scholarly journals miR-194 Suppresses Proliferation and Migration and Promotes Apoptosis of Osteosarcoma Cells by Targeting CDH2

2018 ◽  
Vol 45 (5) ◽  
pp. 1966-1974 ◽  
Author(s):  
Jinglei Miao ◽  
Weiguo Wang ◽  
Song Wu ◽  
Xiaofang Zang ◽  
Yuezhan Li ◽  
...  
Keyword(s):  
Tumour Suppressor ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Migration Assay ◽  
Tumour Suppression ◽  
Normal Bone ◽  
Proliferation Ability ◽  
And Migration ◽  
Normal Bone Tissue ◽  
Proliferation And Migration

Background/Aims: Studies have shown that miR-194 functions as a tumour suppressor and is associated with tumour growth and metastasis. This study intends to uncover the mechanism of tumour suppression by miR-194. The expression of miR-194 in osteosarcoma cell lines and tissues were monitored by real-time PCR. Methods: The proliferation ability was examined by MTT assay. Migration and apoptosis of cells were monitored by migration assay and flow cytometry, respectively. The regulation of miR-194 on CDH2 was determined by luciferase assays and western blot assays. Results: The results showed that miR-194 was significantly reduced in osteosarcoma compared with that in normal bone tissue. Overexpression of miR-194 significantly attenuated the proliferation and migration and induced the apoptosis of osteosarcoma cells. Furthermore, we demonstrated that miR-194 has inhibited the malignant behaviour of osteosarcoma by downregulating CDH2 expression. Conclusions: These findings suggested that miR-194 may act as a tumour suppressor in osteosarcoma. miR-194/CDH2 may be a novel therapeutic target in the treatment of osteosarcoma.

scholarly journals Interfering with pak4 Protein Expression Affects Osteosarcoma Cell Proliferation and Migration

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yuxin Fu ◽  
Lun Fang ◽  
Qipu Yin ◽  
Qi Wu ◽  
Wei Sui ◽  
...  
Keyword(s):  
Protein Expression ◽  
Osteosarcoma Cell ◽  
Mrna Levels ◽  
Osteosarcoma Cells ◽  
Migration Ability ◽  
M Phase ◽  
Underlying Mechanisms ◽  
And Migration ◽  
Proliferation And Migration

Purpose. A number of studies have discovered various roles of PAK4 in human tumors, including osteosarcoma. However, the exact role of PAK4 in osteosarcoma and its mechanism have yet to be determined. Therefore, this study focused on interrogating the PAK4 effect on the proliferation and migration ability of osteosarcoma and its underlying mechanisms. Materials and Methods. Western blot and QRT-PCR were utilized to quantify the PAK4 relative protein and mRNA levels. To measure cellular viability and mobility, the MTT and wound-healing assays were preferred. Results. With the adenovirus-mediated overexpression of PAK4, the proliferation and migration of U2-OS and MG-63 osteosarcoma cells were stimulated. Furthermore, a liposome-mediated knockout of PAK4 will inhibit osteosarcoma cells from proliferating. In terms of mechanism, we observed the positive correlation of PAK4 expression with expression of P21, CyclinD1, CyclinE1, CDK2, and CDK6, which drives G0/G1 to the G2/M phase transition. PAK4 can also activate Erk expression in OS cells and induce EMT. Conclusion. Interfering with PAK4 protein expression has been shown to affect osteosarcoma proliferation and migration.

Using Bioinformatics Analysis to Detect the Effect of Zoledronic Acid on the Biological Behavior of Osteosarcoma Cells

2019 ◽  
Vol 9 (8) ◽  
pp. 1568-1574
Author(s):  
Sheng Li ◽  
Jianjun Li
Keyword(s):  
Cell Proliferation ◽  
Zoledronic Acid ◽  
Side Effects ◽  
Bioinformatics Analysis ◽  
Biological Behavior ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Migration Ability ◽  
And Migration ◽  
Proliferation And Migration

Objective: Osteosarcoma is a malignant bone tumor commonly seen in adolescents. Drug treatment for osteosarcoma is often accompanied by systemic toxicity and side effects, while zoledronic acid has few side effects but has anti-tumor effects. Methods: The bioinformatics analysis and scratch test were used to detect changes in cell proliferation, migration, and apoptosis in two osteosarcoma cell lines 24, 48, and 72 hours after adding zoledronic acid (0, 25, 50, 100, and 200 μM). Flow cytometry and transmission electron microscopy were used to observe the changes in cell apoptosis in the control and experimental groups after a 50% inhibitory dose of zoledronic acid was given. Results: The inhibition of cell proliferation and migration ability, as well as apoptosis increased with the increase in zoledronic acid exposure time and concentration. The 50% inhibitory rate occurred 48 hours after treatment with 100 M zoledronic acid. Conclusion: Zoledronic acid inhibited proliferation and migration and promoted apoptosis of osteosarcoma cells in vitro.

