scholarly journals The regulatory effect of has-circ-0001146/miR-26a-5p/MNAT1 network on the proliferation and invasion of osteosarcoma

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Junjie Wang ◽  
Jiangdong Ni ◽  
Deye Song ◽  
Muliang Ding ◽  
Jun Huang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Survival Rates ◽  
Bone Tumour ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Normal Tissues ◽  
Regulatory Effects ◽  
Proliferation And Invasion

Abstract Osteosarcoma is a malignant bone tumour with the lowest survival rates out of all paediatric cancers and is primarily diagnosed in children and adolescents. MNAT1 is a subunit in the cyclin-dependent kinase-activating kinase complex. Abnormal up-regulation of MNAT1 has been associated with the poor prognosis of multiple cancers. Bioinformatics analysis showed that has-circ-0001146 and miR-26a-5p were involved in the regulation of MNAT1 in osteosarcoma. The present study investigated the regulatory effects of has-circ-0001146 and miR-26a-5p on MNAT1 expression using luciferase reporter and RNA-pull down assays. The effects of the has-circ-0001146/miR26a-5p/Mnat1 network on the proliferation and invasion of osteosarcoma were evaluated by cell viability, apoptosis, migration, and invasion assays. Osteosarcoma tissues showed higher MNAT1 and has-circ-0001146 expression than adjacent normal tissues, although the expression of MNAT1 was not significantly up-regulated in sarcomas according to TCGA databases. As indicated by luciferase reporter and RNA-pull down assays, miR-26a-5p was able to bind to both has-circ-0001146 and MNAT1 mRNA. The depletion of has-circ-0001146 as well as the increase of miR-26a-5p decreased MNAT1 expression in osteosarcoma cells, while the reduction of miR-26a-5p was associated with increased MNAT1 expression. These data suggested that has-circ-0001146 promoted MNAT1 expression by competitively binding to miR-26a-5p with MNAT1 mRNA. The depletion of has-circ-0001146 or MNAT1 or the increase of miR-26a-5p inhibited osteosarcoma cell viability and invasion, and increased apoptosis. Reduction of miR-26a-5p conversely promoted osteosarcoma cell viability and invasion. The present study confirmed that has-circ-0001146 blocked miR-26a-5p targeting MNAT1 in osteosarcoma cells, thereby promoting the malignant behaviours of osteosarcoma cells.

Interaction between miR-572 and PPP2R2C, and their effects on the proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC) cells

2017 ◽  
Vol 95 (5) ◽  
pp. 578-584 ◽  
Author(s):  
Lei Yan ◽  
Kerui Cai ◽  
Jun Liang ◽  
Haifeng Liu ◽  
Yang Liu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Normal Tissues ◽  
Gene Assay ◽  
And Migration ◽  
Proliferation And Invasion ◽  
Lower Expression

We investigated the how miR-572 regulates PPP2R2C, and studied the effects of miR-572 and PPP2R2C on proliferation and migration as well as invasion of nasopharyngeal carcinoma (NPC) cells. NPC tissues and normal tissues were collected, and the expressions of miR-572 and PPP2R2C were detected by real-time PCR. Western blot was applied to detect the expression of PPP2R2C protein. The target relationship between miR-572 and PPP2R2C was confirmed by dual luciferase reporter gene assay. MTT assay and flow cytometry were applied to investigate the viability and apoptosis levels of NPC cells. Transwell as well as wound healing assays were used, respectively, to detect the invasiveness and migration of NPC cells. MiR-572 was highly expressed in NPC tissues as well as NPC cells, and there was lower expression of PPP2R2C in NPC tissues compared with normal samples. MiR-572 could bind to the 3′ UTR of PPP2R2C and decrease its expression. Over-expressed miR-572 and decreased PPP2R2C expression could both inhibit proliferation and invasion and induce apoptosis of NPC cells. Thus, miR-572 promotes the proliferation and invasion of NPC by directly down-regulating PPP2R2C.

scholarly journals Armadillo Repeat-Containing Protein 8 (ARMC8) Silencing Inhibits Proliferation and Invasion in Osteosarcoma Cells

2016 ◽  
Vol 24 (5) ◽  
pp. 381-389 ◽  
Author(s):  
Feng Jiang ◽  
Yan Shi ◽  
Hong Lu ◽  
Guojun Li
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Mesenchymal Transition ◽  
Armadillo Repeat ◽  
Proliferation And Invasion

Armadillo repeat-containing protein 8 (ARMC8) plays an important role in regulating cell migration, proliferation, tissue maintenance, signal transduction, and tumorigenesis. However, the expression pattern and role of ARMC8 in osteosarcoma are still unclear. In this study, our aims were to examine the effects of ARMC8 on osteosarcoma and to explore its underlying mechanism. Our results demonstrated that ARMC8 was overexpressed in osteosarcoma cell lines. Knockdown of ARMC8 significantly inhibited osteosarcoma cell proliferation in vitro and markedly inhibited xenograft tumor growth in vivo. ARMC8 silencing also suppressed the epithelial‐mesenchymal transition (EMT) phenotype, as well as inhibited the migration and invasion of osteosarcoma cells. Furthermore, knockdown of ARMC8 obviously inhibited the expression of β-catenin, c-Myc, and cyclin D1 in MG-63 cells. In conclusion, this report demonstrates that ARMC8 silencing inhibits proliferation and invasion of osteosarcoma cells. Therefore, ARMC8 may play an important role in the development and progression of human osteosarcoma and may represent a novel therapeutic target in the treatment of osteosarcoma.

