Expression Level Of Maternally Expressed Gene 3 Research Articles

Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-κB signaling pathway.

To explore the effects of long non-coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) on proliferation and apoptosis of gallbladder cancer (GBC) cells and its molecular mechanism. The relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using Western blotting, and the changes in nuclear factor-κB (NF-κB) protein in the nucleus were determined after overexpression of lncRNA MEG3. The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-κB signal in GBC cells was activated by lncRNA MEG3. LncRNA MEG3 activates the NF-κB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.

LncRNA MEG3 inhibits proliferation and promotes apoptosis of osteosarcoma cells through regulating Notch signaling pathway.

To explore the effect of long non-coding ribonucleic acid (lncRNA)-maternally expressed gene 3 (MEG3) on the Notch signaling pathway, and its influences on the proliferation and apoptosis of osteosarcoma MG-63 cells. LncRNA MEG3 was overexpressed in osteosarcoma MG-63 cells, and the cells were divided into Blank group, Len-con group, and Len-MEG3 group. The expression level of MEG3 in each group was detected via quantitative Polymerase Chain Reaction (qPCR), the cell proliferation level in each group was detected via Cell Counting Kit-8 (CCK-8) assay, and the apoptosis in each group was detected via Hoechst 33258 staining. Moreover, the content of the inflammatory factors in each group was determined using the Enzyme-Linked Immunosorbent Assay (ELISA), and the expression levels of apoptosis-related proteins and Notch signaling pathway-related proteins were determined through Western blotting. The expression level of lncRNA MEG3 in Len-MEG3 group was significantly higher than that in the Blank group and Len-con group (p<0.01). The overexpression of lncRNA MEG3 could significantly weaken the proliferation (p<0.01) and enhance the apoptosis of osteosarcoma cells (p<0.01). The overexpression of lncRNA MEG3 could significantly increase the content of the inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) (p<0.01), and remarkably decrease the content of the anti-inflammatory factor IL-10 in osteosarcoma cells (p<0.01). Besides, the overexpression of lncRNA MEG3 could evidently raise the expression of Caspase3 (p<0.01) and reduce the Bcl-2/Bax expression in osteosarcoma cells (p<0.01). Finally, the overexpression of lncRNA MEG3 could remarkably reduce the protein expressions of Jagged1, Notch1, and NICD1 in osteosarcoma cells (p<0.01). The overexpression of lncRNA MEG3 can inhibit the proliferation and promote the apoptosis of osteosarcoma MG-63 cells by suppressing the Notch signaling pathway.

Upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in Alzheimer's disease through inactivating the PI3K/Akt signaling pathway.

The purpose of this study was to elucidate the expression of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in rats with Alzheimer's disease (AD) and to explore its potential mechanisms. An AD rat model was induced by microinjection of Aβ25-35 . On the first day after successful modeling, pcDNA3.1 plasmid and pcDNA3.1-MEG3 plasmid were continuously infused into the third ventricle through a micro-osmotic pump to interfere with the expression level of MEG3. The spatial learning ability and memory ability, the histopathological changes of hippocampus tissues, the ultrastructure of hippocampal neurons, astrocyte activation as well as the survival and apoptosis of hippocampal neurons in each group was observed. The expression of apoptosis, PI3/Akt signaling pathway-related proteins, glial fibrillary acidic protein, inflammatory factors, malondialdehyde, glutathione-peroxidase, and superoxide dismutase levels were determined. The deposition of amyloid beta (Aβ) in the hippocampus of rats by was observed by Aβ immunohistochemical staining. Downregulated MEG3 was detected in the tissues of AD rats. In addition, upregulation of MEG3 contributed to an improvement of spatial learning ability and memory ability, inhibited the pathological injury and its apoptosis of hippocampal neurons, decreased Aβ positive expression, inhibited oxidative stress injury and inflammatory injury as well as the activated astrocytes in AD rats via inactivation of the PI3/Akt pathway. Our study highlights that upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in AD through inhibiting the PI3K/Akt signaling pathway.

Research on the correlation of changes in plasma lncRNA MEG3 with change in inflammatory factors and prognosis in patients with traumatic brain injury.

