Expression Of Colon Cancer-associated Transcript-1 Research Articles

Assessment of long noncoding RNA CCAT1 using real time-polymerase chain reaction in colorectal cancer patients

Colorectal cancer (CRC) is linked to high mortality, mainly when discovered in its advanced stages. Several studies have pointed to the role of epigenetic factors in CRC and other cancers. Long non-coding RNAs (lncRNAs) are involved in the initiation, progression, metastasis, and modulation of the response to chemotherapeutic modalities of CRC as vital contributors to epigenetic mechanisms. Colon cancer-associated transcript-1 (CCAT1) is one of the lncRNAs that have been dysregulated in serum samples, providing a non-invasive route for diagnosing CRC patients. This study aimed to determine the role of CCAT1 expression as diagnostic and prognostic markers. We tested the associations of CCAT1 expression with serum carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9). The study included three groups: 41 patients with colorectal cancer, 39 patients with precancerous benign colorectal diseases, and 20 normal control individuals. CEA and CA 19-9 were measured by an immunoassay automated system. The expression level of CCAT1 was assessed by a real-time polymerase chain reaction. There was a statistically significant elevation of serum CEA levels in patients with CRC compared to patients with precancerous benign colorectal diseases. Furthermore, there was no statistically significant difference in serum CA 19-9 levels between all groups (p = 0.102). Interestingly, CCAT1 expression was significantly upregulated in the blood of CRC patients compared to the precancerous benign colorectal diseases group (p = 0.009) and the control group (p<0.001). Also, expression of CCAT1 was significantly elevated in patients with precancerous benign colorectal diseases compared to the control group (p=0.004). In conclusion, measuring the expression level of CCAT1 is more advised than assessment of CEA and CA 19-9 for the early diagnosis and prognosis of colorectal cancer.

Long non-coding RNA CCAT1 sponges miR-490 to enhance cell proliferation and migration of non-small cell lung cancer.

BackgroundNon‐small cell lung cancer (NSCLC) accounts for 85% of lung cancer which is the most frequently diagnosed malignancy in China. Colon cancer associated transcript 1 (CCAT1) acts as an oncogene in enhancing tumor progression. However, the effects of CCAT1 in NSCLC remain unclear. The purpose of this study was to explore the role of CCAT1 in NSCLC.MethodsWound healing and transwell assays were performed to measure cell migration. RT‐qPCR was employed to calculate the mRNA level of CCAT1 and miR‐490.ResultsHigh expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR‐490. CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR‐490 had the opposite effect. CCAT1 could specifically bind to miR‐490 and regulate its expression. MiR‐490 partially reversed the inhibitory effect of CCAT1 on cell proliferation and metastasis.ConclusionsThe CCAT1/miR‐490 molecular axis has been shown to be important for the treatment of NSCLC.

Long Non-coding RNA Colon Cancer-Associated Transcript-1 Promotes Migration, Invasion, and Epithelial Mesenchymal Transition of Lung Adenocarcinoma by Suppressing miR-219-1.

Previous evidence suggests that long non-coding colon cancer-associated transcript-1(CCAT1) plays a pivotal role in the progression of a variety of tumors. However, little is known about its role in lung adenocarcinoma (LAD). In this study, we found LAD tissue samples had a higher expression of CCAT1 but a lower expression of miR-219-1 compared to their adjacent non-tumor tissues. CCAT1 negatively regulated the expression of miR-219-1. miR-219-1 suppressed the proliferation of A549 and H1299 cells. Knockdown of CCAT1 inhibited the proliferation, migration, and invasion of A549 and H1299 cells, which were reversed by the miR-219-1 inhibitor. CCAT1 knockdown increased the expression of E-cadherin but decreased the expressions of N-cadherin and vimentin, which were restored by the miR-219-1 inhibitor. In vivo, knockdown of CCAT1 suppressed the tumor growth of LAD xenografts, which were rescued by the inhibition of miR-219-1. In summary, our findings suggested that CCAT1 promotes the progression of LAD via sponging miR-219-1, providing a potential therapeutic target for LAD.

Long non-coding RNA CCAT1 promotes non-small cell lung cancer progression by regulating the miR-216a-5p/RAP2B axis.

