lncRNAs In Gastric Cancer Research Articles

Identification of differential expression lncRNAs in gastric cancer using transcriptome sequencing and bioinformatics analyses.

The current study aimed to identify novel long non-coding RNAs (lncRNAs) associated with gastric cancer (GC). Transcriptome sequencing of the lncRNAs and mRNAs from GC tissues and normal adjacent tissues was performed. The data were analyzed using bioinformatics analysis, specifically analysis of differentially expressed lncRNAs and mRNA, target gene prediction and functional enrichment analysis. A total of 1,181 differentially expressed mRNA and 390 differentially expressed lncRNAs were identified. The targets of upregulated lncRNAs were significantly enriched in functions associated with collagen fibril organization, whereas the downregulated lncRNA were significantly associated with ion transmembrane transport and regulation of membrane potential. A total of 7 lncRNAs were verified by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Following RT-qPCR validation, AC016735.2, AP001626.1, RP11-400N13.3 and RP11-243M5.2 were considered to be consistent with the prediction of the bioinformatics analysis. Transcriptome sequencing and RT-qPCR experiments identified 4 lncRNAs, including AC016735.2, AP001626.1, RP11-400N13.3 and RP11-243M5.2 to have an important role in the carcinogenesis of GC.

Role of DiGeorge syndrome critical region gene 9, a long noncoding RNA, in gastric cancer.

IntroductionLong non-coding RNAs (lncRNAs) regulate and influence cancer cell development and tumor formation. However, the role for lncRNAs in gastric cancer has not been fully established. In this study, DGCR9, a lncRNA, was significantly upregulated in gastric cancer cell lines.MethodsThe expression levels of DGCR9 in each patient between formalin-fixed, paraffin-embedded (FFPE) gastric cancer tissues and adjacent noncancer tissues (NAT) (n=102) were measured by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The effect of DGCR9 on cellular proliferation, migration, and glucose uptake was investigated in vitro, respectively.ResultsDGCR9 was shown to have increased expression in gastric cancer tissues and in gastric cancer cell lines. Further, DGCR9 was found to be associated with clinicopathological characteristics of patients with gastric cancer. In particular, DGCR9 was positively associated with lymph node invasion and tumor-node-metastasis (TNM) stage in gastric cancer patients. By in vitro functional analysis, knockdown of DGCR9 in gastric cancer cells suppressed cellular proliferation, migration, and glucose uptake. In contrast, overexpression of DGCR9 increased each of these cancer cell characteristics.ConclusionsDGCR9 was upregulated in gastric cancer tissues and was shown to accelerate cellular proliferation, migration, and glucose metabolism, all of which would promote the formation and development of gastric cancer.

Long noncoding RNA PANDAR blocks CDKN1A gene transcription by competitive interaction with p53 protein in gastric cancer

Emerging evidence indicates that lncRNAs play important roles in cancer tumourigenesis and could be used as potential diagnostic biomarkers or therapeutic targets. However, the clinical significance and molecular mechanism of lncRNAs in gastric cancer (GC) is still unclear. The aim of this study was to explore the expression and role of lncRNAs in GC. The relative expression level of lncRNAs in GC samples was examined by an lncRNA microarray analysis, northern blot analysis and qRT-PCR analysis. A Kaplan−Meier survival analysis and univariate and multivariate Cox proportional hazards models were performed to evaluate the clinical and prognostic significance of PANDAR (promoter of CDKN1A antisense DNA damage activated RNA) in GC patients. The binding activity of PANDAR with the p53 protein was analysed by an RNA immunoprecipitation analysis and RNA pull-down analysis. The depletion of PANDAR was conducted using the CRISPR/Cas9 system for PANDAR. The biological functions of PANDAR in GC cells were determined both in vitro and in vivo. Upregulated PANDAR in GC patients was positively correlated with increased tumour size, advanced TNM classification and a poor survival rate in GC patients. The ROC curves identified that the PANDAR level was a marker for discriminating the early-stage tumour group from the healthy group, the metastasis group from the non-metastasis group and the chemoresistance group from the chemosensitive group in GC patients. As a target, the CDKN1A gene was successfully downregulated by PANDAR. PANDAR controlled the transcription of the CDKN1A gene by competitively binding with p53 protein. In combination with a p53 activator (nutlin3), the knockout of PANDAR by CRISPR/Cas9 technology synergistically inhibited GC tumour growth in vivo. Our results suggest that the PANDAR is a powerful diagnostic and therapeutic marker for patients with GC and, combined with other chemotherapeutics, may have distinct antitumour effects.

