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The occurrence and development of breast cancer is a complicated process, in which many kinds of bioactive substances are involved. As a long non-coding RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) not only plays a role in multiple sites of breast cancer, but also plays an important role in the treatment and prognosis evaluation of breast cancer patients. This article reviews the research progress of MALAT1 in breast cancer.
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Objective:To investigate the correlations between expression of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), nuclear-enriched abundant transcript 1 (NEAT1) and their functions on exosome secretion, proliferation and invasion in hepatocellular carcinoma (HCC).Methods:We used small interfering RNA of MALAT1 (si-MALAT1) to knockdown MALAT1 in HuH-7. At the meanwhile, cells which were transfected with si-NC were used as the negative control group. Expression of NEAT1, cell proliferation and invasion function were detected these two groups. HuH-7 cells were transfected with lentivirus NEAT1 over expressing vector (lv-NEAT1) or negative control (lv-control). Expression of exosomes secretion related genes were analyzed between lv-NEAT1 and lv-control groups. Cells of lv-NEAT1 were knockdown MALAT1 expression using si-MALAT1, which could be si-MALAT1+ lv-NEAT1 group. exosomes secretion was detected in si-NC, si-MALAT1 and si-MALAT1+ lv-NEAT1 group. We treated cells (si-MALAT1 group) with exosomes from cells with lv-NEAT1 or lv-control to divide cells as si-MALAT1+ exosomes of lv-NEAT1 cells and si-MALAT1+ exosomes of lv-control groups. Cell proliferation and invasion of cells were detected in two groups.Results:Low expression of NEAT1 were found in MALAT1 knockdown cells compared with si-NC group [(0.72±0.02) vs. (0.98±0.01), P<0.05]. Cells with MALAT1 knockdown shown diminished proliferation [(0.66±0.03) vs. (0.98±0.04), P<0.05)] and invasion [(88.33±7.26) vs. (147.70±13.62), P<0.05)]. Compared with si-NC group, CD9 and CD63 expression were decreased in exosomes of si-MALAT1 group. Compared with si-MALAT1 group, CD9 and CD63 expression was increased in exosomes of si-MALAT1+ lv-NEAT1 group. Compared with si-MALAT1+ exosomes of lv-control group, proliferation [(0.97±0.03) vs. (0.74±0.05), P<0.05)] and invasion [ (132.70±7.36) vs. (98.33±6.01), P<0.05) ] were increased in si-MALAT1+ exosomes of lv-NEAT1 group. Exosomes related genes expression including HSPA8 (5.53±0.31), SLC3A2 (0.32±0.07) and SLC7A5 (0.77±0.45) were changed in lv-NEAT1 group compared with lv-control group [(0.98±0.15), P<0.05]. Conclusion:MALAT1 induced exosomes secretion by NEAT1 and exosomes related genes regulation. This regulation might be related with increased proliferation and invasion function in HCC cells with MALAT1 and NEAT1 abnormal expression.
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Objective:To investigate the expression of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) in bronchopulmonary dysplasia (BPD) of neonatal rats induced by hyperoxia and its effect on alveolar type 2 epithelial cells (AEC Ⅱ).Methods:The lung injury model of neonatal SD rats induced by hyperoxia(model group, n=50, inhaled oxygen concentration of 80%-85%) and the control group(inhaled air, n=50) were prepared.Lung tissue samples were taken and retained on days 1, 3, 7, 14 and 21, and the physiological and pathological changes of lung tissue were detected by paraffin-embedded sections and hematoxylin-eosin staining; The dynamic expression of lncRNA MALAT1 in lung tissue was detected by real-time fluorescent quantitative polymerase chain reaction; The dynamic expression of surfactant protein C(SPC) in lung tissue and AECⅡ was detected by Western blot.AECⅡ was extracted from lung tissue of normal newborn rats, and lncRNA MALAT1 was knocked down by siRNA.The cells were collected and Western blot as well as immunofluorescence were used to detect the changes of SPC. Results:The lung tissue of model group gradually became thickened with alveolar compartments, and the alveolar cavity was enlarged with the disappearance of alveolar spine and other pathological structural changes.Compared with the control group, there was no difference in the expression of lncRNA MALAT1 and SPC in the lung tissue from model group on days 1, 3( P>0.05), but the expression of lncRNA MALAT1 and SPC significantly increased on days 7, 14 and 21( P<0.05). When lncRNA MALAT1 was inhibited, SPC expression showed a decrease trend. Conclusion:Hyperoxia can lead to the stagnation of lung development in neonatal rats, and the structure and function of alveolar disorders are impaired.The expression of lncRNA MALAT1 is involved in the process of hyperoxia-induced BPD in neonatal rats.The increase of lncRNA MALAT1 may promote the proliferation of AECⅡ.
