lncRNA Colon Cancer-associated Transcript 2 Research Articles

LncRNA CCAT2 expression at diagnosis predicts imatinib response in chronic phase chronic myeloid leukemia patients

Long noncoding RNAs (lncRNAs) are identified as key players in the initiation, development, and prognosis of chronic myeloid leukemia (CML). Some lncRNAs are expected to serve as diagnostic biomarkers, predictors of clinical outcomes and therapeutic targets. We aimed to examine the expression of lncRNA colon cancer-associated transcript 2 (CCAT2) in CML patients, as well as to correlate CCAT2 expression with response to imatinib therapy. 43 newly diagnosed patients with chronic phase CML were included, and 30 healthy persons were selected as controls. Real-time reverse transcription PCR was performed to analyze the expression of CCAT2 in peripheral blood mononuclear cells. Our results reported for the first time the upregulated expression of CCAT2 in CML patients as compared with controls (P < 0.001). We demonstrated significant association between CCAT2 expression and therapy response at 3 months, and at 6 months (P = 0.004, and P = 0.005; respectively). Moreover, CCAT2 expression was significantly associated with spleen size (P = 0.006) and EUTOS sore (P = 0.030). LncRNA CCAT2 is highly expressed in the peripheral blood of CML patients, and the enhanced expression at diagnosis is linked to imatinib resistance. CCAT2 is expected to become a reliable molecular marker for predicting imatinib response in chronic phase CML patients.

Expression of lncRNA CCAT2 in children with neuroblastoma and its effect on cancer cell growth.

The aim of this study was to determine the expression of long-chain non-coding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) in children with neuroblastoma and its effect on cancer cell growth. A polymerase chain reaction assay was carried out to quantify lncRNA CCAT2 miRNA in neuroblastoma cells, corresponding paracancerous cells, SH-SY5Y and SK-N-SH cells, and human umbilical vein endothelial cells (HUVEC), and two groups of children with different lncRNA CCAT2 expression were compared in clinical pathological parameters and prognosis. CCAT2-NC and si-CCAT2 were transfected into SH-SY5Y cells, separately. Then a 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay was carried out to analyze the cell proliferation, migration, and invasion ability, a flow cytometry to detect cell apoptosis, and a Western blotting (WB) assay to quantify p53 and Bcl-2 proteins. lncRNA CCAT2 expression in cancer tissues of children with neuroblastoma was notably higher than that in corresponding paracancerous tissues (P < 0.05), and children with different tissue differentiation, tumor staging, and lymph node metastasis (LNM) showed notably different lncRNA CCAT2 expression (P < 0.05). In addition, children with neuroblastoma in the high lncRNA CCAT2 expression group showed lower 3-year survival rate than those in the low expression group (P < 0.05). Multivariate analysis revealed that tissue differentiation, tumor-node-metastasis staging, LNM, and lncRNA CCAT2 expression were all independent risk factors affecting the prognosis of children with neuroblastoma (all P < 0.05). Compared with HUVEC cells, SH-SY5Y and SK-N-SH cells showed notably up-regulated lncRNA CCAT2, and the expression of it in SH-SY5Y was higher than that in SK-N-SH cells (P < 0.05). Compared with the CCAT2-NC group, the si-CCAT2 group presented notably down-regulated CCAT2 (P < 0.05). Moreover, according to the MTT assay, the si-CCAT2 group showed notably weakened cell viability and proliferation than the CCAT2-NC group (both P< 0.05), and SH-SY5Y cells in the former group were less active than those in the latter group in terms of migration and invasion. The cell apoptosis rate of SH-SY5Y cells in the si-CCAT2 was higher than that in the CCAT2-NC. The results suggested that knock down of lncRNA CCAT2 could improve the apoptosis activity of neuroblastoma cells in children. According to the WB assay, the si-CCAT2 group showed notably higher p53 expression and notably lower Bcl-2 protein expression than the CCAT2-NC group (both P < 0.05). LncRNA CCAT2 can inhibit the proliferation of neuroblastoma cells and promote their apoptosis, which provides a basis for the treatment of neuroblastoma.

Erratum.

Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) has been demonstrated to play an important role in diverse tumorigenesis. However, the biological function of lncRNAs in glioma is still unknown. In this study, we found that lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration, and invasion, as well as induced early apoptosis of glioma cells in vitro. Moreover, lncRNA CCAT2 regulated epithelial–mesenchymal transition (EMT)-associated gene expression. In conclusion, lncRNA CCAT2 plays an important role in glioma tumorigenesis and progression and may act as a potential biomarker for therapeutic strategy and prognostic prediction.

