Promotion of tumour proliferation, migration and invasion by miR-92b in targeting RECK in osteosarcoma

2016 ◽  
Vol 130 (11) ◽  
pp. 921-930 ◽  
Author(s):  
Zhenhua Zhou ◽  
Zhiwei Wang ◽  
Haifeng Wei ◽  
Sujia Wu ◽  
Xudong Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Poor Prognosis ◽  
Expression Level ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Cysteine Rich Protein ◽  
Tumour Proliferation

MicroRNAs play important roles in the development of cancers. Although miR-92b has been reported to promote the tumorigenesis of some cancers, its role in osteosarcoma remains unknown. In the present study, we focused on the expression, function and mechanisms of miR-92b in osteosarcoma development. The miRNA miR-92b was up-regulated in osteosarcoma cell lines and tissues; miR-92b up-regulation correlated with poor prognosis in osteosarcoma. Overexpression of miR-92b promoted osteosarcoma cell proliferation, migration and invasion, which was abrogated by miR-92b inhibition. Reversion-inducing, cysteine-rich protein with kazal motifs (RECK) was identified as the direct and functional target of miR-92b in osteosarcoma. Importantly, restoring RECK expression abrogated increases in cell growth, motility and invasiveness induced by miR-92b. RECK was down-regulated in osteosarcoma tissues, and its expression level negatively correlated with miR-92b. Collectively, our results indicate that miR-92b acts as an oncogenic miRNA and may be a therapeutic target in osteosarcoma.

scholarly journals FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Ying Jiang ◽  
Chunlei Zhou ◽  
Qiang Gao ◽  
Zhi-Qi Yin ◽  
Jingwen Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Poor Prognosis ◽  
Migration And Invasion ◽  
Tumor Proliferation ◽  
Osteosarcoma Cell ◽  
Aberrant Expression ◽  
Upstream Gene ◽  
Cancer Types

Aberrant expression of FAM64A was correlated with cell proliferation in various cancer types. We examined the expression of FAM64A and the upstream gene miR-493 in OS. The functions of miR-493 were revealed through extensive experiments. We found an increase of FAM64A gene and protein in OS tissues. Overexpression of FAM64A resulted in promoting tumor proliferation, migration, and invasion. The miR-493 targeted and negatively regulated FAM64A. Our data showed that upregulation of FAM64A in OS correlated with poor prognosis.

scholarly journals TUFT1 promotes osteosarcoma cell proliferation and predicts poor prognosis in osteosarcoma patients

2018 ◽  
Vol 13 (1) ◽  
pp. 396-403 ◽  
Author(s):  
Yao-Ping Yu ◽  
Jian-Guo He ◽  
Ping Li ◽  
Ning-Hui Qiu ◽  
Li-Jun Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Mg63 Cell ◽  
Mapk Signaling ◽  
Gene Expression Omnibus ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Mg63 Cells

AbstractObjectiveThis study is aimed at exploring the role of TUFT1 in osteosarcomas.MethodsWe investigated the expression of TUFT1 in osteosarcoma cell lines and explored the correlation between TUFT1 expression and prognosis in osteosarcoma patients based on the expression data downloaded from Gene Expression Omnibus (GEO) website. The effects of TUFT1 on osteosarcoma cell proliferation, migration and invasion were investigated by silencing TUFT1 in osteosarcoma MG63 cell line. Finally, western blot was performed to determine the expression changes of MAPK signaling pathway related proteins after silencing TUFT1.ResultsWe found that the expression of TUFT1 was significantly up-regulated in osteosarcoma cell lines compared with the normal control. Using Kaplan-Meier analysis, we identified that high TUFT1 expression was positively correlated with poor prognosis in osteosarcoma patients. Furthermore, knockdown of TUFT1 remarkably inhibited MG63 cell proliferation, migration and invasion. Using western blot analysis, we found that the phosphorylation levels of MEK and ERK were reduced obviously in MG63 cells after silencing TUFT1 (p<0.01).ConclusionsOur results demonstrated that TUFT1 plays a promoting role in MG63 cell proliferation and metastasis and has the potential to be a predictor as well as a therapeutic target for osteosarcoma patients.