To study the correlation between the plasma long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and the levels of inflammatory cytokines in patients with traumatic brain injury (TBI) and to evaluate its prognosis to screen new biological targets for the diagnosis and treatment of TBI. 40 patients with TBI (TBI group) and 40 healthy people (control group) were collected and venous blood was drawn. The plasma MEG3 in subjects was quantitatively analyzed via quantitative Polymerase Chain Reaction (qPCR). Moreover, the levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-8] in plasma in each group were detected via enzyme-linked immunosorbent assay (ELISA). Finally, the correlation analysis was performed for the MEG3 expression level and inflammatory cytokine levels in patients with TBI. Patients were divided into high-expression MEG3 group and low-expression MEG3 group, high-level inflammatory cytokine group and low-level inflammatory cytokine group according to the median, followed by prognosis evaluation. The MEG3 expression level in TBI group was significantly decreased compared to that in control group, and the levels of inflammatory cytokines in plasma, including TNF-α, IL-1β, IL-6, and IL-8, were significantly higher than in control group. The results of the correlation analysis showed that the expression level of plasma MEG3 had a significantly negative correlation with the level of each inflammatory cytokine. The prognostic analysis revealed that the prognosis of patients with high MEG3 expression level and low inflammatory cytokine levels was good, while it was poor in patients with low MEG3 expression level and high inflammatory cytokine levels; the difference was significant. In patients with TBI, the expression level of plasma MEG3 is decreased, while the inflammatory cytokine levels are increased, and there is a significantly negative correlation between the two items. The prognosis of patients with high MEG3 expression level and low inflammatory cytokine levels is good so MEG3 and inflammatory cytokines can be used as biomarkers for diagnosis and treatment of TBI, improving the prognosis of patients.

Downregulation of long non-coding RNA MEG3 promotes proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-β1.

Hepatocellular carcinoma is a common malignant cancer with high incidence. And long non-coding RNAs (lncRNAs) play pivotal roles in the development of different types of cancers. In this study, we aimed to investigate the role of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of hepatocellular carcinoma. Expression of MEG3 in tumor tissues and adjacent healthy tissues of hepatocellular carcinoma patients, as well as the serum of both hepatocellular carcinoma patients and healthy controls, was detected by quantitative reverse transcriptase-polymerase chain reaction. The results showed that expression level of MEG3 was significantly lower in tumor tissues than in adjacent healthy tissues. Serum level of MEG3 was also significantly lower in hepatocellular carcinoma patients than in normal controls. The receiver operating characteristic curve analysis was used to evaluate the diagnostic value of MEG3 for hepatocellular carcinoma, and the prognostic value of MEG3 for this disease was analyzed using Kaplan-Meier method. The results indicated that serum level of MEG3 was a diagnostic and prognostic marker for hepatocellular carcinoma. We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-β inhibitor treatment reduced those enhancing effects. MEG3 siRNA silencing also increased the expression level of TGF-β1. These results indicated that downregulation of MEG3 can promote proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-β1 expression.

Baicalin inhibits proliferation and promotes apoptosis of vascular smooth muscle cells by regulating theMEG3/p53 pathway following treatment with ox‑LDL.

Atherosclerosis (AS) is a systemic disease associated with lipid metabolic disorders and abnormal proliferation of smooth muscle cells. Baicalin is a flavonoid compound isolated from the dry roots of Scutellaria baicalensis Georgi and exerts anti-proliferative effects in various types of cells. However, the effect of baicalin on AS remains unclear. In the present study, serum samples were collected from patients with AS and an in vitro model of AS was established using oxidized low-density lipoprotein (ox-LDL)-treated human aorta vascular smooth muscle cells (HA-VSMCs). The siRNA transfection and overexpression efficiency of endogenous maternally expressed gene 3 (MEG3) and the expression level of MEG3 were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of alterations in expression levels of MEG3 were assessed by MTT assay, bromodeoxyuridine incorporation assay, 5-ethynyl-2′-deoxyuridine staining, wound healing assay, immunofluorescence and western blotting in HA-VSMCs. qPCR indicated that the expression of MEG3 was reduced in serum samples from patients with AS and ox-LDL-treated HA-VSMCs, compared with serum samples from healthy patients and untreated HA-VSMCs, respectively. Further experiments indicated that ox-LDL-induced decrease of MEG3 expression was reversed by treatment with baicalin in a concentration-dependent manner. Following treatment with ox-LDL, decreased expression of MEG3 promoted proliferation and migration, and suppressed apoptosis in HA-VSMCs. Furthermore, treatment with baicalin reversed these effects on proliferation and apoptosis in ox-LDL-treated HA-VSMCs. The current study indicated that downregulated expression of MEG3 increased cell cycle-associated protein expression. However, treatment with baicalin inhibited the expression of cell-cycle associated proteins in HA-VSMCs with MEG3 knockdown. In addition, baicalin activated the p53 signaling pathway and promoted the expression and transport of p53 from the cytoplasm to nucleus following MEG3 knockdown in ox-LDL-treated HA-VSMCs. Baicalin inhibited proliferation and promoted apoptosis by regulating the expression of MEG3/p53, indicating that baicalin may serve a role in AS by activating the MEG3/p53 signaling pathway. The present study suggested a potential mechanism underlying the protective role of baicalin in the in vitro model of AS, and these results may be used to develop novel therapeutic approaches for the affected patients.