Long non-coding RNA colon cancer associated transcript-2 from nasopharyngeal carcinoma-derived exosomes promotes angiogenesis

Objective: To evaluate the role of exosomal long non-coding RNA (lncRNA) colon cancer associated transcript-2(CCAT2) in angiogenesis in nasopharyngeal carcinoma(NPC). Methods: Human umbilical vein endothelial cells (HUVECs) were divided into CNE2 supernatant coculture group and NP69 supernatant coculture group. The proliferation ability of HUVEC in each group was examined by CCK8. The lncRNA CCAT2 level in HUVEC was detected using real-time fluorescent quantitative PCR (qRT-PCR). HUVECs were divided into coculture group of serum in patients with NPC and coculture group of serum in healthy donors. The proliferation ability of HUVEC in each group was examined by CCK8. The lncRNA CCAT2 level in each group was detected using qRT-PCR. Exosomes from CNE2,NP69 supernatant were obtained by ultracentrifugation. HUVECs were divided into coculture group of CNE2's supernatant exosomes and coculture group of NP69's supernatant exosomes. Biological experiments like CCK8 were conducted to compare the angiogenesis ability of HUVEC in each group. shRNA transfection was used in HUVEC to suppress the expression of lncRNA CCAT2. Biological experiments like CCK8were conducted to compare the HUVEC's function with different expression of lncRNA CCAT2. CNE2 was transfected with shRNA, the total supernatant exosomal RNA was extracted, and the difference of exosomal lncRNA CCAT2 in CNE2 supernatant with low expression and normal expression of lncRNA CCAT2 was detected by qRT-PCR. The above mentioned two groups of exosomes were cocultured with HUVEC respectively. The difference of lncRNA CCAT2 expression in each group's HUVEC was detected by qRT-PCR and the function of HUVEC was examined with migration assay. GraphPad Prism 8 software was used for graphing and statistical analysis. Results: Compared with those in the NP69 supernatant coculture group, HUVECs in the CNE2 supernatant coculture group showed a higher proliferation ability and higher expression of lncRNA CCAT2(1 vs. 1.40±0.01, t=42.23, P=0.000). Compared with those in serum of healthy donors, HUVECs in serum of patients with NPC showed a higher proliferation ability and the expression of lncRNA CCAT2 increased (1 vs. 1.25±0.03, t=14.43,P=0.001). Compared with those in the coculture group of NP69 cells' supernatant exosomes, HUVEC in the coculture group of CNE2 cells' supernatant exosomes showed a higher proliferation ability and there were more cells that had passed the well during the migration experiment (53.12±2.13 vs. 154.74±4.17, t=37.73, P=0.000) and more knots formed in the tube-formation experiment(10.72±1.02 vs. 53.65±3.21, t=22.63, P=0.000). Compared with those in the sh-NC group, HUVEC in the sh-CCAT2 group showed a lower proliferation ability, and there were less cells that had passed the cell during the migration experiment(401.34±22.15 vs.138.25±6.85, t=23.19, P=0.000) and less MVC in the experiment of subcutaneous stroma embolization in nude mice(41.00±0.32 vs. 27.15±0.23, t=61.53, P=0.000). Compared with the supernatant exosomes in the sh-NC exosome group, the expression of lncRNA CCAT2 was lower in the supernatant exosomes of sh-CCAT2 group (1 vs. 0.65±0.02, t=30.31, P=0.000). Compared with those of the exosomes of sh-NC exosome group, the expression of lncRNA CCAT2 was lower in the HUVEC cocultured with exosomes of the sh-CCAT2 exosome group (1 vs. 0.73±0.01, t=46.77, P=0.000) and the exosomes of sh-CCAT2 exosome group showed a lower migration ability (389.73±26.34 vs. 190.54±8.36, t=12.47, P=0.001) after cocultured with HUVEC. Conclusion: Nasopharyngeal carcinoma-derived exosomal lncRNA CCAT2 could promote angiogenesis.

Vitamin D Suppresses Ovarian Cancer Growth and Invasion by Targeting Long Non-Coding RNA CCAT2.

