In the enrolling studies HOTAIR was investigated in three

In the enrolling studies, HOTAIR was investigated in three studies, MALAT1, PVT1 and Sox2ot were detected in two researches, and with the high levels of the four lncRNAs, the prognosis rate was low in GC. In 2014, Liu et al. revealed that HOTAIR may act as a competitive endogenous RNA (ceRNA), effectively becoming a sink for miR-331-3p, then modulating the derepression of HER2. Meanwhile, they found that the positive HER2/HOTAIR correlation was significantly associated with advanced GC. MALAT1 is originally identified in lung cancer. In 2016, Xia et al. found that MALAT1 could function as an oncogene in GC, and high MALAT1 level could serve as a potential biomarker for the distant metastasis of GC. PVT1 is increased in the GC patients, and the high discover this of PVT1 was significantly correlated with deeper invasion depth and advanced TNM stage of cancer patients. Furthermore, researchers demonstrated that PVT1 played an oncogenic role in gastric cancer partly through epigenetic regulation of p15 and p16. Zhang et al. revealed that high levels of Sox2ot were correlated with malignant status and poor prognosis. Furthermore, silencing Sox2ot expression effectively inhibited GC cell motility and growth in vitro. Our results indicated that these four lncRNAs had a significantly prognostic value in GC. Previous studies revealed that the expression levels of lncRNAs were related to clinicopathological parameters in GC, including lymph node metastasis, tumor differentiation, distant metastasis, invasion depth, TNM stage and some other features. However, in our meta-analysis, we found that dysregulated lncRNAs were associated with the TNM stage and lymph node metastasis. In the enrolling studies, most of these lncRNAs were detected by the single study. Therefore, the possible reason for the uncorrelation between lncRNAs and other clinicopathological characters was the insufficient investigation for each lncRNA. Further studies should be performed to verify these conclusions.
Introduction Cancer is one of the most common diseases and a major public health problem in China and worldwide. Based on GLOBOCAN estimates, about 14.1million new cancer cases and 8.2million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to the developing countries, which currently account for about 57% of cases and 65% ofcancer deaths worldwide. The high morbidity and mortality of cancer are related with the increasing prevalence of risk factors such as overweight, smoking, the increased aging and growth of the population. There are many effective methods to treat the cancer disease. Surgery, radiation therapy and chemotherapy are the major methods in the treatments of cancer today. Primary tumors and large metastases often depend on surgery and radiation therapy. Some disseminated tumors such as breast, prostate and colorectal cancer are treated mainly by chemotherapy. Traditional anticancer chemotherapy agents block cell division and DNA replication. Many of these agents could also target the microtubule dynamics of the mitotic spindle. These early anticancer drugs such as platinum derivatives, nucleoside analogues, topoisomerase inhibitors, taxanes and vinca alkaloids are widely used today. They have great curative effects and slightly prolong survival among patients with childhood leukaemias and testicular carcinoma. However, they are not effective for all types of cancer. Regarding the background and disadvantage of chemotherapy, complementary treatment modalities are being widely explored in recent years. For example, molecular therapy, anti-angiogenesis therapy, immunotherapy, apoptosis regulation, signal-transduction therapy, differentiation therapy, targeted radionuclide therapy and nucleic-acid-based therapies have attracted more attention from the public. Researches are focusing on some new approaches for cancer treatments that involve the specific targets of the cancer disease. Multiple molecular targets and signaling pathways were related to the action of targeted treatment. Targeted treatment exerted its anticancer effects through multiple mechanisms, including proliferation inhibition, apoptosis induction, metastasis suppression, immune function regulation and multidrug resistance reversal.