A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer

Background/Aims: Recent evidence has shown that some long non-coding RNAs (lncRNAs) play important roles in various biological processes. However, the regulatory mechanism of lncRNA in gastric cancer (GC) remains unclear. Methods: We reannotated the GC gene expression profile into a lncRNA-mRNA biphasic profile and integrated the microRNA target data to construct a global GC triple network. A further clustering and random walk with restart analyses was performed on the triple network from the level of topology analyses. Quantitative real-time PCR was used to determine expression of lncRNA RP11-363E7.4. Kaplan-Meier analyses was performed to evaluate the prognostic value of lncRNA RP11-363E7.4. Results: We constructed a gastric cancer lncRNA-miRNA-mRNA network (GCLMN) including six lncRNAs, 332 mRNAs, and 3,707 edges. For the shared lncRNA RP11-363E7.4, the interacting gene and microRNA functional enrichment studies implied that lncRNA RP11-363E7.4 might function as a new regulator in GC. The expression of lncRNA RP11-363E7.4 was downregulated compared with that of paracarcinoma tissues in five GC samples. High expression of lncRNA RP11-363E7.4 was found to be correlated to better overall survival (OS) for GC patients. Conclusions: This study focused on GC lncRNA-miRNA-mRNA regulatory networks, and found that lncRNA RP11-363E7.4 was a new GC risk lncRNA, which might provide novel insight into a better understanding of the pathogenesis of GC.

H19 functions as a competing endogenous RNA to regulate human epidermal growth factor receptor expression by sequestering let‑7c in gastric cancer.

Long non‑coding RNA (lncRNA) H19 has been suggested to serve important roles in the progression of gastric cancer (GC); however, the mechanism involved is largely unknown. The present study aimed to investigate the mechanism underlying the effect of H19 on human epidermal growth factor receptor (HER2) expression. Let‑7c belongs to the let‑7 family, which has been reported to be downregulated in cancers and considered to serve as a tumor suppressor. Let‑7c has been negatively associated with the expression of human epidermal growth factor receptor 2 (HER2). Reverse transcription‑quantitative polymerase chain reaction was used to examine the expression levels of H19 and let‑7c in GC tissues and cell lines. HER2 protein expression levels were examined using immunohistochemistry and western blot analyses. The effect of H19 on let‑7c and HER2 expression was analyzed following transfection of small interfering RNA targeting H19 in GC cells. The results indicated that the expression levels of H19 lncRNA in GC tissue samples were significantly higher when compared with that in matched benign adjacent tissue samples (P<0.001). H19‑silenced GC cells exhibited significantly increased let‑7c expression and decreased HER2 protein expression levels. Assessment of tumor diameter and pathological tumor stage suggested that increased H19 expression was associated with a poorer prognosis in patients with GC. The results of the present study suggest that H19 may function as a competing endogenous RNA to regulate HER2 expression by sequestering let‑7c in GC cells. The present study has aided the understanding of the mechanism of H19 lncRNA in GC, and has provided evidence for the application of lncRNA‑based diagnostic and therapeutic strategies for GC.

Downregulated long non-coding RNA TCONS_00068220 upregulates apoptosis in gastric cancer cells.

Long non-coding RNAs (lncRNAs) are emerging as a fundamental class of biological effect or molecules that perform pivotal functions in the regulation of the genome. With advances in bioinformatics and genomics, extensive identification and characterization of lncRNAs is now possible. They regulate cellular growth, differentiation and apoptosis. Dysregulation of lncRNAs has been associated with numerous types of human cancer. In the present study, the expression profile of differentially expressed genes (DEGs) and lncRNAs in gastric cancer (GC) samples and normal tissue samples was evaluated with bioinformatics. The biological functions of the predicted lncRNA TCONS_00068220 were focused on; the DEGs co-expressed with TCONS_00068220 were enriched in cancer-associated pathways. TCONS_00068220 was demonstrated to be upregulated in GC tissues and cell lines compared with normal controls. In addition, an increased rate of apoptosis was observed in NCI-N87 cells following transfection with small interfering RNA against TCONS_00068220. These data suggest that TCONS_00068220 may be associated with the pathogenesis of GC, and it may serve as a potential therapeutic target.

Integrated analysis of long non-coding RNAs in human gastric cancer: An in silico study.