Ovarian cancer is the most deadly gynecologic cancer among women worldwide. Poor response to current treatment makes it necessary to discover new diagnostic biomarkers to detect the cancer early and develop new and effective prevention strategies. Calcitriol, the active metabolite of vitamin D, protects against multiple cancers through unelucidated mechanisms. The oncogenic long non-coding RNA (lncRNA) CCAT2 (colon cancer associated transcript 2) is overexpressed in ovarian cancer. Here, we foundd that calcitriol inhibited CCAT2 expression in ovarian cancer cell lines. Treatment with calcitriol inhibited ovarian cancer cell proliferation, migration, and invasion. As a result of CCAT2 inhibition, calcitriol decreased the binding of transcription factor TCF7L2 (TCF4) to the MYC promoter, resulting in the repression of c-Myc protein expression. Our results suggest a novel anti-cancer mechanism of vitamin D by targeting CCAT2 in ovarian cancer. The findings may help develop vitamin D as a practical and inexpensive nutraceutical for ovarian cancer prevention.

Increased expression of long non-coding RNA CCAT2 predicts poorer prognosis in patients with hepatocellular carcinoma.

Background:Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is a 1752-bp lncRNA transcribed from m8q24 genomic region. A lot of investigations have confirmed the involvement of CCAT2 in the tumorigenesis of many cancer types. Previous studies found that over-expression of CCAT2 significantly promoted cell migration and proliferation, and inhibited apoptosis of HCC cells. In the present investigation, the clinical value and prognostic significance of CCAT2 were investigated.Methods:The 122 pairs of HCC tissues and adjacent normal liver tissues were acquired between September 2013 and February 2018. The expression levels of CCAT2 in HCC tissues and their corresponding adjacent normal liver tissues were examined by RT-qPCR analysis. Survival was calculated using the Kaplan-Meier method and analyzed using the log-rank test. Independent prognostic indicators were determined in the multivariate analysis using Cox's proportional hazard model.Results:CCAT2 expression levels were significantly increased in HCC tissues compared to that in their normal counterparts (P < .001). CCAT2 expression was significantly correlated with vascular invasion (P = .001), histopathologic grading (P = .001), distant metastasis (P = .002) and TNM stage (P = .018). A Kaplan–Meier survival curve showed that the overall survival rate of HCC patients in high CCAT2 expression group markedly decreased as compared with that of low CCAT2 expression group (P = .016). In addition, COX multivariate analysis showed that high expression of CCAT2 was an independent risk factor for predicting shorter overall survival time in HCC (HR = 2.126, 95%CI:1.273–8.775, P = .021).Conclusions:Taken together, this research revealed that lncRNA CCAT2 may serve as a potential biomarker for predicting overall survival time in HCC.

Long non-coding RNA colon cancer-associated transcript 2 may promote esophageal cancer growth and metastasis by regulating the Wnt signaling pathway.

The aim of this study was to investigate how long non-coding (lnc)RNA colon cancer-associated transcript 2 (CCAT2) regulates the proliferation, invasion and metastasis of esophageal cancer cells via the Wnt signaling pathway. The expression of lncRNA CCAT2 was quantified by reverse transcription-quantitative PCR in four esophageal cancer cell lines (Eca-109, EC9706, KYSE150 and TE-1) and normal human esophageal epithelial cells (HEECs). The effect of silencing CCAT2 (si-CCAT2) and inhibiting Wnt signaling (using the inhibitor FH535) on the proliferation, migration and invasion of Eca-109 cells was measured by MTT, wound-healing and Transwell invasion assays. Flow cytometry was used to evaluate apoptosis in si-CCAT2 Eca-109 cells. The expression of β-catenin and proliferating cell nuclear antigen (PCNA) proteins was detected by immunohistochemistry. The pro-apoptotic protein Bax, cyclin D1 and Wnt target proteins, including c-Myc and adenomatous polyposis coli (APC), were detected by western blotting. LncRNA CCAT2 was highly expressed in the four esophageal cancer cell lines compared with the HEEC cells. The expression of CCAT2 was significantly decreased in si-CCAT2 Eca-109 cells. Treatment with si-CCAT2 and FH535 alone or in combination significantly inhibited the proliferation, migration and invasion of Eca-109 cells. The treatments also promoted apoptosis, upregulated the expression of Bax and APC proteins, and downregulated β-catenin, PCNA, cyclin D1 and c-Myc proteins. In summary, lncRNA CCAT2 is upregulated in esophageal cancer cells and the knockdown of lncRNA CCAT2 inhibits their proliferation, migration and invasion via the Wnt signaling pathway.

The lncRNA CCAT2 rs6983267 G allele is associated with decreased susceptibility to recurrent miscarriage.

