Serum MALAT1 Assumes Signifying Capacity in Gastric Cancer Diagnosis.
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Abstract Background: Gastric cancer (GC) represents one of the most serious cancers worldwide with the increasing mortality. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1), a kind of lncRNAs, has been reported to be involved in the progression of cancers. This study aimed to assess serum expression pattern of MALAT1 and its clinical significance in diagnosis of GC. Methods: Serum specimens were collected from 120 GC patients and 58 healthy individuals. The expression profile of MALAT1 was examined using quantitative real-time polymerase chain reaction (qRT-PCR), and its association with clinical parameters was estimated by chi-square test. The diagnostic value of MALAT1 in GC was evaluated by the receiver operating characteristic (ROC) analysis. Results: Upregulated expression of MALTA1 was found in GC patients compared with the healthy controls (P<0.05). The overexpression of MALAT1 was positively correlated with lymph node metastasis (P=0.041) and TNM stage (P=0.005). An area under the curve (AUC) was 0.897 in ROC analysis, suggesting the high diagnostic value of MALAT1. Conclusion: The expression of MALAT1 was upregulated in GC serum samples, and its expression might serve as a potential diagnostic biomarker in patients with GC.Keywords:
MALAT1
Clinical Significance
Gastric adenocarcinoma
Metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1), a well‑known lncRNA associated with numerous diseases, particularly cancer, has received increased attention. The expression of MALAT1 was determined to be upregulated in numerous types of tumors and MALAT1 exhibited effects on tumor cell proliferation, migration, invasion and apoptosis. The abnormal expression of MALAT1 was identified in almost in every organ of the digestive system. MALAT1 performed an important role in the pathological alterations of organs that are associated with sex hormones and several reproductive system cancers. MALAT1 participates in molecular pathways. In the clinical application of MALAT1, MALAT1 was considered as a potential biomarker for the diagnosis and prediction of cancers, and may also serve as therapeutic target for treatment of specific tumors. This review summarizes the abnormal expression of MALAT1 in cancer, its significant effect on the primary features of cancer, as well as the underlying molecular mechanisms of MALAT1 in various cancers. According to studies on MALAT1, we introduce the upstream and downstream substances associated with the function of MALAT1. These reviewed studies promote the clinical application of MALAT1 in the aspect of diagnosis and treatment of different cancers, and may help point out new study directions for MALAT1.
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Current studies have indicated that long non-coding RNAs (lncRNAs) could act as tumor biomarkers for disease diagnosis and prognosis prediction. In this study, we mainly focused on determining the expression of circulating lncRNAs in patients suffering for hilar cholangiocarcinoma (HC), aiming to reveal the potential lncRNA as a fingerprint.A total 12 lncRNAs were previously proven to be aberrantly expressed in HC tumor tissues. All of the 12 lncRNAs were selected as candidate targets for subsequent circulating lncRNA assay. The candidate lncRNAs were validated by qRT-PCR arranged in training and validation sets. The risk score analysis was employed. Data was presented with receiver operating characteristic curve (ROC).Circulating PCAT1, MALAT1, and CPS1-IT1 were significantly increased in plasma samples of HC patients in both the training set and validation set. Through ROC analysis, we found that the three plasmatic lncRNAs presented the area under ROC curve value (AUC) as 0.784, 0.860, and 0.677. Further combination with the three factors indicated a higher power (AUC, 0.893; sensitivity, 85.5%; specificity, 93.2%).This was the first time to reveal the potential circulating fingerprints for predicting HC. PCAT1, MALAT1, and CPS1-IT1 may act as novel early diagnosis biomarkers for predicting HC.
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Abstract Long non-coding RNAs (lncRNAs) play an important role in gene regulation and show greater tissue specificity and complexity of biological functions. There is on-going research in their contribution in autoimmune diseases like multiple sclerosis (MS). Our study aimed at the evaluation of serum levels of lncRNAs, MALAT1 and lnc-DC in MS patients and the investigation of the association between these lncRNAs and the disease activity. Serum from 45 MS patients and 45 healthy controls was separated. MALAT1 and lnc-DC expression levels were assayed by qRT-PCR. MALAT1 and lnc-DC were significantly increased in MS patients (P=0.004 and P=0.006, respectively) in comparison with controls. There was a significant increase in expression of MALAT1 in secondary progressive MS (SPMS) subgroup compared with controls (P<0.0001); however, significant elevation of lnc-DC was demonstrated in relapsing remitting MS (RRMS) subtype (P=0.003) compared with normal controls. A positive association between the expression levels of MALAT1 and lnc-DC (r = 0.513, P < 0.0001) in MS patients was detected. Moreover, positive correlation was observed between MALAT1and lnc-DC in RRMS (r = 0.569, P = 0.001). Serum levels of MALAT1 and lnc-DC may serve as potential novel molecular biomarkers for MS diagnosis and may provide a new direction for its treatment.
