Journal Article•
lncRNA MEG3 inhibit proliferation and metastasis of gastric cancer via p53 signaling pathway.
01 Oct 2017-European Review for Medical and Pharmacological Sciences (Eur Rev Med Pharmacol Sci)-Vol. 21, Iss: 17, pp 3850-3856
TL;DR: It is found that overexpression of lncRNA MEG3 could decrease the proliferation and metastasis of gastric cancer cells and could also increase the expression of p53.
Abstract: Objective lncRNA MEG3 has been reported as a tumor suppressor gene in many different kinds of cancer, but its role in gastric cancer has not been fully understood. Then, we would like to explore its mechanism in gastric cancer. Patients and methods We first used qRT-PCR to detect the expression of lncRNA MEG3, then CCK8 and wound healing assay were used to detect the effect of lncRNA MEG3 on gastric cancer cells. Western blot assay was used to measure the expression of p53 when lncRNA MEG3 was overexpressed. Results lncRNA MEG3 was highly expressed in the adjacent tissue, compared to the one in gastric cancer tissue. What's more, we also found that overexpression of lncRNA MEG3 could decrease the proliferation and metastasis of gastric cancer cells. Finally, overexpression of lncRNA MEG3 could also increase the expression of p53. Conclusions lncRNA MEG3 could inhibit the proliferation and metastasis of gastric cancer.
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TL;DR: Biological function of MEG3 to repress tumor through regulating the major tumor suppressor genes p53 and Rb, inhibiting angiogenesis-related factor, or controlling miRNAs is highlighted.
Abstract: Long noncoding RNAs (lncRNAs) have recently considered as central regulators in diverse biological processes and emerged as vital players controlling tumorigenesis. Several lncRNAs can be classified into oncogenes and tumor suppressor genes depending on their function in cancer. A maternally expressed gene 3 (MEG3) gene transcripts a 1.6 kb lncRNA whose act as an antitumor component in different cancer cells, such as breast, liver, glioma, colorectal, cervical, gastric, lung, ovarian and osteosarcoma cancer cells. The present review highlights biological function of MEG3 to repress tumor through regulating the major tumor suppressor genes p53 and Rb, inhibiting angiogenesis-related factor, or controlling miRNAs. On the other hand, previous studies have also suggested that MEG3 mediates epithelial-mesenchymal transition (EMT). However, deregulation of MEG3 is associated with the development and progression of cancer, suggesting that MEG3 may function as a potential biomarker and therapeutic target for human cancers.
115 citations
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TL;DR: LncRNA MEG3 was a down‐regulated lncRNA in prostate cancer and impacted the abilities of cell proliferation, migration and invasion, and cell apoptosis rate, this regulation relied on regulating miR‐9‐5p and its targeting gene QKI‐5.
Abstract: This study was designed to detecting the influences of lncRNA MEG3 in prostate cancer. Aberrant lncRNAs expression profiles of prostate cancer were screened by microarray analysis. The qRT-PCR and Western blot were employed to investigating the expression levels of lncRNA MEG3, miR-9-5p and QKI-5. The luciferase reporter assay was utilized to testifying the interactions relationship among these molecules. Applying CCK-8 assay, wound healing assay, transwell assay and flow cytometry in turn, the cell proliferation, migration and invasion abilities as well as apoptosis were measured respectively. LncRNA MEG3 was a down-regulated lncRNA in prostate cancer tissues and cells and could inhibit the expression of miR-9-5p, whereas miR-9-5p down-regulated QKI-5 expression. Overexpressed MEG3 and QKI-5 could decrease the abilities of proliferation, migration and invasion in prostate cancer cells effectively and increased the apoptosis rate. On the contrary, miR-9-5p mimics presented an opposite tendency in prostate cancer cells. Furthermore, MEG3 inhibited tumour growth and up-regulated expression of QKI-5 in vivo. LncRNA MEG3 was a down-regulated lncRNA in prostate cancer and impacted the abilities of cell proliferation, migration and invasion, and cell apoptosis rate, this regulation relied on regulating miR-9-5p and its targeting gene QKI-5.
113 citations
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TL;DR: Several aspects of the participation of MEG3 in carcinogenesis are discussed, and this lncRNA is regarded as a putative cancer biomarker and treatment target.