Genetics might play various roles in susceptibility to recurrent miscarriage, and previous studies suggest that some gene polymorphisms might be associated with abortion and breast cancer onset. Colon cancer-associated transcript 2 (CCAT2) is a novel long noncoding RNA (lncRNA) transcript that might be correlated with susceptibility to multiple cancers, including breast cancer. However, whether lncRNA CCAT2 polymorphisms are related to susceptibility to recurrent miscarriage is unclear. We genotyped two lncRNA CCAT2 polymorphisms (rs6983267 and rs3843549) in 248patients with recurrent miscarriage and 392 controls through a TaqMan real-time polymerase chain reaction assay, and the strength of each association was evaluated via 95% confidence intervals (CIs) and odds ratios (ORs). Our results showed that the rs6983267 G allele in lncRNA CCAT2 was associated with decreased susceptibility to recurrent miscarriage (TG vs. TT: adjusted OR = 0.603; 95% CI = 0.420-0.866; p = 0.0062; GG/TG vs. TT: adjusted OR = 0.620; 95% CI = 0.441-0.873; p = 0.0061). The combined analysis of the two protective polymorphisms (rs3843549 AA and rs6983267 TG/GG) revealed that individuals with two unfavorable alleles exhibited a lower risk of recurrent miscarriage than those with no or only one unfavorable allele (adjusted OR = 0.531; 95% CI = 0.382-0.739). Moreover, the decreased risk associated with the two protective alleles was most obvious in women aged less than 35 years (OR = 0.551; 95% CI = 0.378-0.8803; p = 0.0019) and in women with two to three miscarriages (adjusted OR = 0.466; 95% CI = 0.318-0.683; p < 0.0001). In conclusion, our study indicates that the rs6983267G allele might contribute to a decreased risk of recurrent miscarriage in the South Chinese population.

LncRNA CCAT2 enhances cell proliferation via GSK3β/β-catenin signaling pathway in human osteosarcoma.

Osteosarcoma(OS) is a kind of malignant bone tumor. The aim of the manuscript is to investigate the clinical significance and the functional effects of long non-coding (lncRNA) coloncancer-associated transcript 2 (CCAT2) in osteosarcoma. Expression of CCAT2 was detected by quantitative Real-time PCR (qRT-PCR) in 50 cases of osteosarcoma tissue samples and adjacent normal bone tissues. Kaplan-Meier survival analysis and log-rank test were used to assess the association between CCAT2 expression and prognosis of OS patients. Cell Counting Kit 8 and cell colony formation assays were performed to evaluate cell proliferation. The protein expression of PCNA, p-GSK3β, GSK3β, and β-catenin were analyzed using Western blot analysis. We demonstrated that lncRNA CCAT2 expression was significantly upregulated in OS tissues compared to adjacent normal bone tissues. Higher lncRNA CCAT2 expression positively associated with larger tumor size, advanced tumor stage and poor overall survival (OS) rate of patients. In vitro, knockdown of lncRNA CCAT2 suppressed cell proliferation and colony formation ability. In contrast, overexpression of lncRNA CCAT2 showed promoting cell proliferation effects in OS. Also, we found that knockdown of lncRNA CCAT2 inhibited GSK3β/β-catenin signaling by reducing p-GSK3β and β-catenin expression, but increasing GSK3β expression. Our results showed that CCAT2 is a crucial oncogene in OS and may be a potential therapeutic target of OS.

LncRNA CCAT2 promoted osteosarcoma cell proliferation and invasion.

Long non‐coding RNA (lncRNA) plays important roles in tumour progression. Accumulating studies demonstrated that lncRNA colon cancer‐associated transcript 2 (CCAT2) acted as an oncogene in many tumours. However, the role of CCAT2 in the development of osteosarcoma has not been elucidated. In our study, we indicated that CCAT2 expression was up‐regulated in osteosarcoma tissues and cell lines (SOSP‐9607, MG‐63, U2OS and SAOS‐2). In addition, osteosarcoma cases with higher CCAT2 expression had a poorer disease‐free survival and shorter the overall survival time compared to those with lower expression. Overexpression of CCAT2 promoted osteosarcoma cell proliferation, invasion and cell cycle. Furthermore, ectopic expression of CCAT2 increased the expression of mesenchymal markers N‐cadherin, vimentin and snail and reduced the expression of N‐cadherin marker E‐cadherin. CCAT2 overexpression promoted the LATS2 and c‐Myc expression in osteosarcoma cell. These data indicated that CCAT2 served as an oncogene in osteosarcoma and promoted osteosarcoma cell proliferation, cell cycle and invasion.