LncRNA MEG3 is downregulated in ankylosing spondylitis and associated with disease activity, hospitalization time and disease duration.

Long non-coding (lnc)RNA maternally expressed gene 3 (MEG3) has been proved to participate in osteoporosis, which features inverse pathological changes to those associated with spondylosis. The present study aimed to investigate the involvement of lncRNA MEG3 in ankylosing spondylitis. Blood and open sacroiliac joint biopsies were obtained from ankylosing spondylitis patients and healthy controls, and the expression of MEG3 in those tissues was detected by reverse-transcription-quantitative polymerase chain reaction analysis. Disease activity was evaluated according to the Ankylosing Spondylitis Disease Activity Score established by the International Association of Ankylosing Spondylitis. The diagnostic value of MEG3 expression for ankylosing spondylitis was evaluated by receiver operating characteristic curve analysis. The correlation between MEG3 expression and disease activity was assessed using Pearson correlation analysis. Furthermore, according to the median expression level of MEG3, patients were divided into high-level and low-level groups. The hospitalization time and re-hospitalization rate within 2 years after discharge were compared between these two groups and differences in clinicopathological parameters between the two groups were analyzed using the chi-square test. The results indicated that MEG3 was downregulated in ankylosing spondylitis patients compared with that in healthy controls. Furthermore, MEG3 expression levels may be used to effectively distinguish ankylosing spondylitis patients from healthy controls. The serum levels of MEG3 were not associated with the patients' age, sex or alcohol/tobacco consumption, but closely correlated with disease activity and disease duration. In addition, patients with higher expression levels of MEG3 had a shorter hospitalization time and a lower re-hospitalization rate within 2 years after discharge It was concluded that lncRNA MEG3 is downregulated in ankylosing spondylitis patients and is associated with disease activity, time of hospitalization and disease duration.

The Long Non-coding RNA MEG3/miR-let-7c-5p Axis Regulates Ethanol-Induced Hepatic Steatosis and Apoptosis by Targeting NLRC5

Ethanol (EtOH)-induced hepatic injury, characterized by hepatic steatosis with apoptosis, causes heavy health burden personally and socially. Long non-coding RNAs (lncRNAs) have been implicated in liver diseases. However, the role of lncRNA maternally expressed gene 3 (MEG3) in EtOH-induced hepatic injury remains unknown. The aim of present study was to assess the function of MEG3 and its functional interaction with miR-let-7c-5p in EtOH-induced hepatic injury. Here, we observed that MEG3 and NLRC5 expression was increased and miR-let-7c-5p expression decreased in EtOH-fed mice and EtOH-induced AML-12 cells. Knockdown of MEG3 contributed to attenuation of EtOH-induced steatosis and apoptosis in AML-12 cells. Also, expression level of MEG3 negatively correlated with miR-let-7c-5p expression and positively correlated with NLRC5 expression. In contrary to MEG3, miR-let-7c-5p overexpression attenuated EtOH-induced steatosis and apoptosis, as well as suppressed EtOH-induced increase in NLRC5 expression. By luciferase reporter assay, we concluded that miR-let-7c-5p directly binds to NLRC5 3′-UTR, thereby negatively regulates NLRC5 expression. Our data suggested that lncRNA MEG3 functions as a competing endogenous RNA for miR-let-7c-5p to regulate NLRC5 expression in EtOH-induced hepatic injury.

LncRNA MEG3 ameliorates respiratory syncytial virus infection by suppressing TLR4 signaling.

