The SNHG12 expression is relatively high in PTC tissues and cells. In-vivo/in-vitro experiments prove that SNHG12 can promote the proliferation and metastasis of PTC cells through influencing the Wnt/β-catenin signaling pathway.

Prostate cancer is the second leading cause of cancer‐related deaths among men worldwide. Early diagnosis increases survival rates in patients but the survival rate has remained relatively poor over the past years. Increasing evidence shows that altered metabolism is a critical hallmark in prostate cancer. There is a strong need to explore the molecular mechanisms underlying cancer metabolism for prostate cancer therapy. Whether the aberrant expression of micro RNA (mi RNA ) contributes to cancer metabolism is not fully known. In this study, we found that micro RNA ‐132 (miR‐132) expression is reduced and thus leads to a metabolic switch in prostate cancer cells. miR‐132 performs this role by increasing Glut1 expression, resulting in the enhanced rate of lactate production and glucose uptake. The altered metabolism induced by decreased miR‐132 levels confers the rapid growth of the cancer cells. These data indicate that miR‐132 is involved in regulating the Warburg effect in prostate cancer by inhibiting Glut1 expression.

BackgroundNesfatin-1, recently identified as a satiety regulator, elicits an anti-atherosclerosis effect. Our study was designed to determine whether there is an association between serum nesfatin-1 and the development and severity of peripheral arterial disease (PAD) in patients with type 2 diabetes mellitus (T2DM).Material/MethodsThis cross-sectional study included 355 T2DM patients (200 without PAD and 155 with PAD).ResultsT2DM patients with PAD exhibited marked lower serum nesfatin-1 concentrations than those without PAD. Multivariable logistic regression analysis indicated an inverse association of serum nesfatin-1 concentrations with the development of PAD in T2DM patients (OR 0.008, 95% CI 0.002 to 0.028; P<0.001). Simple linear regression analysis showed a marked correlation between serum nesfatin-1 concentrations and body mass index (BMI), homeostasis model assessment of insulin resistance (HOMA-IR), C-reactive protein (CRP), and ankle-brachial index (ABI) in T2DM patients. By contrast, multivariable analysis showed only BMI and ABI as independent correlates of serum nesfatin-1.ConclusionsOur study shows an association of serum nesfatin-1 concentrations and the development and severity of PAD in T2DM patients.

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