Long non-coding RNA CCAT2 promotes cholangiocarcinoma cells migration and invasion by induction of epithelial-to-mesenchymal transition

Cholangiocarcinoma (CCA) is one of the most aggressive malignancies in humans. Emerging evidence has indicated that abnormally expressed long non-coding RNAs (lncRNAs) could conduce to tumorigenesis and progression. Specifically, colon cancer-associated transcript 2 (CCAT2) has been reported to be overexpressed in several carcinomas. However, its clinical significance and functional roles in CCA is still unknown. qRT-PCR experiments were conducted to assess the CCAT2 expression in CCA tissue samples and cell lines. In addition, the link between CCAT2 expression and clinicopathological characteristics was analyzed. The potential effects of CCAT2 in CCA cells was evaluated in vitro including cell proliferation, colony-forming ability, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT). As a result, CCAT2 was aberrantly overexpressed in CCA tissue samples and cells, and this upregulation was correlated with tumor size, lymph node invasion, TNM stage and postoperative recurrence in CCA patients. Overexpression of CCAT2 could serve as an independent prognostic indicator for CCA. Additionally, overexpression of CCAT2 was a dismal prognostic indicator for patients with CCA. Furthermore, CCAT2 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion, inducing cell apoptosis and reversing the EMT process in HuCCT1 and CCLP1 cells. Collectively, our data illustrated that lncRNA CCAT2 played an oncogenic role in CCA and may offer a potential therapeutic target for treating this fatal disease.

Knockdown of lncRNA CCAT2 inhibits endometrial cancer cells growth and metastasis via sponging miR-216b.

Colon cancer-associated transcript 2 (CCAT2), a novel lncRNA has been reported as an oncogene in several cancers. This study was aimed to explore whether CCAT2 also exerted oncogenic roles in endometrial cancer cells. The expression of CCAT2 in 30 pairs of endometrial cancer and matched non-cancerous tissues were detected by qRT-PCR. Two endometrial cancer cell lines HEC-1-A and RL95-2 were used throughout this study. CCAT2 in cells was silenced by transfection with shRNA targeted CCAT2, then cell growth and metastasis were assessed by performing trypan blue staining, Transwell assay, and flow cytometry. Dual-luciferase reporter assay was used to detect the combination of miR-216b and CCAT2. Besides, the expression of miR-216b and Bcl-2 in cells were overexpressed or suppressed by transfection with their correspondingly mimic/vector or inhibitor/shRNA. qRT-PCR and western blot analysis were performed to detect the expression of Bcl-2 and main factors in PTEN/PI3K/AKT and mTOR signaling pathways. CCAT2 was highly expressed in endometrial cancer tissues when compared to non-cancerous endometrial tissues. Knockdown of CCAT2 inhibited HEC-1-A and RL95-2 cells viability, migration, invasion, but induced apoptosis. CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways. To conclude, these results demonstrated lncRNA CCAT2 was highly expressed in endometrial cancer tissues. Knockdown of CCAT2 inhibited cell growth and metastasis of endometrial cancer cells by sponging miR-216b.

Overexpression of long non-coding RNA colon cancer-associated transcript 2 is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer.

The aim of the present study was to explore the clinicopathological and prognostic significance of long non-coding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) expression in human colorectal cancer (CRC). Expression levels of lncRNA CCAT2 in CRC, adjacent non-tumor and healthy colon mucosa tissues were detected by quantitative polymerase chain reaction. The disease-free survival and overall survival rates were evaluated using the Kaplan-Meier method, and multivariate analysis was performed using Cox proportional hazard analysis. The expression level of lncRNA CCAT2 in CRC tissues was increased significantly compared with adjacent normal tissues or non-cancerous tissues. CCAT2 expression was observed to be progressively increased between tumor-node-metastasis (TNM) stages I and IV. A high level of CCAT2 expression was revealed to be associated with poor cell differentiation, deeper tumor infiltration, lymph node metastasis, distance metastasis, vascular invasion and advanced TNM stage. Compared with patients with low levels of CCAT2 expression, patients with high levels of CCAT2 expression had shorter disease-free survival and overall survival times. Multivariate analyses indicated that high CCAT2 expression was an independent poor prognostic factor. Therefore, increased lncRNA CCAT2 expression maybe a potential diagnostic biomarker for CRC, and an independent predictor of prognosis in patients with CRC.

