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Abstract Recent studies have found that lncRNA-MEG3(MEG3) plays an important role in the development of EMs (Endometriosis), but the specific mechanism needs to be further explored. This study aimed to investigate the effect of MEG3 on the proliferation, invasion of EMs cells. The authors used RT-qPCR to detect the expression of MEG3 and miR-21-5p in EMs tissues and hESCs cells, MTT and Transwell to detect cell proliferation and invasion, western blotting assay to detect the expression of DNMT3B and Twist, MSP to detect the methylation of Twist. The present study's detection results showed that MEG3 was lowly expressed in EMs tissues and hESCs cells, and overexpression of MEG3 could down-regulate miR-21-5p and inhibit endometrial cell proliferation and invasion. In addition, overexpression of MEG3 upregulated the expression of DNMT3B and promoted the methylation of TWIST. In conclusion, the present findings suggest that MEG3 is downregulated in EMs tissues, and overexpression of MEG3 can promote the activity of DNA methyltransferase DNMT3B by downregulating miR-21-5p, thereby promoting the methylation of Twist, downregulating Twist level to inhibits hESCs cells proliferation and invasion.
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Background: Abnormal glucose metabolism is one of the malignant characteristics of tumors. LncRNA plays an important role in the process of aerobic glycolysis of tumors. Aims: To investigate the expression of LncRNA MEG3 in gastric cancer and its correlation with glycolysis. Methods: RT-qPCR was used to detect the mRNA expression of MEG3 in gastric cancer and paracancerous tissue. Immunohistochemical EnVision method was used to detect the protein expressions of PKM2, LDHA, mTOR, HIF-1α in gastric cancer and paracancerous tissue. Relationship between expressions of above-mentioned indices and clinicopathological features of gastric cancer were analyzed. The correlation between MEG3 and glycolysis level of gastric cancer was analyzed by Spearman correlation analysis, and its possible mechanism was explored. Results: The expression of MEG3 in gastric cancer tissue was significantly lower than that in paracancerous tissue (P< 0.05), and was correlated with lymph node metastasis (P<0.05). The positivity rates of expression of PKM2, LDHA, mTOR and HIF-1α in gastric cancer tissue were significantly higher than those in paracancerous tissue, and were correlated with the depth of tumor invasion, lymph node metastasis and pTNM stage (P<0.05). Spearman correlation analysis showed that the expression of MEG3 was negatively correlated with the expressions of PKM2, LDHA, mTOR and HIF-1α (r=-0.346，r= -0.306，r=-0.389, r=-0.338; P<0.05). The expression of MEG3 in HIF-1α
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Objective To investigate the effect and underlying mechanism of lncRNA MEG3 on the radiosensitivity of nasopharyngeal carcinoma cells.Methods this experiment,overexpression control group,MEG3 overexpression group,miR-NC inhibition group,miR-7-5p inhibition group,overexpression control+4 Gy group,MEG3 overexpression+4 Gygroup,miR-NC inhibition+4 Gy group,miR-7-5p inhibition+4 Gy group,MEG3 overexpression + miR-NC overexpression group,MEG3 overexpression + miR-7-Sp overexpression group were established.The expression of miR-7-5p and MEG3 was detected by qRT-PCR.The radiosensitivity of nasopharyngeal carcinoma cells was measured by clone formation assay.Cell apoptosis was assessed by flow cytometry.The fluorescence activity was evaluated by dual luciferase reporter assay.Results MEG3 was lowly expressed in nasopharyngeal carcinoma tissues and cells.Overexpression of MEG3 and inhibition of miR-7-5p expression increased the radiosensitivity of nasopharyngeal carcinoma cells and promoted radiation-induced cell apoptosis.MEG3 could targetedly regulate the miR-7-5p expression.Overexpression of miR-7-5p reversed the effect of overexpression of MEG3 on the sensitization of nasopharyngeal carcinoma cells and the promotion of apoptosis induced by radiation exposure.Conclusions Overexpression of MEG3 increases the radiosensitivity of nasopharyngeal carcinoma cells and promotes radiation-induced cell apoptosis.The mechanism may be related to the down-regulation of miR-7-5p expression.
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@#[Abstract] Objective: To explore the regulatory effect of lncRNA maternal imprinting gene 3 (MEG3) on proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer cells via miR-9-5p/SOCS5 axis. Methods: A total of 20 pairs of cancer and para-cancerous tissue specimens resected from cervical cancer patients in Chongqing Hospital of Traditional Chinese Medicine from January 2017 to June 2019 were collected for this study. Using liposome transfection technology, pcDNA3.1-MEG3,si-MEG3, miR-9-5p mimics, miR-9-5p inhibitor and their control plasmids were transfected into cervical cancer HeLa and SiHa cells respectively to construct overexpression and silence cell model. qPCR was used to detect the expression levels of MEG3, miR-9-5p and SOCS5 in cervical cancer tissues and cell lines. CCK-8 method and Transwell chamber method were used to detect cell proliferation, migration and invasion ability. The expression levels of E-cadherin and vimentin in cells were detected by cellular immunofluorescence experiments. Target genes were predicted through the Online Bioinformatics TargetScan database. Dual luciferase reporter gene assay was used to verify the targeting relationship between miR-9-5p and MEG3, SOCS5, respectively. Results: Compared with para-cancerous tissues and cervical epithelial HcerEpic cells, the expressions of MEG3 and SOCS5 were significantly down-regulated and the expression of miR-9-5p was significantly up-regulated in cervical cancer tissues and cell lines (all P<0.01). TargetScan database analysis and Dual luciferase reporter gene assay confirmed the targeting relationship between miR-9-5p and MEG3 or SOCS5. MEG3 and SOCS5 significantly inhibited while miR-9-5p significantly promoted cell proliferation, migration and invasion ability (all P<0.01). MEG3 and SOCS5 promoted E-cadherin expression and inhibited vimentin expression, while miR-9-5p inhibited E-cadherin expression and promoted vimentin expression (P<0.05 or P<0.01). Conclusion: lncRNA MEG3 regulates proliferation, migration, invasion and EMT of cervical cancer cells via miR-9-5p/SOCS5 axis.