scholarly journals LncRNA TUG1 is upregulated and promotes cell proliferation in osteosarcoma

Open Medicine ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. 163-167 ◽  
Author(s):  
Feng Yun-Bo ◽  
Liu Xiao-Po ◽  
Li Xiao-Li ◽  
Cao Guo-Long ◽  
Zhang Pei ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Promotion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Akt Phosphorylation ◽  
Non Coding Rna ◽  
Human Osteosarcoma Cells ◽  
U2os Cells ◽  
And Function ◽  
Long Non Coding Rna

AbstractObjective: To examine the expression and function of long non-coding RNA taurine up-regulated 1 (TUG1) in human osteosarcoma cells. Methods: Real-time quantitive PCR was used to detect the transcription level of TUG1 in a series of osteosarcoma cell lines. Knockdown of TUG1 in U2OS cells was carried out by transient transfection of siRNAs. MTT assay was performed to access the cell growth rates. Afterwards, RNA and protein of these cells were extracted to analyze the transfection efficient as well as the expression of other molecules. Results: Compared to the normal cell line, TUG1 exhibited a significant upregulation in osteosarcoma cells. Phenotyping analysis showed the growth-promotion activity of TUG1, since knockdown of TUG1 resulted in declined proliferation. We also found that AKT phosphorylation was impaired after TUG1 was inhibited, suggesting that the AKT pathway was involved in the regulation of TUG1 in U2OS cells. Conclusion: Our data provided evidence that TUG1 was upregulated and acted as a possible oncogene via positively regulating cell proliferation in osteosarcoma cells.

scholarly journals Effects of the Long Non-Coding RNA HOST2 On the Proliferation, Migration, Invasion and Apoptosis of Human Osteosarcoma Cells

2017 ◽  
Vol 43 (1) ◽  
pp. 320-330 ◽  
Author(s):  
Wei Wang ◽  
Xiao Li ◽  
Fan-Bin Meng ◽  
Zhen-Xing Wang ◽  
Ren-Tao Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Doubling Time ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Blank Group ◽  
Human Osteosarcoma ◽  
Non Coding Rna ◽  
Human Osteosarcoma Cells ◽  
Long Non Coding Rna

Background/Aims: This study aimed to explore the effects of the long non-coding RNA HOST2 (lnc-HOST2) on the proliferation, migration, invasion and apoptosis of osteosarcoma cells. Methods: Osteosarcoma tissues and adjacent normal tissues from 52 patients were selected. Human osteosarcoma cell lines (SaOS2, HOS, U2OS and MG-63) were collected and cultured; MG-63 cells had the highest lnc-HOST2 expression and thus were used in subsequent experiments. Then, MG-63 cells were transfected and divided into the blank (no transfection), si-CON (transfected with negative control siRNA) and si-lnc-HOST2 (transfected with small interference lnc-HOST2 siRNA) groups. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of lnc-HOST2 in primary tissues and cells. Cell growth was detected using the CCK-8 and colony formation assays. Cell doubling time was detected. Cell migration and invasion were observed using the scratch test and Transwell assays. Cell apoptosis and cell cycle progression of osteosarcoma cells were detected using flow cytometry with annexin V/PI double staining and PI staining, respectively. Results: The level of lnc-HOST2 expression in the si-lnc-HOST2 group was significantly decreased compared to that in the blank and si-CON groups. The OD values in the si-lnc-HOST2 group were significantly lower than those in the blank and si-CON groups. Compared to the blank and si-CON groups, the si-lnc-HOST2 group presented significant decreases in the colony number and healing rates after scratching. The number of invasive cells in the si-lnc-HOST2 group was significantly less than that in the blank and si-CON groups. In the si-lnc-HOST2 group, the cell cycle was mainly halted in the G1 phase, and the apoptosis rate and doubling time in this group were significantly higher than those in the blank group and si-CON group. Conclusions: Inhibition of lnc-HOST2 could suppress the proliferation, migration, and invasion and promote the apoptosis of osteosarcoma cells.

scholarly journals Down-regulation of Long Non-coding RNA TUG1 Inhibits Osteosarcoma Cell Proliferation and Promotes Apoptosis

