lncRNA MEG3 modified epithelial-mesenchymal transition of ovarian cancer cells by sponging miR-219a-5p and regulating EGFR.

This study was aimed to verify whether there existed any associations between long noncoding RNA MEG3/miR-219a-5p/EGFR axis and the development of ovarian cancer (OC). As a whole, we gathered 317 pairs of OC tissues and surgical marginal normal tissues and simultaneously acquired four OC cell lines (ie, A2780, Caov-3, OVCAR-3, and SKOV-3) and human normal ovarian surface epithelial cell line. Moreover, pcDNA3.1-MEG3, si-MEG3, miR-219a-5p mimic, miR-219a-5p inhibitor, pcDNA3.1-EGFR, and si-EGFR were, respectively, transfected into the OC cells, and their impacts on viability, proliferation, apoptosis, invasion, and migration of OC cells were assessed via conduction of MTT assay, colony formation assay, flow cytometry assay, transwell assay, and scratch assay. Ultimately, dual-luciferase reporter gene assay was performed to testify the targeted relationships among maternally expressed gene 3 (MEG3), miR-219a-5p, and estimated glomerular filtration rate (EGFR). It was indicated that underexpressed MEG3 and miR-219a-5p were significantly associated with unfavorable prognosis of patients with OC when compared with overexpressed MEG3 and miR-219a-5p (P < .05). In addition, the OC cells transfected with si-MEG3 or miR-219a-5p inhibitor exhibited stronger viability, proliferation, invasion, and migration than untreated cells (P < .05). Correspondingly, the apoptotic percentage of OC cells was reduced observably under treatments of si-MEG3 and miR-219a-5p inhibitor (P < .05). Moreover, MEG3 exerted modulatory effects on the expression of miR-219a-5p (P < .05), and there was a sponging relationship between them (P < .05). Finally, EGFR expression was modified by both MEG3 and miR-219a-5p significantly (P < .05), and raising EGFR expression could changeover the impacts of MEG3 and miR-219a-5p on the above-mentioned activity of OC cells (P < .05). Conclusively, MEG3 could serve as a promising biomarker for diagnosis and treatment of OC, considering its involvement with OC etiology via regulation of miR-219a-5p/EGFR axis.

Wang L ，Yu M ，Zhao S 《-》

LncRNA MEG3 negatively modified osteosarcoma development through regulation of miR-361-5p and FoxM1.

This study was aimed to figure out whether long noncoding RNA MEG3/miR-361-5p/FoxM1 signaling would contribute to improved proliferation and metastasis of osteosarcoma cells. We altogether collected 204 pairs of osteosarcoma tissues and adjacent normal tissues, and obtained four human osteosarcoma cell lines. Then pcDNA3.1-MEG3, si-MEG3, miR-361-5p mimic, miR-361-5p inhibitor, pcDNA3.1-FoxM1, si-FoxM1, and negative control (NC) were, respectively, transfected into the osteosarcoma cells. Furthermore, real time polymerase chain reaction was utilized to determine the mRNA expressions of maternally expressed gene 3 (MEG3) and miR-361-5p, and western blot analysis was applied for determining the FoxM1 expression. Besides, dual luciferase reporter gene assay was adopted to verify if MEG3 can be directly targeted by miR-361-5p. Finally, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide, colony formation assay, flow cytometry, wound healing assay, and transwell assay were conducted to investigate the influence of MEG3, miR-361-5p, and FoxM1 expressions on the viability, proliferation, apoptosis, migration, and invasion of osteosarcoma cells. MEG3 and miR-361-5p were observed to be significantly downregulated within both osteosarcoma tissues and cell lines, whereas FoxM1 was upregulated in osteosarcoma tissues and cell lines (p < 0.05). MEG3 directly bound to miR-361-5p, and significantly upgraded its expression (p < 0.05). The upregulated MEG3 and miR-361-5p or the downregulated FoxM1 appeared to substantially inhibit proliferation, migration, and invasion of osteosarcoma cells (p < 0.05). Finally, the proliferation, migration, invasion, and motility of osteosarcoma cells within the miR-NC + pcDNA3.1-FoxM1 group and pcDNA + pcDNA-FoxM1 group were markedly promoted when compared with the miR-361-5p mimic group and pcDNA3.1-MEG3 group (p < 0.05). The MEG3/miR-361-5p/FoxM1 axis could potentially serve as therapeutic targets or diagnostic biomarkers for osteosarcoma.