110 citations
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09 Jun 2020TL;DR: LncRNA ADAMTS9-AS2 acted as a tumor suppressor and enhanced cisplatin sensitivity in GC cells by activating NLRP3 mediated pyroptotic cell death through sponging miR-223-3p.
Abstract: The role of LncRNA ADAMTS9-AS2 in the regulation of chemoresistance of gastric cancer (GC) is largely unknown. Here we found that LncRNA ADAMTS9-AS2 was low-expressed in GC tissues and cells compared to their normal counterparts. In addition, LncRNA ADAMTS9-AS2 inhibited miR-223-3p expressions in GC cells by acting as competing endogenous RNA, and the levels of LncRNA ADAMTS9-AS2 and miR-223-3p showed negative correlations in GC tissues. Of note, overexpression of LncRNA ADAMTS9-AS2 inhibited GC cell viability and motility by sponging miR-223-3p. In addition, the levels of LncRNA ADAMTS9-AS2 were lower, and miR-223-3p was higher in cisplatin-resistant GC (CR-GC) cells than their parental cisplatin-sensitive GC (CS-GC) cells. LncRNA ADAMTS9-AS2 overexpression enhanced the cytotoxic effects of cisplatin on CR-GC cells, which were reversed by overexpressing miR-223-3p. Furthermore, LncRNA ADAMTS9-AS2 increased NLRP3 expressions by targeting miR-223-3p, and upregulation of LncRNA ADAMTS9-AS2 triggered pyroptotic cell death in cisplatin treated CR-GC cells by activating NLRP3 inflammasome through downregulating miR-223-3p. Finally, the promoting effects of LncRNA ADAMTS9-AS2 overexpression on CR-GC cell death were abrogated by pyroptosis inhibitor Necrosulfonamide (NSA). Collectively, LncRNA ADAMTS9-AS2 acted as a tumor suppressor and enhanced cisplatin sensitivity in GC cells by activating NLRP3 mediated pyroptotic cell death through sponging miR-223-3p.
88 citations
Cites background from "lncRNA MEG3 inhibit proliferation a..."
...Long non-coding RNAs (LncRNAs) involved in the regulation of gastric cancer pathogenesis according to their differential biological functions [18, 19], for example, LncRNA MEG3 served as a tumor suppressor [19], while LncRNA HOXA11-AS acted as an...
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TL;DR: Lnc-MALAT1 might be interacted with miR-125b to inhibit neuron apoptosis and inflammation while promote neurite outgrowth in AD.
Abstract: Background This study aimed to investigate the effect of long noncoding ribonucleic acids (RNAs) metastasis-associated lung adenocarcinoma transcript 1 (lnc-MALAT1) on regulating neuron apoptosis, neurite outgrowth and inflammation, and further explore its molecule mechanism in Alzheimer's disease (AD). Methods Control overexpression, lnc-MALAT1 overexpression, control shRNA, and lnc-MALAT1 shRNA were transfected into NGF-stimulated PC12 cellular AD model and cellular AD model from primary cerebral cortex neurons of rat embryo, which were established by Aβ1-42 insult. Rescue experiments were performed by transferring lnc-MALAT1 overexpression and lnc-MALAT1 overexpression & miR-125b overexpression plasmids. Neuron apoptosis, neurite outgrowth and inflammation were detected by Hoechst-PI/apoptosis marker expressions, and observations were made using microscope and RT-qPCR/Western blot assays. PTGS2, CDK5 and FOXQ1 expressions in rescue experiments were also determined. Results In two AD models, lnc-MALAT1 overexpression inhibited neuron apoptosis, promoted neurite outgrowth, reduced IL-6 and TNF-α levels, and increased IL-10 level compared to control overexpression, while lnc-MALAT1 knockdown promoted neuron apoptosis, repressed neurite outgrowth, elevated IL-6 and TNF-α levels, but reduced IL-10 level compared to control shRNA. Additionally, lnc- MALAT1 reversely regulated miR-125b expression, while miR-125b did not influence the lnc- MALAT1 expression. Subsequently, rescue experiments revealed that miR-125b induced neuron apoptosis, inhibited neurite outgrowth and promoted inflammation, also increased PTGS2 and CDK5 expressions but decreased FOXQ1 expression in lnc-MALAT1 overexpression treated AD models. Conclusion Lnc-MALAT1 might interact with miR-125b to inhibit neuron apoptosis and inflammation while promote neurite outgrowth in AD.
72 citations