2013 ◽  
Vol 14 (4) ◽  
pp. 2311-2315 ◽  
Author(s):  
Qiang Zhang ◽  
Pei-Liang Geng ◽  
Pei Yin ◽  
Xiao-Lin Wang ◽  
Jin-Peng Jia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Osteosarcoma Cell ◽  
Down Regulation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals AdipoRon Affects Cell Cycle Progression and Inhibits Proliferation in Human Osteosarcoma Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Luigi Sapio ◽  
Ersilia Nigro ◽  
Angela Ragone ◽  
Alessia Salzillo ◽  
Michela Illiano ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Childhood And Adolescence ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Antitumor Effects ◽  
Human Osteosarcoma Cells ◽  
U2os Cells ◽  
The Impact

AdipoRon (AdipoR) is the first synthetic molecule acting as a selective and potent adiponectin receptor agonist. Recently, the possible pharmacological use of AdipoR in different pathological conditions has been addressed. Interestingly, initial evidence suggests that AdipoR may have anticancer properties in different preclinical models, such as pancreatic and ovarian cancer. To our knowledge, so far no research has been directed at determining the impact of AdipoR on osteosarcoma, the most aggressive and metastatic bone malignancy occurring in childhood and adolescence age. Here, we investigate the possible antitumor effects of AdipoR in osteosarcoma cell lines. MTT and cell growth curve assays clearly indicate that AdipoR inhibits, at different extents, proliferation in both U2OS and Saos-2 osteosarcoma cell lines, the latter being more sensitive. Moreover, flow cytometry-based assays point out a significant G0/G1 phase accumulation and a contemporary S phase decrease in response to AdipoR. Consistent with the different sensitivity, a strong subG1 appearance in Saos-2 after 48 and 72 hours of treatment is also observed. The investigation of the molecular mechanisms highlights a common and initial ERK1/2 activation in response to AdipoR in both Saos-2 and U2OS cells. Interestingly, a simultaneous and dramatic downregulation of p70S6K phosphorylation, one of the main targets of mTORC1 pathway, has also been observed in AdipoR-treated Saos-2, but not in U2OS cells. Importantly, a strengthening of AdipoR-induced effects was reported upon everolimus-mediated mTORC1 perturbation in U2OS cells. In conclusion, our findings provide initial evidence of AdipoR as an anticancer molecule differently affecting various signaling pathways involved in cell cycle and cell death in osteosarcoma cells and encourage the design of future studies to further understand its pattern of activities.

scholarly journals Silencing of HuR Inhibits Osteosarcoma Cell Epithelial-Mesenchymal Transition via AGO2 in Association With Long Non-Coding RNA XIST

2021 ◽  
Vol 11 ◽  
Author(s):  
Yongming Liu ◽  
Yuan Zhang ◽  
Jinxue Zhang ◽  
Jingchang Ma ◽  
Xuexue Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blotting ◽  
Epithelial Mesenchymal Transition ◽  
Osteosarcoma Cell ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Lncrna Xist ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

BackgroundOsteosarcoma (OS) is a highly malignant and aggressive bone tumor. This study was performed to explore the mechanisms of HuR (human antigen R) in the progression of OS.MethodsHuR expression levels in OS tissues and cells were detected by immunohistochemistry and western blotting. HuR siRNA was transfected into SJSA-1 OS cells to downregulate HuR expression, and then cell proliferation, migration, and epithelial-mesenchymal transition (EMT) were evaluated. RNA immunoprecipitation was performed to determine the association of the long non-coding RNA (lncRNA) XIST and argonaute RISC catalytic component (AGO) 2 with HuR. Fluorescence in situ hybridization analysis was performed to detect the expression of lncRNA XIST. Western blotting and immunofluorescence assays were performed to observe AGO2 expression after HuR or/and lncRNA XIST knockdown.ResultsKnockdown of HuR repressed OS cell migration and EMT. AGO2 was identified as a target of HuR and silencing of HuR decreased AGO2 expression. The lncRNA XIST was associated with HuR-mediated AGO2 suppression. Moreover, knockdown of AGO2 significantly inhibited cell proliferation, migration, and EMT in OS.ConclusionOur findings indicate that HuR knockdown suppresses OS cell EMT by regulating lncRNA XIST/AGO2 signaling.

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