PurposeThe oncogenic roles of lncRNA LINC01116 have been reported in several types of cancer, while its involvement in gastric cancer is unknown. This study aimed to investigate the involvement of LINC01116 in gastric cancer.MethodsGene expression was detected by qPCR. Correlations were analyzed by linear regression. Overexpression and siRNA silencing techniques were used to analyze gene functions. Cell invasion and migration were analyzed by Transwell assays.ResultsLINC01116 and lncRNA CASC11 were both upregulated in cancer tissues compared to cancer-adjacent tissues. Expression levels of LINC01116 and CASC11 were increased with the increase in clinical stages. Expression levels of LINC01116 and CASC11 were positively correlated. Overexpression of LINC01116 mediated the upregulated CASC11 in gastric cancer cells, and CASC11 overexpression also led to overexpressed LINC01116. Overexpression of LINC01116 and CASC11 led to promoted invasion and migration of gastric cancer cells. Rescue experiments showed that CASC11 knockdown attenuated the effects of LINC01116 overexpression. Overexpression of LINC01116 failed to significantly affect cancer cell proliferation.ConclusionLINC01116 promoted cancer cell invasion and migration in gastric cancer by positively interacting with CASC11.
Background Serum tumor markers including AFU, AFP, CEA, CA199, CA125 and CA724, are of great importance in the diagnosis, prognostic prediction and recurrence monitoring of gastrointestinal malignancies. However, their significance in gastric cancer (GC) patients with neoadjuvant therapy (NCT) is still uncertain. The aim of this study was to evaluate the predictive value of these six tumor markers in locally advanced GC patients who underwent NCT and curative surgery. Methods In total, 290 locally advanced GC patients who underwent NCT and D2 radical gastrectomy were retrospectively analyzed. Data on their tumor markers before (pre-) and after (post-) NCT and pathological characteristics were extracted from the database of our hospital. The optimal cutoff values of the six tumor markers were calculated by the ROC curve and Youden index. Their predictive significance was analyzed and survival curves for overall survival (OS) were obtained by the Kaplan-Meier method. Associations between categorical variables were explored by the chi-square test or Fisher’s exact test. Multivariate analyses were performed by the Cox regression model. Results Pre- and post-CA199, −CA125 and -CA724 could predict overall survival (all P < 0.05), but only the change (diff-) of CA199 was related to prognosis (P = 0.05). In the multivariable analysis, pre- (P = 0.014) and post-CA724 (P = 0.036) remained significant, though diff-CA724 was not an independent prognostic factor (P = 0.581). In addition, pre- and post-CA199, −CA125 and -CA724 were associated with lymph node metastasis (N- vs N+) and pathological stage (I-II vs III) (all P < 0.05). Moreover, post-CA724 was related to the vascular or lymphatic invasion (P = 0.019), while pre-CA724 was not (P = 0.082). However, AFU, AFP and CEA showed no association with survival (P > 0.05). Conclusions CA724 is an independent factor for prognosis and could be used to predict ypN and ypTNM stage in locally advanced GC patients undergoing NCT and curative resection.
Gastric cancer is a common malignant tumor with high occurrence and recurrence and is the leading cause of death worldwide. However, the prognostic value of protein-coding and non-coding RNAs in stage III gastric cancer has not been systematically analyzed. In this study, using TCGA data, we identified 585 long noncoding RNAs (lncRNAs) and 927 protein-coding genes (PCGs) correlated with the overall survival rate of gastric cancer. Functional enrichment analysis revealed that the prognostic genes positively correlated with death rates were enriched in pathways, including gap junction, focal adhesion, cell adhesion molecules (CAMs), and neuroactive ligand-receptor interaction, that are involved in the tumor microenvironment and cell-cell communications, suggesting that their dysregulation may promote the tumor progression. To evaluate the performance of the prognostic genes in risk prediction, we built three multivariable Cox models based on prognostic genes selected from the prognostic PCGs and lncRNAs. The performance of the three models based on features from only PCGs or lncRNAs or from all prognostic genes were systematically compared, which revealed that the features selected from all the prognostic genes showed higher performance than the features selected only from lncRNAs or PCGs. Furthermore, the multivariable Cox regression analysis revealed that the stratification with the highest performance was an independent prognostic factor in stage III gastric cancer. In addition, we explored the underlying mechanism of the prognostic lncRNAs in the Cox model by predicting the lncRNA and protein interaction. Specifically, CTD-2218G20.2 was predicted to interact with PSG4, PSG5, and PSG7, which could also interact with cancer-related proteins, including KISS1, TIMP2, MMP11, IGFBP1, EGFR, and CDKN1C, suggesting that CTD-2218G20.2 might participate in the cancer progression via these cancer-related proteins. In summary, the systematic analysis of the prognostic lncRNAs and PCGs was of great importance to the understanding of the progression of stage III gastric cancer.
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