No abstract

No abstract

No abstract

Cancer Susceptibility Candidate 9 (CASC9) is a novel gene generating long non-coding RNA (lncRNA) with oncogenic potential that was first identified in esophageal cancer. In this study, we have found that CASC9 was overexpressed in gastric cancer (GC) compared to normal gastric tissue. A higher expression level was associated with aggressive pathological characteristics, including deep invasion, poor differentiation and lymph node metastases. In two gastric cancer cell lines, BGC823 and SGC7901, CASC9 were both overexpressed compared to that of normal gastric epithelial cell (GES-1). Moreover, the expression of CASC9 was even higher in BGC823/DR and SGC7901/DR cells that are resistant to paclitaxel or adriamycin. CASC9 knockdown inhibited proliferation and promoted cell apoptosis In BGC823/DR and SGC7901/DR cells. The invasion potential was also significantly inhibited measured by Transwell assay. In addition, CASC9 knockdown in BGC823/DR and SGC7901/DR cells restored chemosensitivity to paclitaxel and adriamycin. This was associated with decreased expression of multidrug resistance 1 (MDR1) protein. Taken together, our data suggest that expression of lncRNA CASC9 correlated with aggressive pathological characteristics of GC, it may serve as a potential oncogene to regulate proliferation, invasion, and chemoresistance of GC cells.

Gastric cancer (GC) is the most common solid tumor in digestive system. Nuclear-enriched abundant transcript 1 (NEAT1) gene is a lncRNA, and reveal potential oncogene role in several malignant tumors. The aim of this study is to investigate the expression and clinical significance of Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) gene and its influence to malignant biologic behaviors and chemotherapy resistance to adriamycin in GC. This study found NEAT1 was up-regulated in GC tissues and cells, especially in in GC adriamycin-resistant cells. NEAT1 silence in SGC7901 cells could inhibit proliferation and invasion ability, and promote cell apoptosis significantly. NEAT1 silence in adriamycin-resistant SGC7901/ADR cells also depressed the half maximal inhibitory concentration (IC50) for adriamycin, chemotherapy resistance to adriamycin was inhibited significantly. NEAT1 knockdown promoted apoptosis in SGC7901/ADR cells induced by adriamycin. In summary, lncRNA NEAT1 is high-expressed in GC and functions as an oncogene to modulate apoptosis, invasion, proliferation and chemotherapy resistance of GC cells, which might be a novel potential therapeutic target for GC.

No abstract

The purpose of this study is to examine the impact of the 2004 and 2005 Diagnosis-Related Group (DRG)-based Prospective Payment Experiments (whereby a ceiling was set on per case payments for 15 DRGs) of the health insurance system in Shanghai using Differences-In-Differences (DID) and Differences-in-Differences-in-Differences (DDD) empirical strategies. The results show that the Length Of Stay (LOS) of all inpatients suffering from the target diseases during the two test periods responded quickly to the experiment (even though only insured inpatients living in Shanghai were eligible for the DRG-based experiments), thus implying that the DRG-based prospective payment system does not induce physicians to significantly reduce inpatient expenditures but does induce them to reduce the LOS of those suffering from the target diseases. Moreover, costs were shifted to uninsured inpatients suffering from the target diseases: their overall inpatient expenditures increased by 33.6 percentage points more than that of uninsured inpatients during the nontest period in 2005. Thus, the experiments were of limited effectiveness, and cost-shifting to uninsured inpatients was observed during at least the latter test period.

No abstract