scholarly journals B7-H6 Is Associated with Poor Prognosis and a Potential Therapeutic Target of T-Lymphoblastic Lymphoma

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 33-33
Author(s):  
Lei Yuan ◽  
Lu Sun ◽  
Yu Zhao ◽  
Hongmei Jing ◽  
Xiaoyan Ke
Keyword(s):  
Cell Proliferation ◽  
Therapeutic Target ◽  
Poor Prognosis ◽  
Elevated Serum ◽  
Lymphoblastic Lymphoma ◽  
Jurkat Cells ◽  
Migration And Invasion ◽  
Serum Lactate Dehydrogenase ◽  
Nuclear Localization Sequence ◽  
The Impact

Background:B7-H6 is a novel co-stimulatory protein that is exclusively expressed on a variety of cancer cells and associated with poor prognosis. T cell lymphoblastic lymphoma (T-LBL) is a highly aggressive hematological malignancy whose treatment requires reliable prognostic biomarkers and therapeutic targets. The rare nature and delayed progression of T-LBL has limited its clinical management. Methods:B7-H6 expression was analyzed by immunohistochemistry (IHC) in 65 T-LBL samples, and its association with clinicopathological characteristics and prognosis was analyzed. Jurkat cell with B7-H6 depletion was constructed to investigate the impact of B7-H6 on cell proliferation, migration, and invasion ability. RNA sequencing was used to explore aberrantly expressing genes. Results:In this study, we used immunohistochemistry to show the expression of B7-H6 in 61.5% (40/65) of the cohort, including 38.5% (25/65) patients with membrane/cytoplasmic expression of B7-H6. Although B7-H6 expression varied across samples and did not correlate with patient survival, it was significantly associated with B symptoms, higher ECOG score (3-4), elevated serum lactate dehydrogenase, and reduced complete remission at interim evaluation. B7-H6 underwent translocation into the nucleus of T-LBL cells and had a specific nuclear localization sequence in the C-terminus. Depleting Jurkat cells of B7-H6 impaired cell proliferation, migration, and invasion. RNAseq showed the differential expression of RAG-1 that could be involved in the tumorigenesis of T-LBL. Conclusions:B7-H6 may serve as a novel prognostic biomarker and therapeutic target of T-LBL. Disclosures Ke: Peking University Third Hospital:Current Employment.

scholarly journals Myc is a prognostic biomarker and potential therapeutic target in osteosarcoma

2020 ◽  
Vol 12 ◽  
pp. 175883592092205 ◽  
Author(s):  
Wenlong Feng ◽  
Dylan C. Dean ◽  
Francis J. Hornicek ◽  
Dimitrios Spentzos ◽  
Robert M. Hoffman ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Prognostic Biomarker ◽  
3D Cell Culture ◽  
Clinical Results ◽  
Osteosarcoma Cell ◽  
Migration Activity ◽  
Cell Proliferation Inhibition