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@#Metastasis-associated lung adenocarcinoma transcript 1(MALAT1)is one of the first identified LncRNA associated with human diseases. Unlike most members of the LncRNA family, MALAT1 is found in almost all human tissues and expressed at a relatively high level. At present, MALAT1 is known to play a vital role in the pathophysiological process of many diseases such as tumors, cardiovascular diseases, and nervous system diseases. In recent years, studies have found that MALAT1 may be involved in many ocular diseases(such as diabetic retinopathy, cataracts, glaucoma, retinoblastoma, neonatal retinopathy, <i>etc</i>.)play an important role in the pathological development process, and it is expected to become an effective target for the diagnosis and treatment of eye diseases. This article summarizes the research progress of eye diseases in which MALAT1 has participated in recent years.
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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in the development of various tumors. Recent studies have shown that MALAT1 is highly expressed in hematological tumors and can participate in development, progression and prognosis of hematological tumors at transcriptional and post-transcriptional levels as a competitive endogenous RNA. Therefore, MALAT1 might be a novel marker as a valuable basis for the diagnosis, treatment and prognosis evaluation of hematological tumors.
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BACKGROUND: Previous study demonstrated that hypoxia preconditioning promoted mesenchymal stem cells survival and their therapeutic efficacy, and this effect was mediated by hypoxia induced factor-1α (HIF-1α). However, specific downstream mechanism remained unclear. OBJECTIVE: To observe the influence of hypoxia preconditioning on the survival and vascularization potential of bone marrow mesenchymal stem cells in vitro and explore the regulatory mechanism of HIF-1α/MALAT1/VEGFA pathway. METHODS: Bone marrow mesenchymal stem cells were obtained and cultured in vitro. Cells were divided into hypoxia (1% O2) and normoxia control groups (20% O2), and cultured for 24 hours. Cells proliferation, apoptosis and vascularization were evaluated. The expression of HIF-1α, MALAT1, and VEGFA was detected. HIF-1α and MALAT1 were inhibited by their siRNAs separately. HIF-1α siRNA scramble and MALAT1 siRNA scramble were used as negative controls before hypoxia preconditioning. Alterations of the molecules were examined and compared in different groups. RESULTS AND CONCLUSION: (1) Compared with the normoxia control group, cell viability was significantly enhanced; and cell apoptosis percentage was significantly declined in the hypoxia group; vascular lumen like structure was also increased significantly in the hypoxia group (P < 0.01); expression of HIF-1α, MALAT1, and VEGFA was significantly increased in the hypoxia group (P < 0.01). (2) After the inhibition of HIF-1α and hypoxia preconditioning, both MALAT1 and VEGFA expression levels were significantly reduced (P < 0.01). The expression of VEGFA was also significantly suppressed after the blockage of MALAT1 (P < 0.01). (3) This study suggested that hypoxia preconditioning effectively promoted bone marrow mesenchymal stem cell survival and vascularization through the activation of HIF-1α/MALAT1/VEGFA pathway.
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Hepatocellular carcinoma (HCC) has the features of high incidence rate, low survival rate, poor treatment outcome, and complex pathogenesis. In recent years, many studies have shown that long non-coding RNA (lncRNA) MALAT1 is upregulated in HCC and can promote the proliferation, invasion, and metastasis of HCC cells, and it can also guide the diagnosis, prognostic evaluation, and treatment of HCC in clinical practice. This article reviews the current status of research on lncRNA MALAT1 in HCC and discusses its expression pattern, mechanism of action, and clinical significance in predicting and monitoring the progression of HCC, so as to gain a deep understanding of the role of lncRNA MALAT1 in the progression of HCC. It is pointed out that lncRNA MALAT1 is expected to become a potential biomarker for the diagnosis and prognostic evaluation of HCC and may be used as a therapeutic target in clinical practice.