Accumulating evidence highlights the important role of long non-coding RNAs (lncRNAs) in a large number of biological processes. However, the knowledge of genome scale expression of lncRNAs and their potential biological function in gastric cancer is still lacking. Using RNA-seq data from 420 gastric cancer patients in The Cancer Genome Atlas (TCGA), we identified 1,294 lncRNAs differentially expressed in gastric cancer compared with adjacent normal tissues. We also found 247 lncRNAs differentially expressed between intestinal subtype and diffuse subtype. Survival analysis revealed 33 lncRNAs independently associated with patient overall survival, of which 6 lncRNAs were validated in the internal validation set. There were 181 differentially expressed lncRNAs located in the recurrent somatic copy number alterations (SCNAs) regions and their correlations between copy number and RNA expression level were also analyzed. In addition, we inferred the function of lncRNAs by construction of a co-expression network for mRNAs and lncRNAs. Together, this study presented an integrative analysis of lncRNAs in gastric cancer and provided a valuable resource for further functional research of lncRNAs in gastric cancer.

The role of miRNA and lncRNA in gastric cancer.

Gastric cancer is one of the most common cancers and has the highest mortality rate worldwide. It is worthwhile to explore the mechanism of gastric cancer progression. An increasing number of studies have found that non-coding RNAs including miRNA and lncRNA play important roles in gastric cancer progression. This review summarized the role of ectopic miRNA in gastric cancer proliferation, growth, migration, invasion and apoptosis. Meantime, aberrantly expressed miRNA also received a great deal of attention as potential biomarker for gastric cancer diagnosis and therapy. Over the last decade, lncRNA was considered to regulate gastric cancer progression at the transcript and post-transcript level. At the transcript level, lncRNA induced gastric cancer progression by changing chromatin modification and mRNA stabilization to regulate mRNA and miRNA expression. Furthermore, lncRNA regulated gastric cancer progression by completely combining with miRNA to produce ceRNA or promote protein stabilization at the post-transcript level. Greater attention of miRNA and lncRNA in gastric cancer can provide new insight of mechanism of cancer development and may be acted as a new anticancer target.

E2F1 induces TINCR transcriptional activity and accelerates gastric cancer progression via activation of TINCR/STAU1/CDKN2B signaling axis

Recent evidence indicates that E2F1 transcription factor have pivotal roles in the regulation of cellular processes, and is found to be dysregulated in a variety of cancers. Long non-coding RNAs (lncRNAs) are also reported to exert important effect on tumorigenesis. E2F1 is aberrantly expressed in gastric cancer (GC), and biology functions of E2F1 in GC are controversial. The biological characteristics of E2F1 and correlation between E2F1 and lncRNAs in GC remain to be found. In this study, integrated analysis revealed that E2F1 expression was significantly increased in GC cases and its expression was positively correlated with the poor pathologic stage, large tumor size and poor prognosis. Forced E2F1 expression promotes proliferation, whereas loss of E2F1 function decreased cell proliferation by blocking of cell cycle in GC cells. Mechanistic analyses indicated that E2F1 accelerates GC growth partly through induces TINCR transcription. TINCR could bind to STAU1 (staufen1) protein, and influence CDKN2B mRNA stability and expression, thereby affecting the proliferation of GC cells. Together, our findings suggest that E2F1/TINCR/STAU1/CDKN2B signaling axis contributes to the oncogenic potential of GC and may constitute a potential therapeutic target in this disease.

LncRNAs act as prognostic biomarkers in gastric cancer: A systematic review and meta-analysis

Gastric cancer (GC) is one of the leading causes of cancer-related death. The 5-year overall survival (OS) rate of patients is extremely low and to find a new marker is urgently needed. Increasing studies indicate that long noncoding RNAs (lncRNAs) are abnormally expressed in GC. However, the results of these studies were conflicting and inconclusive, especially in the aspects of tumor prognosis. Therefore, we performed a systematic review and meta-analysis to investigate the clinical values, including prognosis and clinicopathology of different lncRNAs in GC. A total of 38 studies including 34 on OS, 17 on disease-free survival (DFS), 1 on progression-free survival (PFS), 1 on disease-specific survival (DSS), and 34 on clinicopathological features were identified from the databases. Our results indicated that the levels of lncRNAs were associated with the OS (hazard ratios [HR]=1.44, 95% confidence interval [95% CI]=1.23–1.69, P<0.001), PFS (HR=2.32, 95% CI=1.10–5.28, P=0.001) and DSS (HR=2.65, 95% CI=1.53–3.60, P=0.009). However, there was no relationship between lncRNAs and DFS (HR=1.25, 95% CI=0.90–1.74, P=0.11). Moreover, lncRNAs were related to lymph node metastasis (odds ratios [OR]=1.67, 95% CI=1.21–2.31, P=0.002) and TNM (OR=1.93, 95% CI=1.27–2.92, P<0.001). In conclusion, our present meta-analysis indicated that lncRNAs could function as potential prognostic markers in GC.

