This meta-analysis suggests that patients with DM are at greater risk of GERD than those who do not have DM.

Recently, the long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was reported to be involved in the pathogenesis of several cancers, including human colorectal cancer (CRC). However, the molecular basis for cancer initiation, development, and progression remains unclear. In this study, we observe that upregulated PVT1 is associated with poor prognosis and bad clinicopathological features of CRC patients. In vitro means of PVT1 loss in a CRC cell line inhibit cell proliferation, migration, and invasion. Furthermore, dual-luciferase reporter and RNA pull-down assays indicated that PVT1 binds to miR-16-5p, which has been shown to play strong tumor suppressive roles in CRC. Targeted loss of miR-16-5p partially rescues the suppressive effect induced by PVT1 knockdown. Vascular endothelial growth factor A (VEGFA), a direct downstream target of miR-16-5p, was suppressed by PVT1 knockdown in CRC cells. Overexpression of VEGFA is known to modulate the AKT signaling cascade by activating vascular endothelial growth factor receptor 1 (VEGFR1). We, therefore, show that PVT1 loss combined with miR-16-5p overexpression reduces tumor volume maximally when propagated within a mouse xenograft model. We conclude that the PVT1-miR-16-5p/VEGFA/VEGFR1/AKT axis directly coordinates the response in CRC pathogenesis and suggest PVT1 as a novel target for potential CRC therapy.

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Long noncoding RNAs (LncRNAs) have been identified in multiple human cancer types, including lung cancer. An increasing number of studies have indicated that lncRNAs can function as important gene regulators. However, the biological mechanism of LINC00961 in lung cancerremains poorly understood. In our current study, we recognized lncRNA LINC00961, and we observed that it was significantly reduced in human non-small cell lung cancer (NSCLC) tissues. LINC00961 was elevated by infecting LV-LINC00961, while decreased by LV-shLINC00961 in H226 and A549 cells. Furthermore, it was shown that LINC00961 overexpression greatly inhibited lung cancer cell proliferation, whereas downregulated LINC00961 induced cell proliferation. In addition, further experiments showed that restoration of LINC00961 could dramatically increase apoptotic ratios of NSCLC H226 and A549 cells, and knockdown of LINC00961 exhibited an opposite effect. Moreover, Western blot analysis showed that upregulation of LINC00961 repressed proliferating cell nuclear antigen expression and increased Bax expression, indicating that it acts as an important pro-apoptosis gene. Conversely, inhibition of LINC00961 induced proliferating cell nuclear antigen expression and restrained Bax protein levels. Taking these together, LINC00961 might play a tumor suppressive role in NSCLC progression, and it could serve as a novel prognostic biomarker in NSCLC diagnosis and treatment.