The long non-coding RNA colon cancer-associated transcript 1 (CCAT1) has been investigated to involve in the progression of non-small cell lung cancer (NSCLC). Thus, this study aims to explore the detailed molecular mechanisms of CCAT1 in NSCLC. The expression of CCAT1, miR-216a-5p, RAP2B, Bax, Bcl-2, and cleaved caspase 3 was detected by qRT-PCR or Western blot. Cell proliferation, apoptosis, migration, and invasion were analyzed using cell counting kit-8, flow cytometry or Transwell assays, respectively. The interaction between miR-216a-5p and CCAT1 or RAP2B was analyzed by luciferase reporter, RNA immunoprecipitation, and pull-down assays. The expression of CCAT1 was elevated in NSCLC, and CCAT1 deletion could inhibit NSCLC cell proliferation, migration, and invasion but induce apoptosis in vitro as well as imped tumor growth in vivo. MiR-216a-5p was confirmed to be a target of CCAT1, and silencing miR-216a-5p could reverse CCAT1 depletion-mediated inhibitory effects on cell tumorigenesis in NSCLC. Besides that, miR-216a-5p was decreased in NSCLC, and miR-216a-5p restoration inhibited cell tumorigenesis by regulating RAP2B, which was verified to be a target of miR-216a-5p. Additionally, co-expression analysis suggested that CCAT1 indirectly regulated RAP2B level by targeting miR-216a-5p in NSCLC cells. Taken together, CCAT1 deletion could inhibit cell progression in NSCLC through miR-216a-5p/RAP2B axis, indicating a novel pathway underlying NSCLC cell progression and providing new potential targets for NSCLC treatment.

LncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miR-219-1.

Gastric cancer (GC) is one of the most malignant tumors that seriously threatenhuman health. Increased reports have indicated that long noncoding RNAs (lncRNAs) areassociated with GC. This study aims to investigate the regulatory role of colon cancer-associated transcript-1 (CCAT1) in GC. The results exhibited the fact that CCAT1 was expressed higher in 57 GC tissue samples than in 57 paired adjacent normal tissue samples. The expression of CCAT1 was also increased in GC cell lines (MKN45, Hs746T, and SGC-7901) compared with the gastric epithelial cell line GES-1. Besidesthis, decreased cell proliferation with increased cell apoptosis wasdetected in SGC-7902 cells transfected with CCAT1 short hairpin RNA (shRNA). At the same time, a lower cell invasion ability was measured in SCG-7901 cells transfected with CCAT1 shRNA.In addition, miR-219-1 was predicted and convinced a direct target of CCAT1. The expression of miR-219-1 was decreased in GC tissues and GC cell lines. Further studies demonstrated that the roles of CCAT1 in cell proliferation, apoptosis, and invasion were inhibited by miR-219-1. Finally, in vivo experiment indicated that tumor growth of GC was suppressed through knockdown of CCAT1. In conclusion, these results suggested that CAT1 promotes the tumorigenesis and progression of GC by negatively regulating miR-219-1.

RETRACTED: Ginsenoside Rg3 inhibits cell growth, migration and invasion in Caco-2 cells by downregulation of lncRNA CCAT1

Colorectal cancer (CRC) is a troublesome disease with high morbidity and mortality. Ginsenoside Rg3 possesses anti-cancer properties. Colon Cancer Associated Transcript 1 (CCAT1) participates in the genesis, development, invasion and metastasis of colorectal cancer. In our study, we explored the effects of Rg3 on CRC cell line Caco-2 by regulating CCAT1. CRC tissue was obtained from hospital and Caco-2 cells were purchased. Caco-2 cells were treated with Rg3 and/or transfected with pc- CCAT1 or pcDNA3.1. The group without Rg3 treatment was treated as control. Cell viability, cell apoptosis, cell migration and invasion were detected by Cell Counting Kit-8 assay, flow cytometry and Transwell chamber migration/invasion assay, respectively. The expression of CyclinD1, apoptosis related proteins (p53, Bcl-2, Bax, pro-/Cleaved-Caspase-3), migration and invasion related proteins (MMP-9 and vimentin), and phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT) related proteins (p/t-PI3K, p/t-AKT) were examined by western blot. The expression of CCAT1 was measured by quantitative real time RCR (qRT-PCR). Rg3 significantly decreased cell viability, migration and invasion, and promoted apoptosis. Meanwhile, the expression of Cyclin D1, matrix metalloproteinase (MMP)-9 and vimentin was downregulated. The expression of apoptosis-related proteins p53, Bax, and Cleaved-Caspase-3 were upregulated while Bcl-2 was downregulated by the treatment of Rg3 compared with control. Furthermore, CCAT1 was upregulated in CRC tissue and Rg3 negatively regulated CCAT1 expression. Transfection with pc-CCAT1 led to the opposite results as compared with transfection with pcDNA3.1 in Rg3 treated cells. In addition, Rg3 decreased the phosphorylation of PI3K and AKT. Ginsenoside Rg3 inhibits migration and invasion, and promotes apoptosis of Caco-2 cells by suppression expression of LncRNA CCAT1.

