LncRNA MEG3 impacts proliferation, invasion, and migration of ovarian cancer cells through regulating PTEN

Wang, Juelan; Xu, Wenqian; He, Yi; Qi, Xia; Liu, Siwei

doi:10.1007/s00011-018-1186-z

Cited by 60 publications

(46 citation statements)

References 29 publications

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“…Overall, our in vitro and in vivo experimental studies demonstrated that exogenous MEG3 expression is able to revert the malignant phenotype in HGSOC. Indeed, in line with recent literature data [22,28], we proved that over-expression of MEG3 inhibited cell proliferation, plate colony formation, migration, and invasion ability, as well as spheroid formation and tumor growth in mice.…”

Section: Discussionsupporting

confidence: 90%

“…On the other hand, recent studies have implicated MEG3 in the regulation of different oncogenic and tumor-suppressive gene networks, possibly through an activity as a molecular decoy for cancer-associated microRNAs [28,30]. Indeed, one of the most interesting mechanisms of action reported for MEG3 is the positive regulation of PTEN expression in ovarian cancer cells [22]. Although driver pathways for this modulation have not been entirely clarified, one possibility is that MEG3 could act as competitive endogenous RNA for miR-214 [31] that, in turn, negatively regulates PTEN protein expression [32].…”

Section: Discussionmentioning

confidence: 99%

“…Due to recent studies showing a role for phosphatase and tensin homologue (PTEN) in mediating MEG3 tumor suppressor activity in ovarian cancer cells [22], we evaluated PTEN expression in stably transfected HEY pcDNA and pMEG3 cells. Western blot analysis showed a relevant protein increase in pMEG3 overexpressing cells compared to controls ( Figure 4E; Figure S1: Uncropped blots of Figure 4E; Table S2: Densitometric analysis of Figure 4E); notably, this modulation was supported by the concomitant decrease in mTOR (Mammalian target of rapamycin) phosphorylation ( Figure 4E; Figure S1: Uncropped blots of Figure 4E; Table S2: Densitometric analysis of Figure 4E), in line with literature findings of key pathways regulated by PTEN [23].…”

Section: Meg3 Overexpression Upregulated Ptenmentioning

confidence: 99%

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Clinical Value of lncRNA MEG3 in High-Grade Serous Ovarian Cancer

Buttarelli

Donato

Raspaglio

et al. 2020

Cancers

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Long non-coding RNAs (lncRNAs) are emerging as regulators in cancer development and progression, and aberrant lncRNA profiles have been reported in several cancers. Here, we evaluated the potential of using the maternally expressed gene 3 (MEG3) tissue level as a prognostic marker in high-grade serous ovarian cancer (HGSOC), the most common and deadliest gynecologic malignancy. To the aim of the study, we measured MEG3 transcript levels in 90 pre-treatment peritoneal biopsies. We also investigated MEG3 function in ovarian cancer biology. We found that high MEG3 expression was independently associated with better progression-free (p = 0.002) and overall survival (p = 0.01). In vitro and in vivo preclinical studies supported a role for MEG3 as a tumor suppressor in HGSOC, possibly through modulation of the phosphatase and tensin homologue (PTEN) network. Overall, results from this study demonstrated that decreased MEG3 is a hallmark for malignancy and tumor progression in HGSOC.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Meg3 Overexpression Upregulated Ptenmentioning

confidence: 99%

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Clinical Value of lncRNA MEG3 in High-Grade Serous Ovarian Cancer

Buttarelli

Donato

Raspaglio

et al. 2020

Cancers

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“…Additionally, mounting studies also verified that lncRNA MEG3 inhibited tumor initiation and progression [15]. For example, lncRNA MEG3 inhibits breast cancer growth via upregulating endoplasmic reticulum stress and activating NF-κB and p53 [29]; lncRNA MEG3 impacts proliferation, invasion, and migration of ovarian cancer cells through regulating PTEN [30]. E-cadherin has been implicated in a number of signaling pathways that enhance cell-cell adhesion and cell-cell interactions [31].…”

Section: Discussionmentioning

confidence: 93%

LncRNA MEG3 promotes melanoma growth, metastasis and formation through modulating miR-21/E-cadherin axis