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Aims: The purpose of this study was to investigate the potential correlation between metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and the transcription factor BTB and CNC homology 1 (BACH1) and their clinicopathological significance in triple-negative breast cancer (TNBC). Subjects and Methods: MALAT1 and BACH1 were detected by immunohistochemistry using TNBC tissue microarrays of 240 patients. The association between MALAT1 and BACH1 expression levels was statistically analyzed. Moreover, the prognostic roles as well as clinical and pathological significance of MALAT1 and BACH1 expression in TNBC were determined. Statistical Analysis Used: Two-tailed Pearson correlation was used to examine the correlation of BACH1 and MALA1 expression. Comparisons of clinicopathological variables between different BACH1 and MALA1 expression groups were performed using χ2 tests. Overall survival (OS) and disease-free survival (DFS) curves were plotted with the Kaplan-Meier method and the differences in OS and DFS between three groups were compared by the log-rank test. Multiple comparisons were performed using χ2 tests for subsequent individual group comparisons. Results: MALAT1 and BACH1 expression was significantly correlated with tumor-node-metastasis stage, distant metastasis, pathological stage, and survival outcomes of patients. Patients with high MALAT1 and BACH1 expression exhibited shorter overall survival and disease-free survival. Conclusions: These findings provide further insight into the expression pattern of MALAT1 and BACH1 in TNBC and suggest them as prognostic biomarkers for TNBC
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Objective: To investigate the regulatory effect of long chain non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) adsorbing microRNA-124 (miR-124) on osteogenic differentiation of mesenchymal stem cells (MSCs). Methods: C3H10T1/2 cells derived from mouse embryos were cultured in vitro, then randomly divided into control group (group A), lncRNA MALAT1 no-load plasmid group (group B), lncRNA MALAT1 overexpression plasmid group (group C), lncRNA MALAT1 small interfering RNA (siRNA) group (group D), and lncRNA MALAT1 siRNA negative control group (group E). The cells were transfected into plasmids and siRNA, then induced to differentiate into osteoblasts. Alkaline phosphatase (ALP) and alizarin red staining were used to detect the osteogenic differentiation of cells in each group, real-time fluorescence quantitative (qRT-PCR) analysis was used to detect the expressions of lncRNA MALAT, miR-124, and osteogenesis-related genes such as Runt-related transcription factor 2 (Runx2), osteopontin (OPN), and osteocalcin (OCN) in each group. Double luciferase reporter gene was used to detect the targeting regulation of lncRNA MALAT1 to miR-124. Results: The relative contents of ALP positive cells, mineralized nodule, and the relative mRNA expressions of lncRNA MALAT1, Runx2, OPN, and OCN in group C were significantly higher than those in other groups ( P0.05). The results of double luciferase reporter gene assay showed that lncRNA MALAT1 targeting down-regulated the expression of miR-124. Conclusion: LncRNA MALAT1 can targeting down-regulate the expression of miR-124 and promote the osteogenic differentiation of MSCs.
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The aim of this study was to identify some biomarkers for predicting lymph node metastasis and prognosis of human epidermal growth factor receptor 2 (Her-2)-positive breast cancer (BC). We analyzed correlations between microRNAs (miRNAs) and the prognosis of patients with BC based on data collected from The Cancer Genome Atlas (TCGA) database. The expression levels of miR-455, miR-143, and miR-99a were measured in clinical samples of Her-2-positive BC patients with different degrees of lymph node metastasis. We investigated the impacts of overexpressed miR-455 on the proliferation and invasiveness of MDA-MB-453 cells and measured its effects on the expression of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of miR-455 was significantly and positively correlated to the prognosis and overall survival (OS) of the BC (P=0.028), according to TCGA information. The expression level of miR-455 was positively correlated with OS and relapse-free survival (RFS) of patients with Her-2-positive BC, and was negatively correlated with the number of metastatic lymph nodes (P<0.05). Transwell assay suggested that MDA-MB-453 cells became much less invasive (P<0.01) after being transfected with miR-455 mimics. During the qRT-PCR, the expression level of MALAT1 declined significantly after transfection (P<0.01). Overexpressed miR-455 significantly inhibited the proliferation and migration of MDA-MB-453 cells and the expression of MALAT1. We conclude that miR-455 may be a useful potential biomarker for forecasting lymph node metastasis and the prognosis of Her-2-positive BC patients. miR-455 may play an important role in lymph node metastasis of BC by interacting with MALAT1.