Shen B ，Zhou N ，Hu T ，Zhao W ，Wu D ，Wang S ... -  《-》

The encouraging role of long noncoding RNA small nuclear RNA host gene 16 in epithelial-mesenchymal transition of bladder cancer via directly acting on miR-17-5p/metalloproteinases 3 axis.

The present investigation was intended to elucidate whether long noncoding RNA small nuclear RNA host gene 16 (SNHG16) could regulate the epithelial-mesenchymal transition process of bladder cancer cells by directing expressions of miR-17-5p and metalloproteinases 3 (TIMP3). To elucidate the point, we collected 275 pairs of bladder cancer tissues and corresponding adjacent normal tissues, as well as four bladder cancer cell lines and the normal human bladder epithelial cell line. Moreover, pcDNA3.1-SNHG16, si-SNHG16, miR-17-5p mimic, miR-17-5p inhibitor, pcDNA3.1-TIMP3, and si-TIMP3 were prepared for transfection, and CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, and transwell assay were carried out. Finally, the dual luciferase reporter gene assay was performed to figure out whether targeted regulations were present among SNHG16, miR-17-5p, and TIMP3. The laboratory findings demonstrated that the bladder cancer patients carrying under-expressed SNHG16 or miR-17-5p were associated with extended survival time when compared with those possessing overexpressed SNHG16 and miR-17-5p (P < 0.05). Furthermore, overexpression of SNHG16 and miR-17-5p both enhanced the viability, proliferation, migration, and invasion (P < 0.05), and simultaneously suppressed their apoptosis (P < 0.05). Transfections of pcDNA3.1-SNHG16 and si-SNHG16, respectively, resulted in overexpression and under-expression of miR-17-5p, and the dual luciferase reporter gene assay demonstrated a targeted relationship between SNHG16 and miR-17-5p (P < 0.05). Besides, the expression of TIMP3 was subjected to targeted regulation of miR-17-5p (P < 0.05), and its overexpression could reverse the effects of miR-17-5p on proliferation and metastasis (P < 0.05). Conclusively, purposeful modification of SNHG16/miR-17-5p/TIMP3 signaling might be conducive to postpone the aggravation of bladder cancer.

Peng H ，Li H 《-》

LncRNA XIST facilitates proliferation and epithelial-mesenchymal transition of colorectal cancer cells through targeting miR-486-5p and promoting neuropilin-2.

This study was designed to acertain whether the long noncoding RNA (lncRNA) X-inactive specific transcript (XIST)/miR-486-5p/neuropilin-2 (NRP-2) pathway might promote the viability and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells. In this investigation, we included 317 pathologically confirmed CRC patients and purchased several human CRC cells (i.e. HCT116, HT29, SW620, and SW480). Moreover, pcDNA3.1-XIST, si-XIST, miR-486-5p mimic, miR-486-5p inhibitor, and pcDNA3.1-NRP-2 were transfected into the CRC cells. And the dual-luciferase reporter gene assay managed to verify the targeted relationships among XIST, miR-486-5p, and NRP-2. Ultimately, the MTT assay, flow cytometry, colony formation assay, and transwell assay were carried out to assess the influence of XIST, miR-486-5p, and NRP-2 on the proliferation, apoptosis, migration, and invasion of CRC cells. Our study results demonstrated that CRC tissues and cells were detected with significantly elevated XIST and NRP-2 expressions as well as markedly reduced miR-486-5p expression when compared with normal tissues and cells (all p < 0.05). Besides this, the highly expressed XIST and NRP-2, as well as the lowly expressed miR-486-5p all could substantially encourage proliferation and EMT of CRC cells and simultaneously restrict apoptosis of the cells ( p < 0.05). Moreover, XIST was found to directly target miR-486-5p, and NRP-2 was directly targeted and modulated by miR-486-5p. Finally, CRC cells of the miR-NC + pcDNA3.1-NRP-2 groups showed stronger proliferation, viability, and EMT than those of miR-NC and miR-486-5p mimic groups ( p < 0.05). In conclusion, the XIST/miR-486 -5p/NRP-2 axis appeared to participate in the progression of CRC, which could assist in developing efficacious therapies for CRC.

Liu A ，Liu L ，Lu H 《-》

lncRNA MIAT Regulates Cell Growth, Migration, and Invasion Through Sponging miR-150-5p in Ovarian Cancer.

Zhou S ，Xu A ，Song T ，Gao F ，Sun H ，Kong X ... -  《-》