Long non-coding RNA MEG3 functions as a tumour suppressor and has prognostic predictive value in human pancreatic cancer

Abstract

Long non-coding RNA (lncRNA) MEG3 has been demonstrated to be a tumour suppressor in many malignancies. However, the functional role of MEG3 in pancreatic cancer (PC) is unclear. In this study, the expression pattern of MEG3 was evaluated in 25 samples of microdissected PC tissues and 8 PC cell lines and was compared to the expression in adjacent non‑cancerous tissues and a human pancreatic normal epithelial cell line. Loss of MEG3 expression was observed in both the cancerous tissues and cancer cell lines. Although the absence of expression of MEG3 was not statistically correlated to either histological grade or TNM stage in the 25 cases, the prognosis was significantly worse. MEG3 knockdown enhanced cell proliferation, promoted cell migration and invasion, induced epithelial‑mesenchymal transition (EMT), increased the sphere‑forming ability and cancer stem cell (CSC) properties, and decreased the chemosensitivity to gemcitabine in vitro. In contrast, forced expression of MEG3 resulted in a reverse effect. In conclusion, MEG3 functions as a tumour suppressor in human PC. The underlying cause of the poor prognosis induced by low levels of MEG3 expression in PC patients might involve EMT induction, enhanced CSC phenotypes and reduced chemoresistance, all of which might be associated with Snail activation.

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

“…One of the most significant differences was that deceased MEG3 expression has great importance in AD. MEG3 was described as a tumor suppressor, and the poor expression of MEG3 resulted from gene deletion, hypermethylation or promoter hypermethylation of the intergenic differentially methylated region could result in tumorigenesis which is in line with the results of our study.…”

“…Aβ [25][26][27][28][29][30][31][32][33][34][35] powder (1 mg; Lot: 111M4775V; 98% purity; Sigma Inc) dissolved by 0.5 mL sterile normal saline was prepared into a 2 μg/μL working fluid (3 nmol/uL), and then sealed and decomposed in a sterile incubator at 3°C for 1 week to produce Aβ [25][26][27][28][29][30][31][32][33][34][35] in an aggregate state. The rats were intraperitoneally injected with 1% pentobarbital sodium for anesthesia.…”

“…With reference to the stereotaxic map of rat's brain, Bregma point was used as a base point with a microsyringe. Aβ [25][26][27][28][29][30][31][32][33][34][35] (5 μL) working fluid in aggregate state was injected slowly into the right ventricle at AP0.3 mm, ML2.0 mm, and DV4.0 mm. The syringe was placed for 10 minutes to avoid leakage.…”

“…YI ET AL. | 18055 2.7 | Immunohistochemical staining Hippocampal tissues were selected, fixed in 4% 1phosphofructaldolase (PFA), blocked with 5% goat serum, supplemented with the primary antibody against Aβ [25][26][27][28][29][30][31][32][33][34][35] (1:100; Lot: 980287 W; Beijing Bioss Biotechnology Co Ltd) and glial fibrillary acidic protein (GFAP; 1:250; ab33922; purchased from Abcam). The slices of hippocampal tissues were supplemented with the secondary antibody (Boster Biological Technology), and S-P compound.…”

“…Image-Pro Plus 6.0 software (Media Cybernetics Corporation) was applied to calculate the average number of GFAP positive cells by randomly selected five visual fields under 100 times of a light microscope, with the same exposure condition. The mean optical density of Aβ [25][26][27][28][29][30][31][32][33][34][35] positive expression was determined.…”