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Objective: To investigate the expression of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in plasma of patients with oral squamous cell carcinoma (OSCC) and its clinical significance. Methods: 70 OSCC patients and 50 healthy controls were included. The relative expression of MALAT1 in plasma was examined by quantitative realtime PCR. The expression of MALAT1 in plasma in 15 OSCC patients was analyzed retrospectively 30 days after operation. Results: The expression level of MALAT1 in plasma of OSCC patients was significantly higher than that of healthy controls(P＜ 0. 001). The expression level of MALAT1 in OSCC patients was significantly correlated with TNM stage, tumor differentiation and lymph node metastasis(P＜ 0. 05). After operation the expression level of MALAT1 in plasma of OSCC patients was significantly decreased(P＜ 0. 001). The AUC of the diagnosis of OSCC with MALAT1 was 0. 814, and the sensitivity and specificity were 87. 43％ and 72. 00％ respectively. Conclusion: MALAT1 can be used as an auxiliary diagnostic marker for OSCC.
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Objective To observe the expressions of long noncoding RNA (IncRNA)metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and nuclear factor etythroid-2 related factor 2 (Nrf2) in lung tissues of hyperoxia-exposed premature neonatal rats,and explore the role of MALAT1 and Nrf2 in hyperoxia-induced lung injury.Methods Pregnant Sprague-Dawley (SD) rats were given cesarean section on the 21st day of gestation.After feeding for 24 h,a total of 80 premature rats were randomly divided into the air group and hyperoxia group.The rats in the air group were fed in the indoor environment[fraction of inspiration O2 (FiO2) =210 mL/L] and those in the hyperoxia group were fed in a high-oxygen box (FiO2 ＞ 850 mL/L).Eight premature rats from each group were sacrificed and lung tissue samples were collected at 5 experimental time points (1st,4th,7th,10th,14th day),respectively.Hematoxylin-eosin staining was used to observe pathological changes in lung tissues.Real-time quantitative polymerase chain reaction (qPCR) and Western blot were used to detect the expression level of MALAT1and Nrf2.Results Compared with the air group,the degree of alveolarization in lung tissues of the hyperoxia group rats was reduced,and radial alveolar count (RAC) decreased on the 1st day,but there was no significant difference between 2 groups (P ＞0.05),when they decreased on the 4th(3.14 ± 0.23),7th(5.25 ± 0.38),10th (4.41 ± 0.44),14th (3.41 ± 0.13) day of exposure,the differences were statistically significant (all P ＜ 0.05).Compared with the air group,the RNA expression of MALAT1 of hyperoxia group preterm rats decreased after the 1 st day(0.527 ± 0.124) of exposure,increased after the 4th (0.538 ±0.128),7th (0.748 ±0.071) day,decreased after the 10th (0.519 ± 0.081)day,and the differences were statistically significant (all P ＜ 0.05),but it continually became weak on the 14th day,but there was no significant difference between 2 groups (P ＞ 0.05).Compared with the air group,the mRNA expression of Nrf2 of hyperoxia group preterm rats decreased after the 1st day(0.791 ± 0.031) of exposure,increased after the 4th (0.977 ± 0.189),7 th (1.369 ± 0.100),10th (1.094 ± 0.104) day,and the differences were statistically significant (all P ＜ 0.05),and it decreased after the 14th day,but there was no significant difference between 2 groups (P ＞0.05).The hyperoxia group had significantly higher expression of free Nrf2 protein and lower expression of Nrf2-Keapl protein than those of the air group at all time points.Within the hyperoxia group,the RNA expression of MALAT1 was positively correlated with RAC and Nrf2 (r =0.517,0.533,all P ＜ 0.001).Conclusions Lung injury is gradually aggravated over the time of hyperoxia exposure.The level of lncRNA MALAT1 is associated with the severity of lung injury and the level of Nrf2 mRNA,suggesting that IncRNA MALAT1 and the Nrf2 target gene signaling pathway might be involved in the development of hyperoxia-induced lung injury in neonatal premature rats together.