CCAT1 lncRNA Promotes Inflammatory Bowel Disease Malignancy by Destroying Intestinal Barrier via Downregulating miR-185-3p.

The long noncoding RNA (lncRNA) colon cancer-associated transcript-1 (CCAT1) has been reported to play a vital role in the development of cancer. Although the link between inflammation and cancer initiation is well established, whether CCAT1 is involved in inflammation and promotes inflammatory bowel disease (IBD) malignancy remains undetermined. We aimed to investigate the expression of CCAT1 in IBD and the effect of CCAT1 overexpression on intestinal epithelial barrier function. The relationship between CCAT1 and the inflammation-related pathway was analyzed in both colorectal cancer (CRC) and IBD patients. Gene expression was detected by real-time polymerase chain reaction and Western blot. Transepithelial electrical resistance (TEER) and FD-4 flux measurement were used to test the effect of CCAT1 and miR-185-3p on intestinal epithelial barrier function. Luciferase assay was performed to validate the target site of miR-185-3p on 3'-UTR of MLCK mRNA. Gene set enrichment analysis revealed that several inflammation-related genes were enriched in the CCAT1 high-expressed group of CRC patients. The relationship between CCAT1 and inflammation activation in IBD patients was further confirmed. CCAT1 expression positively correlated with MLCK, which acts as a protein kinase to phosphorylate myosin light chain and induces tight junction protein distribution, whereas it was negatively correlated with miR-185-3p in IBD tissues. We also determined that CCAT1 overexpression increased Caco-2 monolayer permeability and upregulated MLCK. Furthermore, CCAT1-induced MLCK overexpression and IBD disease progression were significantly attenuated by miR-185-3p. The CCAT1/miR-185-3p/MLCK signaling pathway is strongly activated to destroy barrier function and promotes the pathogenesis of IBD.

CX-3543 Promotes Cell Apoptosis through Downregulation of CCAT1 in Colon Cancer Cells.

Aim Colon cancer-associated transcript-1 (CCAT1), located in the vicinity of transcription factor c-Myc, was first identified in colon cancer. A small-molecule compound CX3543 (Quarfloxin) selectively targeting Myc G-quadruplexes has entered phase II clinical trials for neuroendocrine carcinomas. The aim of the study was to explore the relationship between CX3543, CCAT1, and cell apoptosis in colon cancer cells. Methods Semiquantitative PCR was used to detect the relative expression of CCAT1 in colon cancer (CC) tissues and HT29 cell lines. Real-time PCR (RT-PCR) was also used to investigate the expression of CCAT1 and c-Myc after HT29 cells being treated by CX3543 for 24 h. Cell apoptosis assay and cell proliferation assay were conducted in HT29 cells after being treated by CX3543. Results The results showed that the expression of CCAT1 was remarkably increased in CC tissues and HT29 cells compared to controls. CX3543 treatment reduced the expression of c-Myc and CCAT1 and promoted cell apoptosis and inhibited cell proliferation. After the expression of CCAT1 was inhibited by sh-CCAT1 transfection, the cell apoptosis rate was higher than that of control group. After the cells were treated by CCAT1 overexpression plasmid transfection and CX3543, the cell apoptosis rate was lower than that of control group. In vivo results showed that CX3543 inhibited the xenograft tumor growth of rats through downregulation of CCAT1. Conclusion Our study demonstrated that CX3543 could inhibit the progression of colon cancer by downregulating CCAT1 expression and might be a potential drug for the treatment of colon cancer.

Overexpression of the long noncoding RNA CCAT1 promotes metastasis via epithelial-to-mesenchymal transition in lung adenocarcinoma.