Maternally expressed gene 3 (MEG3), a long noncoding RNA (lncRNA) has been dysregulated in various tumors. However, the expression level and functional role of MEG3 in the progression of respiratory syncytial virus (RSV) infection remains to be elucidated. The present study quantified the expression level of MEG3 in the nasopharyngeal (NPA) samples of RSV‑infected patients and in BEAS‑2B cells infected with RSV. The findings of the present study demonstrated that the expression level of lncRNA MEG3 was reduced in the NPA samples of RSV‑infected patients and in BEAS‑2B cells infected with RSV. Invitro transfection revealed increased mRNA expression levels of toll‑like receptor 4 (TLR4), tumor necrosis factor‑α (TNFα) and interleukin (IL)‑8 following RSV infection in BEAS‑2B cells. Additionally, ectopic expression of MEG3 reduced the expression level of TLR4, subsequently suppressing the mRNA expression levels of TNFα and IL‑8, indicating the protective role of MEG3 in the process of RSV infection. It is of note, that RSV infection‑induced p38 mitogen activated protein kinase (MAPK) and nuclear factor‑κB (NF‑κB) activation was partly abolished by overexpression of MEG3. In conclusion, to the best of our knowledge, the present study provided the first evidence that lncRNA MEG3 expression level was reduced in the NPA samples of patients with RSV infection and RSV‑infected cells. Additionally, it was demonstrated that MEG3 protected human airway epithelial cells from RSV infection, primarily by suppressing TLR4‑dependent p38 MAPK and NF‑κB signaling.

Long non-coding RNA MEG3 inhibits the proliferation and metastasis of oral squamous cell carcinoma by regulating the WNT/β-catenin signaling pathway.

This study aimed to investigate how long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) inhibits the growth and metastasis of oral squamous cell carcinoma (OSCC) by regulating WNT/β-catenin signaling pathway in order to explore the antitumor effect of MEG3 and to provide a potential molecular target for the treatment of OSCC. The RT-qPCR technique was used to quantitatively analyze the expression of MEG3 in cancer and adjacent tissues collected from the patients after surgery. Using the Lipofectamine method, the MEG3 overexpression vector and the siRNA interference vector were constructed and transfected into SCC15 and Cal27 cells, respectively, followed by cell proliferation, apoptosis and metastasis analyses. The semi-quantitative analysis of the expression of the β-catenin protein in transfected cells was performed by the western blot analysis, and the activity of the WNT/β-catenin signaling pathway was analyzed using the TOP/FOP flash reporters. In addition, the cells were treated with decitabine to investigate the correlation between the MEG3 expression and the DNA methylation. Results showed that the expression level of MEG3 was significantly decreased in OSCC (p<0.05) and overexpression of MEG3 inhibited the proliferation and metastasis of cancer cells and promoted apoptosis. Importantly, MEG3 played a role as a tumor suppressor by inhibiting the WNT/β-catenin signaling pathway. In addition, the expression of the MEG3 was significantly affected by the degree of DNA methylation. It was concluded that the lncRNA MEG3 can inhibit the growth and metastasis of OSCC by negatively regulating the WNT/β-catenin signaling pathway.

Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer.

Maternally expressed gene 3 (MEG3), a long non-coding RNA (lncRNA), has tumor-suppressor properties and its expression is lost in several human tumors. However, its biological role in esophageal squamous cell carcinoma (ESCC) tumorigenesis is poorly defined. The present study determined the role and methylation status of MEG3 in esophageal cancer cells and ESCC clinical specimens, and further observed the competing endogenous RNA (ceRNA) activity of MEG3 in the pathogenesis and development of ESCC. Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Upregulation of MEG3 led to the inhibition of proliferation and invasiveness of the cancer cells. The aberrant promoter hypermethylation of MEG3 indicates silencing of its expression. Furthermore, MEG3 acts as a ceRNA to regulate the expression of E-cadherin and FOXO1 by binding hsa-miR-9. Upregulation of miR-9 was detected in esophageal cancer cell lines and ESCC tissues, and miR-9 promoted esophageal cancer cell proliferation and invasion. Finally, downregulation and hypermethylation of MEG3 was associated with ESCC patients' survival.Implications: MEG3 functions as a tumor-suppressive lncRNA and aberrant promoter hypermethylation is critical for MEG3 gene silencing in ESCC. In addition, MEG3 acts as a ceRNA to regulate expression of E-cadherin and FOXO1 by competitively binding miR-9 and may be used as a potential biomarker in predicting ESCC patients' progression and prognosis. Mol Cancer Res; 15(7); 800-10. ©2017 AACR.

Promoter hypermethylation-mediated downregulation of miR-770 and its host gene MEG3, a long non-coding RNA, in the development of gastric cardia adenocarcinoma.