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Colorectal cancer is one of the most familiar malignant neoplasms,but the pathogenesis of colorectal cancer is not clear now.Recently the studies show that the long non-coding RNA(lncRNA)plays a regulatory role in various systemic tumors,including colorectal cancer.LncRNA is a non-coding RNA over 200 nucleotides.Five types of lncRNA including H19,colorectal cancer-associated transcript 1(CCAT1),HOX transcriptional antisense RNA(HOTAIR),lung adenocarcinoma-associated transcription factor 1(MALAT1),maternal imprinted expression gene 3(MEG3)are closely related to colorectal cancer.They are well correlated with the occurrence,development,clinical staging,overall survival,and prognosis of colorectal cancer.Therefore,lncRNA is expected to be a new marker for the diagnosis and evaluation of colorectal cancer in clinical work.
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Objective. To explore the link between the expression of long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and IL-6/signal trans ducers and activators of transcription 3(STAT3) signaling pathway in isoniazid induced rats liver injury. Methods. Fifty-six specific pathogen-free (SPF) SD rats were randomly divided into experimental group (48 rats) and control group (8 rats), each with half females and half males. The rats in experimental group were given isoniazid of 63 mg/ (kg•d) for 3, 7, 10, 14, 21 and 28 d, with 8 rats at the same time point of each day. The rats in control group were given distilled water by intragastric administration. Serum levels of ALT and AST were measured by automatic biochemical analyzer; SYBR green real-time polymerase chain reaction was used to test the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA in the liver. Results. Liver tissue injury occurred after 7 days and worsened with the extention of administration time. Compared with the rats in the control group, the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA as well as ALT and AST showed a trend of increase (P<0.01). The expression of ALT, AST and lncRNA MALAT1 declined at different degrees on 28 (P<0.05). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels were positively correlated (P<0.01). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels had a positive correlation with the contents of ALT and AST (P<0.01). Conclusion. The expression level of lncRNA MALAT1 in isoniazid induced liver injury rat models showed an abnormal rising trend, and the positive detection time preceded that of ALT and AST. The mechanism may be related to the activation of IL-6/STAT3 signaling pathway.
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Objective To explore the link between the expression of long non-coding RNA(lncRNA)metastasis associated lung adenocarcinoma transcript 1(MALAT1)and IL-6/signal trans ducers and activators of transcription 3(STAT3)signaling pathway in isoniazid induced rats liver injury. Methods Fifty-six specific pathogen-free(SPF)SD rats were randomly divided into experimen?tal group(48 rats)and control group(8 rats),each with half females and half males. The rats in experimental group were given isonia?zid of 63 mg/(kg·d)for 3,7,10,14,21 and 28 d,with 8 rats at the same time point of each day. The rats in control group were giv?en distilled water by intragastric administration. Serum levels of ALT and AST were measured by automatic biochemical analyzer;SYBR green real-time polymerase chain reaction was used to test the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA in the liver. Results Liver tissue injury occurred after 7 days and worsened with the extention of administration time. Compared with the rats in the control group,the expression level of lncRNA MALAT1 and IL-6/STAT3 mRNA as well as ALT and AST showed a trend of increase(P<0.01). The expression of ALT,AST and lncRNA MALAT1 declined at different degrees on 28(P<0.05). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels were positively correlated(P<0.01). LncRNA MALAT1 and IL-6/STAT3 mRNA expression levels had a positive correlation with the contents of ALT and AST(P<0.01). Conclusion The expression level of lncRNA MALAT1 in isoniazid induced liver injury rat models showed an abnormal rising trend,and the positive detection time preceded that of ALT and AST. The mechanism may be related to the activation of IL-6/STAT3 signaling pathway.