Background: Over the past four decades, outcomes for osteosarcoma patients have plateaued as there have been few emerging therapies showing clinical results. Thus, the identification of novel biomarkers and therapeutic strategies are urgently needed to address these primary obstacles in patient care. Although the Myc-oncogene has known roles in oncogenesis and cancer cell growth, its expression and function in osteosarcoma are largely unknown. Methods: Expression of Myc was determined by Western blotting of osteosarcoma cell lines and patient tissues, and by immunohistochemistry of a unique osteosarcoma tissue microarray (TMA) constructed from 70 patient samples with extensive follow-up data. Myc specific siRNA and inhibitor 10058-F4 were applied to examine the effect of Myc inhibition on osteosarcoma cell proliferation. The clonogenicity and migration activity was determined by clonogenic and wound-healing assays. A mimic in vivo assay, three-dimensional (3D) cell culture model, was performed to further validate the effect of Myc inhibition on osteosarcoma cell tumorigenic markers. Results: Myc was significantly overexpressed in human osteosarcoma cell lines compared with normal human osteoblasts, and also highly expressed in fresh osteosarcoma tissues. Higher Myc expression correlated significantly with metastasis and poor prognosis. Through the addition of Myc specific siRNA and inhibitor, we significantly reduced Myc protein expression, resulting in decreased osteosarcoma cell proliferation. Inhibition of Myc also suppressed the migration, clonogenicity, and spheroid growth of osteosarcoma cells. Conclusion: Our results support Myc as an emerging prognostic biomarker and therapeutic target in osteosarcoma therapy.

scholarly journals Downregulation of miR-1826 Indicates a Poor Prognosis for Osteosarcoma Patients and Regulates Tumor Cell Proliferation, Migration, and Invasion

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Peng Li ◽  
Lei Wei ◽  
Wenshuai Zhu
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Cox Regression ◽  
Clinical Stage ◽  
Prognostic Significance ◽  
Prognostic Indicator ◽  
Migration And Invasion ◽  
Kaplan Meier ◽  
Low Levels

Background. Osteosarcoma (OS) is the most frequent bone tumor with high metastasis. This study is aimed at assessing the expression and prognostic significance of microRNA-1826 (miR-1826) in OS patients, as well as its biological function in tumor progression. Methods. Quantitative Real-Time PCR was employed to measure the expression of miR-1826 in OS tissues and cell lines. Kaplan-Meier survival analysis and Cox regression model were used to evaluate the prognostic value of miR-1826. CCK-8 and Transwell assay were conducted to investigate the effect of miR-1826 on OS cell proliferation, migration, and invasion. Results. miR-1826 expression was downregulated in OS tissues and cell lines and associated with OS patients’ clinical stage and distant metastasis. Low levels of miR-1826 were related with shorter survival time and determined as an independent prognostic indicator for the overall survival of OS patients. The overexpression of miR-1826 in OS cells led to inhibited cell proliferation, migration, and invasion. Conclusion. The decreased expression of miR-1826 predicts a poor prognosis in OS patients, and its overexpression inhibits OS cell proliferation, migration, and invasion. This newly identified miR-1826 provides a novel sight into the pathogenesis of OS and offers a candidate prognostic biomarker and therapeutic target for OS treatment.

scholarly journals LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Si Chen ◽  
Weiguo Li ◽  
Ai Guo
Keyword(s):  
Cell Proliferation ◽  
Overall Survival ◽  
Poor Prognosis ◽  
Histological Grade ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Loss Of Function ◽  
Osteoblast Cell Line ◽  
Enneking Stage

Abstract lncRNA LOXL1 antisense RNA 1 (lncRNA LOXL1-AS1) was recently found to function as oncogenic lncRNA in glioblastoma, prostate cancer, and medulloblastoma. The role of LOXL1-AS1 in osteosarcoma was still unknown. In our study, we found LOXL1-AS1 expression levels were higher in osteosarcoma tissues and cell lines than normal bone tissues and normal osteoblast cell line, respectively. Moreover, high-expression of LOXL1-AS1 was correlated with Enneking stage, tumor size, distant metastasis, histological grade, and overall survival time in osteosarcoma patients. Furthermore, LOXL1-AS1 overexpression acted as an independent poor predictor for overall survival in osteosarcoma patients. The loss-of-function studies showed knockdown of LOXL1-AS1 dramatically inhibited osteosarcoma cell proliferation, migration, and invasion through suppressing PI3K-AKT pathway. In conclusion, LOXL1-AS1 predicts clinical progression and poor prognosis in osteosarcoma patients and functions as oncogenic lncRNA to regulate cell proliferation, cell cycle, migration, and invasion.