Clinical significance of the long noncoding RNA RP11-19P22.6-001 in gastric cancer.

Long non-coding RNAs (lncRNAs) play roles in carcinogenesis; however, the significance of most lncRNAs in gastric cancer is unclear. To explore the diagnostic value of the long noncoding RNA RP11-19P22.6-001 in gastric cancer. RP11-19P22.6-001 levels in gastric cancer tissues and paired non-tumor tissues were analyzed by quantitative reverse transcription-polymerase chain reaction. Since RP11-19P22.6-001 acts in cis to regulate nitric oxide synthase 2 (NOS2), we also analyzed NOS2 expression and its correlation with gastric cancer. Finally, to analyze the potential diagnostic values of RP11-19P22.6-001, a receiver operating characteristic (ROC) curve was constructed. RP11-19P22.6-001 expression was significantly downregulated in 70.91% (78/110) of gastric cancer tissues compared to that of adjacent normal tissues. However, NOS2 was upregulated in 75.45% (83/110) of gastric cancer tissues. RP11-19P22.6-001 expression levels were associated with invasion, lymph node metastasis, and TNM stage. The areas under the ROC curves (AUC) were 0.662 and 0.671 for RP11-19P22.6-001 and NOS2, respectively. More importantly, the combined use of these parameters increased the AUC to 0.704. RP11-19P22.6-001 and NOS2 may be new biomarkers for the diagnosis and prognosis of gastric cancer. The combined use of lncRNAs and their target genes may be a promising method to increase the diagnostic value of lncRNAs in cancer.

Screening and verification of key long chain noncoding RNA of gastric cancer with genetic risk

Objective To screen and verify the expression profiles of long non-coding RNAs (lncRNAs) in gastric cancer (GC) with genetic risk. Methods Microarray analysis was performed in 5 pairs GC tissues with Agilent Array platform to measure the expression levels of lncRNAs and mRNAs and to investigate the expression differences of lncRNAs in GC, and hierarchical clustering used to screen out the differently expressed lncRNAs. In order to verify the reliability of the chip, 4 abnormal expression of lncRNAs were randomly selected, and real time polymerase chain reaction (RT-PCR) was detected in 72 pairs of gastric cancer tissues and their matched normal tissues. Results Compared with the normal tissues, the expression of 2 times higher than those in the gastric cancer tissues was determined as the differential expression. It were found that 1 300 of them were up-regulated in lncRNAs and down-regulated in 1 807 lncRNAs. If this standard was 10 times, it was found that 55 of them were up-regulated and down-regulated in 372 lncRNAs. The results of 4 lncRNAs (H19, HOTAIRM1, HCG18 and LNC00261) showed that there was no significant difference between RT-PCR detection and chip detection (H19: t=1.332, P=0.314; HOTAIRM1: t=0.913, P=0.458; HCG18: t=1.517, P=0.269; LINC00261: t=0.176, P=0.876). Conclusion Some of the lncRNAs are abnormally expressed in tissues with a genetic risk of gastric cancer, which are likely to be the key risk factors for gastric cancer. Key words: Gastric Carcinoma; Heredity; Risk; Long non-coding RNAs; Microchip

Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

Background/Aims: The colorectal neoplasia differentially expressed (CRNDE) gene is a long noncoding RNA (lncRNAs) that is upregulated in colorectal cancer and glioma. Here, we investigated the regulatory function of CRNDE in gastric cancer (GC). Methods: CRNDE and miR-145 expression were assayed by qRT-PCR, and E2F3 protein expression was measured by western blotting. A luciferase reporter assay was used to detect the direct regulation of miR-145 by CRNDE. Cell viability and colony formation of human GC cells were detected using MTT and colony formation assay, respectively. Results: CRNDE was highly expressed in GC cell lines and tissues; overexpression of CRNDE increased GC cell viability and promoted colony formation. Knockdown of CRNDE did not result in loss of expression-related effects on cell proliferation and colony formation. Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145. Conclusion: CRNDE acted as a growth-promoting lncRNA in GC and maybe a potential target of GC treatment.