The long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) has been identified as an oncogene in multiple types of human malignancy, and the aberrant expression of CCAT1 has been associated with the tumorigenesis and progression of cancer. However, the underlying mechanism of how CCAT1 affects malignant behaviors in lung adenocarcinoma cells remains unknown. In the current study, the expression of CCAT1 was identified to be increased in lung adenocarcinoma tissues (n=96) by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its expression level was associated with epidermal growth factor receptor (EGFR) expression (P=0.011), lymphatic metastasis (P=0.003) and tumor node metastasis (TNM) stage (P=0.003). In vitro, by using Transwell assays, the overexpression of CCAT1 was demonstrated to promote the migration and invasion of H358 lung adenocarcinoma cells; while downregulation of CCAT1 expression inhibited H1650 cell migration and invasion. Furthermore, western blot analysis indicated that aberrant CCAT1 expression may induce epithelial-to-mesenchymal transition (EMT) by regulating the expression levels of EMT markers (E-cadherin, N-cadherin and vimentin). In conclusion, these results indicate that CCAT1 is able to promote the metastasis of lung adenocarcinoma cells by inducing EMT.

LncRNA colon cancer-associated transcript 1 (CCAT1) promotes proliferation and metastasis of ovarian cancer via miR-1290.

Ovarian cancer is one of the leading causes of cancer-related death in women, but treatment remained unsatisfactory. Studies have shown that lncRNA colon cancer-associated transcript 1 (CCAT1) plays an important regulatory role in different cancers, but its role in ovarian cancer remained largely unclear. Quantitative Real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of lncRNA CCAT1 in ovarian cancer and adjacent tissue, and analysis was applied to explore the relationship between expression and clinical characteristic. After lncRNA CCAT1 suppression, Cell Counting Kit-8 (CCK8) and wound-healing assay were used to detect the proliferation and metastasis ability of ovarian cancer, respectively. qRT-PCR showed that lncRNA CCAT1 was highly expressed in ovarian cancer tissue, compared with adjacent tissue. Moreover, we found that the expression of lncRNA CCAT1 was closely related to prognosis, tumor size, and lymph node metastasis. We also found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer. In this study, we found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer, and was closely related to prognosis, proliferation, and metastasis.

Long noncoding RNA colon cancer associated transcript‑1 promotes the proliferation, migration and invasion of cervical cancer.

Previous studies have revealed significant roles for long noncoding RNA (lncRNA) in the tumorigenesis, metastasis and invasion of various tumors, including cervical cancer. The present study aimed to investigate the potential roles of lncRNA colon cancer associated transcript 1 (CCAT1) in the metastasis and invasion of cervical cancer, and to reveal the potential underlying mechanism. The mRNA expression of lncRNA CCAT1 in cervical cancer tissue was measured using the reverse transcription‑quantitative polymerase chain reaction, and the association between lncRNA CCAT1 and the metastasis of cervical cancer was analyzed. The effects of lncRNA CCAT1 expression on HeLa cell viability, and migration and invasion were also analyzed by MTT and Transwell assays. The results demonstrated that lncRNA CCAT1 was highly expressed in the cervical cancer tissue compared with the adjacent normal tissue. High expression of lncRNA CCAT1 was positively associated with tumor size, and there was correlation between high lncRNA CCAT1 expression and a poor survival rate of cervical cancer. The cell viability, and migratory and invasive abilities were suppressed by silencing CCAT1. The results of the present study indicate that lncRNA CCAT1 was highly expressed in cervical cancer, and may serve important roles in promoting the progression and metastasis of cervical cancer.

CCAT-1 promotes proliferation and inhibits apoptosis of cervical cancer cells via the Wnt signaling pathway.

Though the long noncoding RNA colon cancer associated transcript-1 (CCAT-1) has been shown to be involved in tumors of other tissues, its involvement in cervical cancer is still unknown. Therefore, the aim of this study was to investigate the molecular mechanism of CCAT-1 in cervical cancer. We quantified the expression of CCAT-1 long noncoding RNA in samples of cervical cancer tissue by real-time PCR. Effects of CCAT-1 expression on the proliferation and apoptosis of HeLa and CaSki cells were assessed by cell-count, colony-formation, and flow cytometry assays. Binding of the c-Myc protein to the CCAT-1 promoter was confirmed by chromatin immunoprecipitation. Finally, TOP-Flash and western blotting were used to examine the regulation of the Wnt/β-catenin pathway by CCAT-1. The results showed that compared with adjacent normal tissue, the expression of CCAT-1 in cervical cancer tissue was significantly upregulated. CCAT-1 expression was related to the stage and size of the tumor and recurrence prognosis. Then, we showed through functional assays that CCAT-1 could promote proliferation and inhibit apoptosis of cervical cancer cells. Furthermore, chromatin immunoprecipitation showed that c-Myc protein could promote CCAT-1 expression by binding to its promoter. Finally, fluorescent-reporter assays and western blotting showed that CCAT-1 could activate the Wnt/β-catenin pathway. In conclusion, we showed that CCAT-1 can be activated by the c-Myc protein and it can promote proliferation and inhibit apoptosis in cervical cancer cells by regulating the Wnt/β-catenin pathway. CCAT-1 might serve as a good prognostic indicator and target for treatment of cervical cancer.