scholarly journals LncRNA RBM5-AS1 Promotes Osteosarcoma Cell Proliferation, Migration, and Invasion

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Biyong Deng ◽  
Runsang Pan ◽  
Xin Ou ◽  
Taizhe Wang ◽  
Weiguo Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Western Blotting ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Pediatric Age Group ◽  
The Relationship

Purpose. Osteosarcoma (Os) is the most frequent malignant tumor of the bone in the pediatric age group, and accumulating evidences show that lncRNAs play a key role in the development of Os. Thus, we investigated the role of RBM5-AS1 and its molecular mechanism. Methods. The expression of RBM5-AS1 in Os tissues and cell lines was detected by real-time polymerase chain reaction (QPCR). The effect of RBM5-AS1 on the proliferation of Os cells was detected using CCK8 assays and flow cytometry. The effect of RBM5-AS1 on the migration and invasion of Os cells was detected by transwell assays. And we performed QPCR and western blotting assays to investigate the relationship between RBM5-AS1 and RBM5. Finally, western blotting assays were performed to explore the mechanism of RBM5. Results. LncRNA RBM5-AS1 was overexpressed in the Os tissues and cell lines. And lncRNA RBM5-AS1 promoted Os cell proliferation, migration, and invasion in vitro and tumor growth in vivo. LncRNA RBM5-AS1 targets RBM5 in Os cells. Conclusion. To sum up, the results showed that lncRNA RBM5-AS1 promotes cell proliferation, migration, and invasion in Os.

scholarly journals FBXW7 circular RNA regulates proliferation, migration and invasion of colorectal carcinoma through NEK2, mTOR, and PTEN signaling pathways in vitro and in vivo

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Haoran Lu ◽  
Baofu Yao ◽  
Xinyuan Wen ◽  
Baoqing Jia
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Circular Rna ◽  
Migration And Invasion ◽  
Potential Therapeutic Target

Abstract Backgrounds A number of circular RNAs (circRNAs) have been identified in various cancer including F-box and WD repeat domain containing 7 (FBXW7) circular RNA (circ-FBXW7), which can suppress glioma cell growth. However, the role of circ-FBXW7 in colorectal cancer (CRC) remains unclear. We aimed to investigate the effect and mechanisms of circ-FBXW7 on CRC progression. Methods The expression of circ-FBXW7 in CRC patients was detected by PCR. Stably knockdown of circ-FBXW7 (si circ-FBXW7) cell lines and overexpression of circ-FBXW7 (oe circ-FBXW7) cell lines were constructed by small interfering RNA method and plasmids transfection in CRC SW480 and SW620 cells. The functional experiments including cell proliferation, migration and invasion were carried out by cell counting kit-8 (CCK-8) assay, wound healing assay and trans well assay. The xenograft animal models were established to evaluate the effect and the underlying molecular mechanisms of circ-FBXW7 on CRC progression. Results CRC samples had a significantly lower level of circ-FBXW7 compared to normal tissue. si circ-FBXW7 notably promoted the proliferation, colony formation, cell migration and invasion of CRC cell in vitro. On contrast, circ-FBXW7 overexpressed significantly suppressed CRC cell proliferation, migration and invasion. Similarly, si circ-FBXW7 stimulated the tumor growth and circ-FBXW7 overexpression repressed the tumor progression in SW480 and SW620 tumor models, which suggested that circ-FBXW7 could serve as a target biomarker of CRC. Further study found that si circ-FBXW7 up-regulated the mRNA and protein expressions of NEK2 and mTOR, and diminished the PTEN expression. Whereas, overexpressed circ-FBXW7 induced the tumor suppression via reversing the expressions of NEK2, mTOR, and PTEN. Conclusion circ-FBXW7 plays a major role in controlling the progression of CRC through NEK2, mTOR, and PTEN signaling pathways and may be a potential therapeutic target for CRC treatment. Graphical abstract Circ-FBXW7 controls the progression of CRC through NEK2, mTOR, and PTEN signaling pathways and its overexpression inhibits colorectal cancer cell migration and invasion, suggesting the potential therapeutic target for CRC treatment.