Posttranscriptional inhibition of γ-adducin promotes the proliferation and migration of osteosarcoma cells

2021 ◽  
pp. 030089162110506
Author(s):  
Zhigang Suo ◽  
Xiucai Ma ◽  
Yueping Ding ◽  
Yu Zhou ◽  
Xiangguo Duan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Annexin V ◽  
Suppressor Gene ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Luciferase Reporter Gene ◽  
And Migration ◽  
Proliferation And Migration

Objective: The expression of cytoskeleton-related protein γ-adducin (ADD3) was abnormally reduced in some tumors. Functional experiments demonstrated that it could inhibit the malignant progression of lung cancer and glioma, whereas the involvement of ADD3 in osteosarcoma was not clear. This study aimed to investigate the role of ADD3 in osteosarcoma and its upstream regulatory mechanisms. Methods: ADD3 was knocked down by siRNA transfection and the expression level of ADD3 was determined using quantitative real-time PCR assay and Western blot. CCK-8 assay and colony formation were performed to detect the capacity of cell proliferation. Transwell assay and PI and Annexin V-FITC staining were used to determine cell migration and apoptosis, respectively. Luciferase reporter experiment was performed to investigate the interaction between ADD3 and miR-23b-3p. Results: Based on gene silencing assays, we showed that knockdown of ADD3 suppressed apoptosis and promoted the proliferation and migration of osteosarcoma cells, revealing inhibitory effects of ADD3 in osteosarcoma. Luciferase reporter gene assays confirmed that miR-23b-3p could bind to the 3'-UTR of ADD3. Upregulation of miR-23b-3p not only inhibited the expression of ADD3, but also released the tumor suppressive role of ADD3 on the proliferation and migration of osteosarcoma cells. Conclusions: Our study found that ADD3 functioned as a tumor suppressor gene during osteosarcoma development. The abnormal upregulation of miR-23b-3p targeted the expression of ADD3 and resulted in accelerated osteosarcoma cell proliferation and migration. Thus, the miR-23b-3p/ADD3 axis contributes to the development of osteosarcoma and ADD3 is a key driver of malignancy.

miR-208a-3p promotes NSCLC proliferation and migration by suppressing lncRNA-MEG3 expression

2021 ◽  
Author(s):  
Linfei Yang ◽  
Qian Li ◽  
Hai Zhong ◽  
Liang Ye ◽  
Surong Fang ◽  
...  
Keyword(s):  
Protein Extraction ◽  
Underlying Mechanism ◽  
In Vitro Assays ◽  
Cell Viability Assay ◽  
Migration Assay ◽  
Normal Tissues ◽  
Viability Assay ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background The disordered expression of maternally expressed gene 3 (MEG3) has been observed in non-small-cell lung cancer (NSCLC). However, the molecular mechanism accounting for this abnormal expression is not fully understood. Methods MEG3 expression was detected by qRT-PCR in 51 cases of NSCLC and adjacent normal tissues. Then, the relationship between MEG3 and miR-208a-3p was assessed in vitro by cell viability assay, cell migration assay, protein extraction and western blot analysis. Resoults We observed that MEG3 expression was decreased in NSCLC tissues. And MEG3 expression was negatively related to lymph node metastasis and differentiation. Moreover, MEG3 expression is regulated by miR-208a-3p expression by overexpression and knockout experiments. Furthermore, we focused on the underlying mechanism of MEG3 downregulation. We found that the overexpression of miR-208a-3p reduced the level of MEG3 expression based on computational predictions and in vitro assays. Using CCK-8 and transwell migration assays, we found that the overexpression of miR-208a-3p can increased proliferation and apoptosis in NSCLC cells. Moreover, the depletion of MEG3 rescued the proliferation and migration induced by miR-208a-3p knockdown. Conclusion Taken together, the results of this study reveal that miR-208a-3p promotes NSCLC tumorigenesis by negatively regulating MEG3 expression and functions as an oncogenic miRNA in NSCLC.

scholarly journals WIN55,212-2-Induced Expression of Mir-29b1 Favours the Suppression of Osteosarcoma Cell Migration in a SPARC-Independent Manner

2019 ◽  
Vol 20 (20) ◽  
pp. 5235 ◽  
Author(s):  
Antonietta Notaro ◽  
Sonia Emanuele ◽  
Fabiana Geraci ◽  
Antonella D’Anneo ◽  
Marianna Lauricella ◽  
...  
Keyword(s):  
Cell Migration ◽  
Extracellular Vesicles ◽  
Cannabinoid Receptors ◽  
Matricellular Protein ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Independent Manner ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
And Migration

WIN55,212-2 (WIN) is a synthetic agonist of cannabinoid receptors that displays promising antitumour properties. The aim of this study is to demonstrate that WIN is able to block the migratory ability of osteosarcoma cells and characterize the mechanisms involved. Using wound healing assay and zymography, we showed that WIN affects cell migration and reduces the activity of the metalloproteases MMP2 and MMP9. This effect seemed to be independent of secreted protein acidic and rich in cysteine (SPARC), a matricellular protein involved in tissue remodeling and extracellular matrix deposition. SPARC release was indeed prevented by WIN, and SPARC silencing by RNA interference did not influence the effect of the cannabinoid on cell migration. WIN also increased the release of extracellular vesicles and dramatically upregulated miR-29b1, a key miRNA that modulates cell proliferation and migration. Interestingly, reduced cell migration was observed in stably miR-29b1-transfected cells, similarly to WIN-treated cells. Finally, we show the absence of SPARC in the extracellular vesicles released by osteosarcoma cells and no changes in SPARC level in miR-29b1 overexpressing cells. Overall, these findings suggest that WIN markedly affects cell migration, dependently on miR-29b1 and independently of SPARC, and can thus be considered as a potential innovative therapeutic agent in the treatment of osteosarcoma.

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