Progress in relationship between long non-coding RNAs and gastric cancer

Long non-coding RNAs (lncRNAs) are a group of regulatory and non-coding RNA molecules which are longer than 200 nucleotides. They are involved in a variety of biological processes such as cell proliferation, differentiation and apoptosis mainly by regulation of gene expression at various levels, including epigenetics, transcription and post-transcription. The evidence has demonstrated that many lncRNAs are dysregulated and closely related to tumorigenesis, progression and prognosis in gastric cancer. Based on an introduction to lncRNAs and the domestic and foreign research status, this review summarizes the function, regulatory mechanisms, potential diagnostic and therapeutic values of lncRNAs in gastric cancer. Key words: Stomach neoplasms; Long non-coding RNAs; Epigenetics

Plasma lncRNA-GACAT2 is a valuable marker for the screening of gastric cancer

Long non-coding RNAs (lncRNAs) are crucial in contributing to gastric tumorigenesis and development. However, the diagnostic value of the majority of lncRNAs in gastric cancer (GC) are not clear. The present study investigated the diagnostic value of gastric cancer associated transcript 2 (GACAT2), a lncRNA that is aberrantly expressed in GC tissues. A total of 343 plasma samples from 80 healthy individuals, 29 patients with gastric dysplasia (GD) and 117 paired preoperative and postoperative patients with GC were collected. Plasma GACAT2 levels were subsequently measured by reverse transcription-quantitative polymerase chain reaction. Finally, the associations between plasma GACAT2 levels and various clinicopathological features of patients with GC were assessed. The results demonstrated that plasma GACAT2 levels in preoperative patients with GC were significantly higher than those in the postoperative group (P=0.031). Compared with healthy individuals, plasma GACAT2 levels were significantly increased in patients with GD (P<0.001) and preoperative patients with GC (P=0.040). Moreover, the individual relative changes of plasma GACAT2 expression following surgery were significantly associated with lymphatic metastasis (P=0.034), distal metastasis (P=0.035) and perineural invasion (P=0.039). Therefore, the results of the current study suggest that plasma-based GACAT2 may be developed as a tumor marker to screen and predict the prognosis of GC patients.

Long noncoding RNA ZFAS1 promotes gastric cancer cells proliferation by epigenetically repressing KLF2 and NKD2 expression.

Recently, long noncoding RNAs have been emerged as critical regulators of human disease and prognostic markers in several cancers, including gastric cancer. In this study, we globally assessed the transcriptomic differences of lncRNAs in gastric cancer using publicly available microarray data from Gene Expression Omnibus (GEO) and identified an oncogenetic lncRNA ZFAS1, which may promote gastric tumorigenesis. ZFAS1 has been found to be upregulated and function as oncogene in colorectal cancer and hepatocellular carcinoma, but its expression pattern, biological function and underlying mechanism in gastric cancer is still undetermined. Here, we reported that ZFAS1 expression is also overexpressed in gastric cancer, and its increased level is associated with poor prognosis and shorter survival. Knockdown of ZFAS1 impaired gastric cancer cells proliferation and induced apoptosis in vitro, and inhibited tumorigenicity of gastric cancer cells in vivo. Mechanistically, RNA immunoprecipitation and RNA pull-down experiment showed that ZFAS1 could simultaneously interact with EZH2 and LSD1/CoREST to repress underlying targets KLF2 and NKD2 transcription. In addition, rescue experiments determined that ZFAS1 oncogenic function is partly dependent on repressing KLF2 and NKD2. Taken together, our findings illuminate how ZFAS1 over-expression confers an oncogenic function in gastric cancer.

LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.

Long noncoding RNAs (lncRNAs) play crucial roles in tumorigenesis. However, the mechanisms of most lncRNAs in cancers are largely unknown. Because the RNA component of mitochondrial RNA processing endoribonuclease (RMRP) is one of the dysregulated lncRNAs in gastric cancer, this study explored its molecular mechanisms in carcinogenesis. RMRP levels in 792 tissues, plasma and gastric juices from patients with various stages of gastric tumorigenesis were analyzed by quantitative reverse transcription-polymerase chain reaction. Overexpression and RNA interference were used to manipulate RMRP expression by RMRP expression vector and small interfering RNAs, respectively. Its mechanisms were evaluated by flow cytometry, real-time cell analysis, plate colony formation assays, and xenograft models. RMRP levels in tissue, plasma and gastric juices from patients with gastric cancer were significantly different from those from controls. Its levels were significantly associated with Borrmann type and metastasis. Plasma and gastric juice RMRP had higher sensitivity and specificity than commonly used markers (such as carcinoembryonic antigen and carbohydrate antigen 19–9). Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression. RMRP plays a crucial role in gastric cancer occurrence and can be used as a novel biomarker for gastric cancer.