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Objective To investigate the effect of atorvastatin on the expressions of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)and inflammation factors in human umbilical vein endothelial cells (HUVECs) stimulated by high glucose. Methods The expression of MALAT1 in HUVECs incubated with high glucose(30 mmol/L) for different time periods were detected by real-time PCR. Under high glucose condition, the expressions of MALAT1, interleukin-6(IL-6), and interleukin-8 (IL-8) in HUVECs were detected after MALAT1 was silenced by siRNA or atorvastatin was added. Results (1) After HUVECs were incubated with high glucose for different time periods, the expressions of MALAT1 were increased to some extent(P<0.05), with the peak at 12h (P<0.01). The levels of IL-6 and IL-8 expression and secretion were increased after HUVECs were stimulated by high glucose for 12h (P<0.05). (2)The silence of MALAT1 markedly suppressed high glucose-stimulated expression and secretion of IL-6 and IL-8 (P<0.05). (3) Atorvastatin significantly inhibited high glucose-stimulated expressions of MALAT1, IL-6, and IL-8(all P<0.05). Conclusions High glucose induces the secretion of inflammatory factors by stimulating MALAT1 expression in endothelial cells. Atorvastatin significantly inhibits high glucose-stimulated MALAT1 expression and decreases inflammatory reaction.
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Objective: To observe the effects of follistatin (FST)on the skeletal muscle wasting of cancer cachexia mice and the expressions of Mstn, LncRNA-MALAT1 and Caspase-3, and to elucidate its associated molecular mechanisms.Methods:Thirty-two BALB/c mices were randomly assigned into:healthy control (HC) group,FST prevention (FP)group,FST treatment (FT)group and cancer cachexia (CC)group.The murine colon adenocarcinoma CT26 cells were inoculated subcutaneously into the mices in FP, FT and CC groups to establish the cancer cachexia models. The body weight, spontaneous activity and tumor growth were daily monitored.The mice in FP and FT groups were administrated with FST intraperitoneally on day 6 and 12 after inoculation.The samples were collected on day 20.The tumor and gastrocnemius weights of the mice were detected. The biochemical metabolism indexes and myofiber cross-sectional area of gastrocnemius tissue were detected.The mRNA expression levels of Mstn,Caspase-3 and LncRNA-MALAT1 were examined by Real-time PCR.The protein expression levels of Mstn and Caspase-3 were measured by Western blotting method. Results:Compared with CC group,the body weights,spontaneous activities,gastrocnemius weights and myofiber cross-sectional areas were increased (P <0.05);the serum levels of glucose,total protein and albumin of the mice in FP and FT groups were increased (P <0.05).The protein and mRNA expression levels of Mstn and Caspase-3 in gastrocnemius of the mice in CC group were significantly higher and the expression level of LncRNA-MALAT1 was significantly lower than those in HC group (P < 0.05).The mRNA and protein expression levels of Mstn and Caspase-3 in FP and FT groups were reduced and the expression level of LncRNA-MALAT1 was increased compared with CC group (P < 0.05).The prevention effect in FP group is better than FT group (P < 0.05). Conclusion:FST may alleviate the muscle wasting of the mice with cancer cachexia by inhibiting the expression of Mstn,thus upregulating the expression of LncRNA-MALAT1 which in turn to suppress the expression of Caspase-3.
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Objective To evaluate the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) in ovarian cancer cell lines, and to investigate the biological effects of down-regulated MALAT-1 on OVCAR3 cells.Methods qRT-PCR analysis was used to examine the expression level of MALAT-1 gene in ovarian cancer cells, including ES-2, A2780, SKOV3 and OVCAR3 cell lines.For functional research, four shRNA oligos specially targeting MALAT-1 and a empty vector were designed and constructed into pGPU6/GFP/Neo, then transfected into OVCAR3 cells.qRT-PCR was used to confirm the effective suppression of MALAT-1.Changes of proliferation and adhesion of cells were analyzed by CCK-8 and adhesion assays.Wound-healing, transwell migration and invasion assays were used to examine migration and invasion of MALAT-l-silencing cells in vitro.Results The expression of MALAT-1 gene in OVCAR3 cells was high, and qRT-PCR results confirmed successfully the knockdown of MALAT-1 after transient transfection.After successful suppression of MALAT-1, the proliferation, wound-healing and adhesion ability in vitro were inhibited to some degree.In transwell migration assay, the number of migration cells in MALAT-1-silencing group was 52.17±4.48, which is much less than that in the negative and control groups (286.50± 12.23 and 295.67±6.96, respectively).In invasion assay, the number of invasion cells passing the transwell membrane in MALAT-1-silencing group (37.33±2.40) was also decreased significantly, compared to that in the negative and control groups (239.00±15.72 and 222.67±20.85, P ＜ 0.05).Conclusions shRNA-mediated silence of MALAT-1 can effectively inhibit the proliferation, adhesion, migration and invasion abilities of ovarian cancer cell line OVCAR3 in vitro, indicating MALAT-1 is expected to be a target gene for the treatment of ovarian cancer.