Maternally expressed gene 3 (MEG3) is an imprinted gene located at 14q32 which encodes an lncRNA and is downregulated in an expanding list of cancer cell lines and primary human cancers. The miR-770 is transcribed from the intronic sequence of MEG3 and MEG3 may be the host gene for miR-770. However, the biological role of MEG3 and miR-770 in gastric cardia adenocarcinoma (GCA) development and prognosis is poorly defined. The present study was to investigate the function and methylation status of MEG3 in GCA, and further to detect the functional association of miR-770 and its host gene MEG3 in GCA carcinogenesis and prognosis. MEG3 and miR-770 was significantly downregulated in GCA patients and cell lines, and their expression was associated with TNM stage and lymph node metastasis. Overexpression of MEG3 and miR-770 inhibited gastric cancer cell proliferation and invasion in vitro. Furthermore, the expression level of MEG3 and miR-770 was significantly increased in cancer cells after treated with 5-Aza-dC. The aberrant hypermethylation of proximal promoter and enhancer region of MEG3 was detected in GCA tissues. In addition, the proximal promoter and enhancer region hypermethylation and dysregulation of MEG3 and miR-770 were associated with poorer GCA patients' survival. These findings suggest that miR-770 and its host gene MEG3 may play tumor suppressor role and hypermethylation of proximal promoter and enhancer region may be one of the critical mechanisms in inactivation of MEG3 and miR-770 in GCA development. MEG3 and miR-770 may be used as potential biomarkers in predicting GCA patients' prognosis.

Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis

Long non-coding RNAs(lncRNAs) play important roles in diverse biological processes. Although downregulation of lncRNA maternally expressed gene3(MEG3) has been identified in several types of cancers, little is known concerning its biological role and regulatory mechanism in hepatoma. Our previous studies demonstrated that MEG3 induces apoptosis in a p53-dependent manner. The aim of the present study was to determine whether endoplasmic reticulum(ER) stress is involved in MEG3‑induced apoptosis. Recombinant lentiviral vectors containing MEG3(Lv‑MEG3) were constructed and transfected into HepG2 cells. A 3‑(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, RT‑PCR, flow cytometry, western blot analysis, immunofluorescence and immunohistochemistry were applied. Transfected HepG2 cells were also transplanted into nude mice, and the tumor growth curves were determined. The results showed that the recombinant lentivirus of MEG3 was transfected successfully into the HepG2 cells and the expression level of MEG3 was significantly increased. Ectopic expression of MEG3 inhibited HepG2 cell proliferationinvitro andinvivo, and also induced apoptosis. Ectopic expression of MEG3 increased ER stress‑related proteins 78‑kDa glucose‑regulated protein(GRP78), inositol‑requiring enzyme1(IRE1), RNA‑dependent protein kinase‑like ER kinase(PERK), activating transcription factor6(ATF6), C/EBP homologous protein(CHOP), caspase‑3, aswellas p53 and NF‑κB expression accompanied by NF‑κB translocation from the cytoplasm to the nucleus. Furthermore, inhibition of NF‑κB with Bay11‑7082 decreased p53 expression in the MEG3‑transfected cells. These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF‑κB signaling is required for p53 activation in ER stress.

Role of long non-coding RNA maternally expressed gene 3 on cell proliferation and apoptosis of clear cell renal cell carcinoma

Objective To examine the expression of long non-coding RNA maternally expressed gene 3 (MEG3) in human clear cell renal cell carcinoma tissues (ccRCC) and cell lines. And to analyze the effects of MEG3 overexpression on the proliferation and apoptosis of ccRCC cells. Methods Real-time quantitative polymerase chain reaction (Real-time PCR) was carried out to measure the expression level of MEG3 in ccRCC specimens and cell lines compared with respective controls. After MEG3 was stabilized overexpressed in 786-O cells, methyl thiazol tetrazolium (MTT) and flow-cytometric assays were performed to evaluate the effects of MEG3 on cell proliferation and apoptosis. Protein levels of growth-or apoptosis-related molecules were then determined by Western blotting. Results MEG3 expression was decreased in ccRCC specimens and cell lines compared with respective controls. Overexpression of MEG3 in ccRCC cell line 786-O [0.51±0.02 vs. 11.26±1.89 for pcDNA3.1 and pcDNA3.1-MEG3 cell lie respectively with statistical difference (P<0.05)] resulted in delayed cell proliferation rate and induction of cell apoptosis[(7.02±1.21)% vs. (13.95±5.48)%] in vitro. Cyclin D1 and B cell lymphoma/leukemia-2 associated X protein (bax) protein levels were affected by MEG3 overexpression in these cell lines. Conclusion MEG3 was down-regulated in ccRCC, in which it functions as a potent tumor suppressor by regulating cell proliferation and apoptosis processes. Key words: Long non-coding RNA; Maternally expressed gene 3; Clear cell renal cell carcinoma; Cell proliferation; Apoptosis