Knockdown of Long Noncoding RNA CCAT2 Inhibits Cellular Proliferation, Invasion, and Epithelial-Mesenchymal Transition in Glioma Cells.

Long noncoding RNA (lncRNA) colon cancer-associated transcript 2 (CCAT2) has been demonstrated to play an important role in diverse tumorigenesis. However, the biological function of lncRNAs in glioma is still unknown. In this study, we found that lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration, and invasion, as well as induced early apoptosis of glioma cells in vitro. Moreover, lncRNA CCAT2 regulated epithelial–mesenchymal transition (EMT)-associated gene expression. In conclusion, lncRNA CCAT2 plays an important role in glioma tumorigenesis and progression and may act as a potential biomarker for therapeutic strategy and prognostic prediction.

LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) remains one of the most important death-related diseases, with poor effective diagnosis and less therapeutic biomarkers. LncRNA colon cancer-associated transcript 2 (CCAT2) was identified as an oncogenic lncRNA and over-expressed in many tumor cells. The aims of this study were to detect the correlation between CCAT2 and its regulatory genes and then explore the potential mechanism between them in NSCLC. In this study, qRT-PCR was used to detect CCAT2, Pokemon and p21 expression. Western-blot was used to detect protein levels of Pokemon and p21. CCK-8 assay and Transwell chambers were used to assess cell viability and invasion. CCAT2 and Pokemon were over-expressed in NSCLC tissue and cells. In NSCLC cells, CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21; then CCAT2 overexpression revealed an opposite result. In addition, over-expressed Pokemon reversed the results that induced by si-CCAT2, while down-regulation of Pokemon significantly reversed the results that induced by CCAT2 overexpression. The results indicated that CCAT2 promotes tumorigenesis by over-expression of Pokemon, and the potential mechanism might relate to the Pokemon related gene p21.

The long non-coding RNA CCAT2 is up-regulated in ovarian cancer and associated with poor prognosis.

BackgroundOvarian cancer is a malignant tumor with a poor prognosis. Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are emerging regulators in cancer biology, and can be used as potential biomarkers for cancer diagnosis, prognosis and targeted therapy. The lncRNA CCAT2 (colon cancer associated transcript 2) was recently shown to be involved in several cancers; however, its role in ovarian cancer remains unknown.MethodsExpression levels of the lncRNA CCAT2 in ovarian cancer tissues, adjacent normal tissues, and cell lines were assessed by quantitative real-time PCR. Then, the associations of CCAT2 expression levels with clinicopathological features and prognosis were evaluated. In addition, CCAT2 functions in tumor progression and invasion were further determined by siRNA-induced CCAT2 silencing in vitro.ResultsExpression levels of the lncRNA CCAT2 in ovarian cancer tissues and cell lines were significantly higher compared with values obtained for adjacent non-tumor tissues and normal ovarian epithelial cells. Interestingly, higher CCAT2 expression levels were associated with a shorter overall survival (P = 0.006) and disease-free survival (P = 0.001) in ovarian cancer patients. In addition, CCAT2 expression was positively correlated with FIGO stage (P = 0.002), tumor grade (P = 0.006) and distant metastasis (P < 0.001). Moreover, CCAT2 knockdown in ovarian cancer cells markedly suppressed cell proliferation, migration, and invasion.ConclusionsThe lncRNA CCAT2 is a novel factor involved in ovarian cancer progression, and constitutes a potential prognostic biomarker and therapeutic target for patients with ovarian cancer.

LncRNA CCAT2 predicts poor prognosis and regulates growth and metastasis in small cell lung cancer.

LncRNA colon cancer-associated transcript 2 (CCAT2) was firstly discovered and found overexpressed in colorectal cancer, and identified as is oncogenic lncRNA. However, the significance of CCAT2 in small cell lung cancer (SCLC) remains unclear. The expression of CCAT2 in SCLC tissues and cell lines was detected, and the association between CCAT2 expression and clinicopathological factors was analyzed. Cell proliferation and invasion assays were conducted by using SCLC cell lines transfected with CCAT2-siRNA or NC-siRNA. In our results, CCAT2 expression was elevated in SCLC tissues and cell lines, and correlated with malignant status and poor prognosis of SCLC patients. Furthermore, knockdown of CCAT2 expression effectively suppressed SCLC cell growth and metastasis in vitro. In conclusion, CCAT2 serves as an oncogenic lncRNA, and an independent unfavorable prognostic factor in SCLC patients.