Long noncoding RNAs in gastric cancer: functions and clinical applications.

Over the last two decades, genome-wide studies have revealed that only a small fraction of the human genome encodes proteins; long noncoding RNAs (lncRNAs) account for 98% of the total genome. These RNA molecules, which are >200 nt in length, play important roles in diverse biological processes, including the immune response, stem cell pluripotency, cell proliferation, apoptosis, differentiation, invasion, and metastasis by regulating gene expression at the epigenetic, transcriptional, and posttranscriptional levels. However, the detailed molecular mechanisms underlying lncRNA function are only partially understood. Recent studies showed that many lncRNAs are aberrantly expressed in gastric cancer (GC) tissues, gastric juice, plasma, and cells, and these alterations are linked to the occurrence, progression, and outcome of GC. Here, we review the current knowledge of the biological functions and clinical aspects of lncRNAs in GC.

Emerging roles of non-coding RNAs in gastric cancer: Pathogenesis and clinical implications.

Gastric cancer is a leading cause of cancer-related deaths. However, the mechanisms underlying gastric carcinogenesis remain largely unclear. The association of non-coding RNAs (ncRNAs) with cancer has been widely studied during the past decade. In general, ncRNAs have been classified as small ncRNAs, including microRNAs (miRNAs), and long non-coding RNAs (lncRNAs). Emerging evidence shows that miRNAs and lncRNAs play key roles in the formation and progression of many cancers. In this review, we focus on the regulation of miRNAs and lncRNAs in gastric cancer. miRNAs and lncRNAs appear to be involved in gastric tumor growth, invasion, and metastasis and in establishment of the gastric tumor microenvironment through various mechanisms. Furthermore, we also discuss the possibilities of establishing miRNAs and lncRNAs as potential biomarkers and therapeutic targets for gastric cancer. Taken together, we summarize the emerging roles of ncRNAs in gastric cancer development and their possible clinical significance.

Differential expression profiles of long non-coding RNAs reveal potential biomarkers for identification of human gastric cancer.

Gastric cancer (GC) is one of the most lethal malignancies worldwide. To reduce its high mortality, sensitive and specific biomarkers for early detection are urgently needed. Recent studies have reported that tumor-specific long non-coding RNAs (lncRNAs) seem to be potential biomarkers for the early diagnosis and treatment of cancer. In the present study, lncRNA and mRNA expression profiling of GC specimens and their paired adjacent non-cancerous tissues was performed. Differentially expressed lncRNAs and mRNAs were identified through microarray analysis. The function of differential mRNA was determined by gene ontology and pathway analysis and the functions of lncRNAs were studied by constructing a co-expression network to find the relationships with corresponding mRNAs. We connected the co-expression network, mRNA functions, and the results of the microarray profile differential expression and selected 14 significantly differentially expressed key lncRNAs and 21 key mRNAs. Quantitative RT-PCR (qRT-PCR) was conducted to verify these key RNAs in 50 newly diagnosed GC patients. The data showed that RP5-919F19, CTD-2541M15 and UCA1 was significantly higher expressed. AP000459, LOC101928316, RP11-167N4 and LINC01071 expression was significantly lower in 30 advanced GC tumor tissues than adjacent non-tumor tissues P<0.05. Then, we further validated the above significant differential expression candidate lncRNAs in 20 early stage GC patients. Results showed that CTD-2541M15 and UCA1 were significantly higher expressed, AP000459, LINC01071 and MEG3 expression was significantly lower in 20 early stage GC patient tumor tissues than adjacent non-tumor tissues (P<0.05). In addition, expression of these lncRNAs shows gradual upward trend from early stage GC to advanced GC. Furthermore, conditional logistic regression analysis revealed the aberrant expression of CTD-2541M15, UCA1 and MEG3 closely linked with GC. There is a set of differentially expressed lncRNAs in GC which may be associated with the progression and development of GC. The differential expression profiles of lncRNAs in GC may be promising biomarkers for the early detection and early screening of high‑risk populations.