Expression and clinical significance of long non-coding RNA CCAT1 in gastric cancer

Objective: To investigate the expression and clinical significance of long non-coding RNA colon cancer associated transcript-1 (CCAT1) in gastric cancer (GC), and to further explore the effect of CCAT1 on cell proliferation of GC. Methods: The mRNA expressions of CCAT1 in GC tissues and matched adjacent normal tissues from 62 patients who received resection for gastric carcinoma between January 2013 and May 2015 in Nanjing Medical University Affiliated Wuxi Second Hospital and expressions in GC cell lines were assessed by quantitative real-time PCR (qRT-PCR). The clinical significance of CCAT1 expression was then analyzed. The expressions of CCAT1 in MGC-803 and SGC-7901 cells were inhibited by small interfering RNA (siRNA) transfection. The effect of CCAT1 on cell proliferation was studied by cell counting kit (CCK)-8 assay. Results: The expressions of CCAT1 mRNA in GC tissues were significantly higher than in the normal tissues (3.39±2.37 vs 1.28±0.74, P<0.05). Compared with immortalized human gastric epithelial cell line (GES-1), the expressions of CCAT1 mRNA were significantly higher in GC cell lines MGC-803 and SGC-7901 (3.07±0.69, 2.23±0.32 vs 1.01±0.12, both P<0.05). Besides, the expression of CCAT1 varied significantly among patients with different TNM stage, depth of invasion, and lymph node metastasis (χ(2) =5.199, 5.395, 9.239, all P<0.05). The results of CCK-8 assay showed that down-regulation of CCAT1 in MGC-803 and SGC-7901 cells significantly inhibited the cell proliferation (both P<0.05). Conclusions: CCAT1 is up-regulated in GC and may be significantly correlated with the progression of GC. Decreased expression of CCAT1 can suppress the proliferation of GC cells. CCAT1 might be used as a novel target for GC early diagnosis and treatment.

LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein.

This study was to investigate the involvement of long non-coding RNA (lncRNA) colon cancer-associated transcript-1 (CCAT1) in renal cell carcinoma (RCC) and to further uncover its underlying mechanism. In this study, the expression of CCAT1 and Livin of RCC tissues or cells was determined using qRT-PCR (quantitative real-time PCR) and western blot, respectively. RNA pulldown and RIP (RNA-Binding Protein Immunoprecipitation) assays were performed to examine the sequence interaction between CCAT1 and Livin. The viability and apoptosis of RCC cells was assessed by MTT(3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and TUNEL (TdT-mediated dUTP nick end labeling) assays, respectively. Mice of tumor animal models were established to observe the effect of CCAT1 on RCC tumor growth. The relative expression of CCAT1 in RCC tissues and cell lines was obviously higher than that of the control. CCAT1 knockdown could reduce cell viability and increase the apoptosis of RCC cells in vitro. Furthermore, Livin was significantly inhibited by CCAT1 silencing; RNA pulldown and RIP assays showed that CCAT1 was physically associated with Livin protein. Moreover, Livin overexpression not only significantly inhibited RCC cell apoptosis and increased cell viability, but completely reversed the si-CCAT1-mediated repression of cell viability. More importantly, CCAT1 silencing could inhibit the growth of RCC in vivo that was accompanied by the reduction of Livin in RCC tissues. CCAT1 inhibits RCC cell apoptosis and increases cell viability through up-regulation of Livin.

Long non-coding RNA CCAT1 is overexpressed in oral squamous cell carcinomas and predicts poor prognosis.