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Non-coding RNAs are becoming major players in disease pathogenesis such as cancer. Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a nuclear enriched long non-coding RNA that is generally overexpressed in patient tumors and metastases. Overexpression of MALAT1 has been shown to be positively correlated with tumor progression and metastasis in a large number of tumor types including breast tumors. Surprisingly, a recent report by Kim et al shows a metastasis suppressive role for Malat1. Here, we discuss these results in the context of a large body of published literature that support a pro-tumorigenic role for MALAT1 in order to gain potential insights into the basis of these observed differences.
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The mammalian genome is pervasively transcribed and the functional significance of many long non-coding RNA (lncRNA) transcripts are gradually being elucidated. Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is one of the most well-studied lncRNAs. MALAT1 is a highly conserved nuclear retained lncRNA that is abundantly expressed in cells and tissues and has been shown to play a role in regulating genes at both the transcriptional and post-transcriptional levels in a context-dependent manner. However, Malat1 has been shown to be dispensable for normal development and viability in mice. Interestingly, accumulating evidence suggests that MALAT1 plays an important role in numerous diseases including cancer. Here, we discuss the current state-of-knowledge in regard to MALAT1 with respect to its function, role in diseases, and the potential therapeutic opportunities for targeting MALAT1 using antisense oligonucleotides and small molecules.
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Background/Aims: LncRNAs have been reported to be vital regulators of the progression of osteosarcoma, although the underlying mechanisms are not completely understood. Methods: The levels of MALAT1 and miR-129-5p expression were measured using qRT-PCR. Cell growth was determined using the CCK-8 and colony formation assays. Cell migration and invasion were detected using the wound healing and Transwell invasion assays, respectively. Tumor growth was determined with a xenograft model. Results: MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. Overexpression of MALAT1 promoted osteosarcoma cell proliferation, migration, and invasion in vitro and enhanced tumor growth in a tumor xenograft mouse model. MALAT1 promoted osteosarcoma progression by modulating stem cell-like properties. Moreover, rescue experiment and luciferase reporter assay results indicated that MALAT1 modulates RET expression by sponging miR-129-5p in osteosarcomas. Furthermore, MALAT1 augmented the expression of downstream proteins of the RET-Akt pathway. MALAT1 was consistently significantly increased in osteosarcoma tissues and MALAT1 expression was positively correlated with tumor size and metastasis. High expression of MALAT1 was significantly associated with poor outcomes in patients with osteosarcomas. MALAT1 expression was positively related to RET and negatively related to miR-129-5p in osteosarcoma samples and xenograft tumors. MALAT1 functioned as an oncogenic lncRNA in osteosarcomas and was as an independent prognostic indicator. Conclusion: Our data revealed for the first time that MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway and provides potential therapeutic targets for osteosarcoma treatment.
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Mounting evidence shows that the long non-coding RNA MALAT1 plays a pivotal role in tumorigenesis and metastasis, but the functional significance of MALAT1 in bladder transitional cell carcinoma (BTCC) remains unclear. MALAT1 expression was measured in 56 BTCC patients and 2 BTCC cell lines by real-time PCR. The effects of MALAT1 on BTCC cells were investigated by over-expression approaches
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Malat1 is a long noncoding RNA with a wide array of functions, including roles in regulating cancer cell migration and metastasis. However, the nature of its involvement in control of these oncogenic processes is incompletely understood. In the present study, we investigate the role of Malat1 and the effects of Malat1 KO in a breast cancer cell model. Our selection of Malat1 as the subject of inquiry followed initial screening experiments seeking to identify lncRNAs which are altered in the presence or absence of Nischarin, a gene of interest previously discovered by our lab. Nischarin is a well characterized tumor suppressor protein and actively represses cell proliferation, migration, and invasion in breast cancer. Our microarray screen for lncRNAs revealed multiple lncRNAs to be significantly elevated in cells ectopically expressing Nischarin compared to control cancer cells, which have only marginal Nisch expression. Using these cells, we assess how the link between Nischarin and Malat1 affects cancer cell function, finding that Malat1 confers an inhibitory effect on cell growth and migration which is lost following Malat1 KO, but in a Nisch-dependent context. Specifically, Malat1 KO in the background of low Nischarin expression had a limited effect on cell functions, while Malat1 KO in cells with high levels of Nischarin led to significant increases in cell proliferation and migration. In summary, this project provides further clarity concerning the function of Malat1, specifically in breast cancer, while also indicating that the Nischarin expression context is an important factor in the determining how Malat1 activity is governed in breast cancer.
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