Zhu

et al. 2020

Cancer Cell Int

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Background: Melanoma is the most aggressive type of skin cancer with high mortality rate and poor prognosis. lncRNA MEG3, a tumor suppressor, is closely related to the development of various cancers. However, the role of lncRNA MEG3 in melanoma has seldom been studied. Methods: RT-PCR was used to examine the expressions of lncRNA MEG3 and E-cadherin in melanoma patients and cell lines. Then, the biological functions of lncRNA MEG3 and E-cadherin were demonstrated by transfecting lncRNA MEG3-siRNA, lncRNA MEG3-overexpression, E-cadherin-siRNA and E-cadherin-overexpression plasmids in melanoma cell lines. Moreover, CCK8 assay and colony formation assay were utilized to assess the cell proliferation; Transwell assay was performed to evaluate the cell invasive ability; and tumor xenografts in nude mice were applied to test the tumor generation. Additionally, the target interactions among lncRNA MEG3, miR-21 and E-cadherin were determined by dual luciferase reporter assay. Finally, RT-PCR and WB were further conducted to verify the regulatory roles among lncRNA MEG3, miR-21 and E-cadherin. Results: The clinical data showed that lncRNA MEG3 and E-cadherin expressions were both declined in carcinoma tissues as compared with their para-carcinoma tissues. Moreover, lncRNA MEG3 and E-cadherin expressions in B16 cells were also higher than those in A375 and A2058 cells. Subsequently, based on the differently expressed lncRNA MEG3 and E-cadherin in these human melanoma cell lines, we chose B16, A375 and A2058 cells for the following experiments. The results demonstrated that lncRNA MEG3 could suppress the tumor growth, tumor metastasis and formation; and meanwhile E-cadherin had the same effects on tumor growth, tumor metastasis and formation. Furthermore, the analysis of Kaplan-Meier curves also confirmed that there was a positive correlation between lncRNA MEG3 and E-cadherin. Ultimately, dual luciferase assays were further used to verify that lncRNA MEG3 could directly target miR-21 which could directly target E-cadherin in turn. Additionally, the data of RT-PCR and WB revealed that knockdown of lncRNA MEG3 in B16 cells inhibited miR-21 expression and promoted E-cadherin expression, but overexpression of lncRNA MEG3 in A375 and A2058 cells presented completely opposite results. Conclusion: Our findings indicated that lncRNA MEG3 might inhibit the tumor growth, tumor metastasis and formation of melanoma by modulating miR-21/E-cadherin axis.

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“…Surveying the function of lncRNAs globally (Figure 2b), 120 are considered as oncogenes, 114 confirmed and six putative; and 29 are considered as tumor suppressor genes, 25 confirmed and four putative. SPRY-IT1 [26], MEG3 [122,123], XIST [54,99] and TTN-AS1 [65,124] statuses remain unclear because the shreds of evidence collected are ambiguous. The experimental data about TC0101686, TC0100223, TC0901107, and TC1500845 show only that they are transcriptionally activated by estrogens.…”

Section: Lncrnas Implicated In Oc Development and Progressionmentioning

confidence: 99%

The Challenges and Opportunities of LncRNAs in Ovarian Cancer Research and Clinical Use

Salamini-Montemurri

Lamas-Maceiras

Barreiro-Alonso

et al. 2020

Cancers

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Ovarian cancer is one of the most lethal gynecological malignancies worldwide because it tends to be detected late, when the disease has already spread, and prognosis is poor. In this review we aim to highlight the importance of long non-coding RNAs (lncRNAs) in diagnosis, prognosis and treatment choice, to make progress towards increasingly personalized medicine in this malignancy. We review the effects of lncRNAs associated with ovarian cancer in the context of cancer hallmarks. We also discuss the molecular mechanisms by which lncRNAs become involved in cellular physiology; the onset, development and progression of ovarian cancer; and lncRNAs' regulatory mechanisms at the transcriptional, post-transcriptional and post-translational stages of gene expression. Finally, we compile a series of online resources useful for the study of lncRNAs, especially in the context of ovarian cancer. Future work required in the field is also discussed along with some concluding remarks.

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LncRNA MEG3 impacts proliferation, invasion, and migration of ovarian cancer cells through regulating PTEN

Cited by 60 publications

References 29 publications

Clinical Value of lncRNA MEG3 in High-Grade Serous Ovarian Cancer

Clinical Value of lncRNA MEG3 in High-Grade Serous Ovarian Cancer

LncRNA MEG3 promotes melanoma growth, metastasis and formation through modulating miR-21/E-cadherin axis

The Challenges and Opportunities of LncRNAs in Ovarian Cancer Research and Clinical Use

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