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Objective To investigate the significance of metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in the occurrence and development of non-small cell lung cancer(NSCLC).Methods Eighty-six NSCLC lung tissue samples and 86 corresponding adjacent tissues were collected.Real-time quantitative polymerase chain reaction (RT-PCR) was used to detect MALAT1 mRNA expression.The correlation analysis of the gender,age,carcinoma embryonic antigen (CEA),clinical stage,and the degree of differentiation was performed.Results MALAT1 expression levels showed an average 2.16-fold increase in NSCLC lung tissues(87.23 ±9.72) when compared with adjacent tissues(40.38 ± 5.49),the difference was statistically significant (t =7.894,P ＜ 0.01).There was no significant difference between gender,age,histological type,tumor diameter,CEA level in terms of MALAT1 expression (P ＞ 0.05).There was significant differences between pathological stage (Ⅰ stage =52.38％ (11/21),Ⅱ stage =76.00％ (19/25),Ⅲ stage =97.50％ (39/40),x2 =11.839,P =0.042),tumor differentiation (High differentiated =39.13％ (9/23),moderately differentiated =74.47％ (35/47),low differentiated =100％ (16/16),x2 =15.383,P =0.032)and lymph node metastasis (with =97.22％ (35/36),no =46.00％ (23/50),x2 =23.947,P =0.030).Conclusion MALAT1 might be involved in the development of NSCLC,and could be an auxiliary diagnosis marker.
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Objective To investigate the significance of metastasis associated lung adenocarcinoma transcript 1 ( MALAT1 ),cyclooxygerase-2 ( COX-2 ),beta catenin ( β-catenin )、matrix metalloproteinase (MMP)-3 and MMP-9 in the occurrence and development of colorectal carcinoma.Methods Real-time PCR was used to detect MALAT1,COX-2,β-catenin,MMP-3 and MMP-9 rnRNA expression in samples from 30 fresh colorectal carcinomas and 30 corresponding adjacent tissues.And the correlation analysis of the gender and age of patients,CEA,immune cellular factors ( CD4 and CD8 ),clinical stages,and the degree of differentiation was undertaken.Results The expression levels of MALAT1,COX-2,β-catenin and MMP-9 were significantly different between colorectal carcinoma tissues and adjacent colorectal tissues (P ＜ 0.05 ).MMP-3 showed no significant difference (P ＞ 0.05).MALAT1,COX-2,β-catenin and MMP-9 expression levels showed an average 2.22-fold,1.86-fold,2.16-fold,0.58-fold ( P ＜ 0.01 ) increase in colorectal carcinoma tissues when compared with adjacent colorectal tissues respectively.There were negative correlation between MALAT1 and β-cateuin ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( r =- 0.346,P =0.030).While there were positive correlation between MMP-9 and β-catenin ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( r =0.312,P =0.047 ).There were significant difference between male patients and female patients in terms of COX-2 and MMP-9 (colorectal carcinoma tissues vs adjacent colorectal tissues) (P =0.047; P =0.018).There were significant difference between patients with tumor marker CEA increase and patients without CEA increase in terms of COX-2 ( colorectal carcinoma tissues vs adjacent colorectal tissues) ( P =0.021 ).Conclusion MALAT1,COX-2,MMP-9 and β-catenin have significance in the occurrence and development of colorectal carcinoma,while MMP-3 has no significant reference value. The negative correlation between MAL(A)T-1 and β-catenin and the positive correlation between MMP-9 and β-catenin might show some interaction relationship in the development of colorectal carcinoma.The expression differences of COX-2 and MMP-9 (colorectal carcinoma tissues vs adjacent colorectal tissues) in male and female patients suggest that above two genes may affect the occurrence ratio of colorectal carcinoma.Detecting of COX-2 maybe helpful to the tumor marker CEA during the diagnosis of colorectal carcinoma.