invasion of PCa cells (DU145 and 22RV1; P<0.01). Meanwhile, the 3T3L1 cells can increased expression of CAMKK2 in PCa cells ( P<0.01). CAMKK2 reversed the invasive effects of preadipocyte cells on the PCa cells. Conclusions:Our study demonstrates that the preadipocyte may promote the PCa cell invasion possibly by mediating the CAMKK2 expression.