Oral squamous cell carcinoma (SCC) is the most common malignant tumor in India with 5-year survival rates totaling <50%. Recently, dysregulation of non-coding RNA was reported as a potential hallmark of carcinogenesis. Colon Cancer Associated Transcript 1 (CCAT1), an lncRNA located in chromosome 8q24, close to the c-Myc gene, has been reported to be overexpressed in many human cancers. In the present study, the authors analyzed the expression of CCAT1, c-Myc and the miRNAs miR155-5p, let7b-5p, miR490-3p and miR218-5p sponged by CCAT1 in 60 oral tumor and 8 normal tissue samples by reverse transcription-quantitative polymerase chain reaction. CCAT1 was significantly overexpressed in 27% (16/60) of oral tumors. Interestingly, a high level of c-Myc expression was observed in all CCAT1 overexpressing cases (P=0.0473). Furthermore, CCAT1 overexpression significantly downregulated miR155-5p (P=0.03) and let7b-5p (P<0.0001). Oral cancer cases expressing high level of CCAT1 (P=0.01) presented poor therapeutic outcome. To the best of the authors' knowledge, this is the first study to report the overexpression of the CCAT1 in oral SCCs, and the results suggested that CCAT1 overexpression may sponge miR155-5p and let7b-5p, and may account for poor treatment response.

CCAT1: a pivotal oncogenic long non‐coding RNA in human cancers

Long non-coding RNAs (lncRNAs) compose a group of non-protein-coding RNAs - more than 200 nucleotides in length. Recent studies have shown that lncRNAs play important roles in different cellular processes, including proliferation, differentiation, migration and invasion. Deregulation of lncRNAs has been widely reported in human tumours, in which they are able to function as either oncogenes (on the one hand) or tumour suppressor genes (on the other). Deregulation of CCAT1 (colon cancer-associated transcript-1), an oncogenic lncRNA, has been documented in different types of malignancy, such as gastric cancer, colorectal cancer and hepatocellular carcinoma. In this regard, enforced expression of CCAT1 exerts potent tumorigenic effects by promoting cell proliferation, invasion and migration. Recent evidence has also shown that CCAT1 may serve as a prognostic cancer biomarker. In this review, we provide an overview of current evidence relating to the role and biological function of CCAT1 in tumour development.

Colon Cancer Associated Transcript-1 (CCAT1) Expression in Adenocarcinoma of the Stomach.

Background: Long non-coding RNAs (lncRNAs) have been shown to have functional roles in cancer biology and are dys-regulated in many tumors. Colon Cancer Associated Transcript -1 (CCAT1) is a lncRNA, previously shown to be significantly up-regulated in colon cancer. The aim of this study is to determine expression levels of CCAT1 in gastric carcinoma (GC).Methods: Tissue samples were obtained from patients undergoing resection for gastric carcinoma (n=19). For each patient, tumor tissue and normal appearing gastric mucosa were taken. Normal gastric tissues obtained from morbidly obese patients, undergoing laparoscopic sleeve gastrectomy served as normal controls (n=19). A human gastric carcinoma cell line (AGS) served as positive control. RNA was extracted from all tissue samples and CCAT1 expression was analyzed using quantitative real time-PCR (qRT-PCR).Results: Low expression of CCAT1 was identified in normal gastric mucosa samples obtained from morbidly obese patients [mean Relative Quantity (RQ) = 1.95±0.4]. AGS human gastric carcinoma cell line showed an elevated level of CCAT1 expression (RQ=8.02). Expression levels of CCAT1 were approximately 10.8 fold higher in GC samples than in samples taken from the negative control group (RQ=21.1±5 vs. RQ=1.95±0.4, respectively, p<0.001). Interestingly, CCAT1 expression was significantly overexpressed in adjacent normal tissues when compared to the negative control group (RQ = 15.25±2 vs. RQ=1.95±0.4, respectively, p<0.001). Tissues obtained from recurrent GC cases showed the highest expression levels (RQ = 88.8±31; p<0.001). Expression levels increased with tumor stage (T4- 36.4±15, T3- 16.1±6, T2- 4.7±1), however this did not reach statistical significance (p=0.2). There was no difference in CCAT1 expression between intestinal and diffuse type GC (RQ=22.4±7 vs. 22.4±16, respectively, p=0.9). Within the normal gastric tissue samples, no significant difference in CCAT1 expression was observed in helicobacter pylori negative and positive patients (RQ= 2.4±0.9 vs. 0.93±0.2, respectively, p=0.13).Conclusion: CCAT1 is up-regulated in gastric cancer, and may serve as a potential bio-marker for early detection and surveillance.