scholarly journals Silencing of LINC00707 suppresses cell proliferation, migration, and invasion of osteosarcoma cells by modulating miR-338-3p/AHSA1 axis

2021 ◽  
Vol 16 (1) ◽  
pp. 728-736
Author(s):  
Xiao-rong Zhang ◽  
Jian-li Shao ◽  
Heng Li ◽  
Liang Wang
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Osteoblastic Cell ◽  
Osteosarcoma Cell ◽  
Osteoblastic Cell Line ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets ◽  
Competitive Endogenous Rna

Abstract Osteosarcoma is the most common type of primary malignant tumor of the bone, with a high metastatic rate and poor prognosis. Therefore, it is important to further elucidate the molecular mechanisms involved in the development of osteosarcoma and explore new molecular therapeutic targets. Long intergenic nonprotein-coding RNA 707 (LINC00707) is an oncogenic gene in several cancers. In this study, we further clarified its role and regulatory mechanism in osteosarcoma. We found that LINC00707 levels are significantly higher in the osteosarcoma cell lines SW 1353, HOS, U-2 OS, MG-63, and Saos-2 compared to those in human fetal osteoblastic cell line hFOB1.19. LINC00707 silencing suppressed cell proliferation, migration, and invasion of MG-63 and Saos-2 cells. Moreover, LINC00707 can act as a competitive endogenous RNA of miR-338-3p, and miR-338-3p inhibitor and AHSA1 overexpression alleviated the effect of LINC00707 silencing. In conclusion, we demonstrated high expression of LINC00707 in osteosarcoma cell lines and that silencing LINC00707 suppresses cell proliferation, migration, and invasion by targeting the miR-338-3p/AHSA1 axis in MG-63 and Saos-2 cells. These findings suggest that LINC00707 may serve as a potential target for osteosarcoma treatment.

scholarly journals MiR-566 mediates cell migration and invasion in colon cancer cells by direct targeting of PSKH1

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ying Zhang ◽  
Siqi Zhang ◽  
Jian Yin ◽  
Ruisi Xu
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Survival ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Reporter Assays ◽  
And Migration ◽  
Colon Epithelial Cell

Abstract Background Colorectal cancer (CRC), a common malignancy worldwide, and microRNAs (miRs) have been suggested to play roles in the disease. MiR-566 expression has been shown to be reduced in CRC, but its functions and mechanisms are still unclear. Methods Cell viability was assessed by using the CellTiter 96 AQueous One Solution Cell Proliferation kit. Cell proliferation was measured with MTT assay. Cell metastasis were measured by transwell assay. Luciferase reporter assays was used to confirm the target of MiR-566. PSKH1 expression was measured by RT-PCR and western blot. Results In the present study, we first observed that miR-566 was expressed in several CRC cell lines (SW480, SW620, LoVo, HT29 and Caco-2) at low levels compared to control colon epithelial cell lines (FHC). Further study showed that miR-566 overexpression suppressed cell survival and impeded cell proliferation, whereas inhibition of its expression enhanced cell survival and proliferation. Transwell assays showed that cell invasion and migration were reduced in cells overexpressing miR-566 and increased in those with inhibition of miR-566. Further analysis confirmed that PSKH1 is a target of miR-566. MiR-566 overexpression significantly inhibited PSKH1 expression and reintroduction of PSKH1 partially reversed the effects of miR-566 on CRC cell growth and metastasis in SW480 and Caco-2 cells. Conclusions Taken together, the data show that CRC cell growth and metastasis can be significantly suppressed by miR-566 through targeting PSKH1.

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