scholarly journals The proliferation and invasion of osteosarcoma are inhibited by miR-101 via targetting ZEB2

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Haopeng Lin ◽  
Xiaodong Zheng ◽  
Ting Lu ◽  
Yang Gu ◽  
Canhao Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Bone Cell ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Direct Target ◽  
Proliferation And Invasion

AbstractHaving a better grasp of the molecular mechanisms underlying carcinogenesis and progression in osteosarcoma would be helpful to find novel therapeutic targets. Different types of cancers have presented abnormal expression of miRNA-101 (miR-101). Nevertheless, we still could not figure out what expression of miR-101 in human osteosarcoma is and its biological function. Thus, we conducted the present study to identify its expression, function, and molecular mechanism in osteosarcoma. We detected the expression of miR-101 in osteosarcoma samples and cell lines. The effects of miR-101 on osteosarcoma cells’ proliferation and invasion were evaluated. Luciferase reporter assay was applied to identify the direct target of miR-101. Compared with adjacent normal specimens and normal bone cell line by using qPCR, the expression levels of miR-101 in osteosarcoma specimens and human osteosarcoma cell lines distinctly decreased. According to function assays, we found that overexpression of miR-101 significantly inhibited the cell proliferation and invasion in osteosarcoma cells. Moreover, we confirmed that zinc finger E-box binding homeobox 2 (ZEB2) was a direct target of miR-101. In addition, overexpression of ZEB2 could rescue the inhibition effect of proliferation and invasion induced by miR-101 in osteosarcoma cells. MiR-101 has been proved to be down-regulated in osteosarcoma and has the ability to suppress osteosarcoma cell proliferation and invasion by directly targetting ZEB2.

scholarly journals Long Non-Coding RNA Urothelial Carcinoma Associated 1 Promotes Proliferation, Migration and Invasion of Osteosarcoma Cells by Regulating microRNA-182

2018 ◽  
Vol 51 (3) ◽  
pp. 1149-1163 ◽  
Author(s):  
Qiang Li ◽  
Wanying Xing ◽  
Xilong Gong ◽  
Yueshu Wang
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Key Factors ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Luciferase Activity Assay

Background/Aims: Previous studies demonstrated the oncogenic roles of lncRNA UCA1 in osteosarcoma. This study aimed to explore the internal molecular mechanism of UCA1 on promoting osteosarcoma cell proliferation, migration and invasion. Methods: qRT-PCR was conducted to measure the expression levels of UCA1, miR-182 and TIMP2. Cell transfection was used to change the expression levels of UCA1, miR-182 and TIMP2. Cell viability, migration, invasion and apoptosis were measured using CCK-8 assay, two-chamber migration (invasion) assay and Guava Nexin assay, respectively. The associations between UCA1, miR-182 and iASPP were analyzed by dual luciferase activity assay. The protein expression levels of key factors involved in cell apoptosis, PI3K/AKT/GSK3β pathway and NF-κB pathway, as well as p53, Rb, RECQ family and iASPP were evaluated by western blotting. Results: UCA1 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of UCA1 inhibited OS-732 cell viability, migration and invasion, but promoted cell apoptosis. miR-182 was up-regulated in OS-732 cells after UCA1 knockdown and participated in the effects of UCA1 on OS-732 cells. TIMP2 was downstream factor of miR-182 and involved in the regulatory roles of miR-182 on OS-732 cell viability, migration, invasion, apoptosis, as well as PI3K/AKT/GSK3β and NF-κB pathways. UCA1 knockdown up-regulated p53, Rb and RECQL5 levels in OS-732 cells, while down-regulated the expression of iASPP. TGF-β or TNF-α treatment could enhance the expression of UCA1 in OS-732 cells. Conclusion: Our research verified that UCA1 exerted oncogenic roles in osteosarcoma cells by regulating miR-182 and TIMP2, as well as PI3K/AKT/GSK3β and NF-κB pathways.

scholarly journals CircSAMD4A contributes to cell doxorubicin resistance in osteosarcoma by regulating the miR-218-5p/KLF8 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 848-859
Author(s):  
Wei Wei ◽  
Liefeng Ji ◽  
Wanli Duan ◽  
Jiang Zhu
Keyword(s):  
Cell Cycle ◽  
Cell Viability ◽  
Circular Rna ◽  
Resistant Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Osteosarcoma Cells

AbstractCircular RNA sterile alpha motif domain containing 4A (circSAMD4A) was found to be differentially expressed in osteosarcoma and contributed to the tumorigenesis of osteosarcoma. However, the role of circSAMD4A in doxorubicin (DXR) resistance of osteosarcoma is yet to be elucidated. Levels of circSAMD4A, microRNA (miR)-218-5p and Krüppel-like factor 8 (KLF8) were detected using quantitative reverse transcription-polymerase chain reaction. Western blot was applied to detect the protein levels of KLF8, cyclin D1 and p21. Cell viability, cell cycle, migration and invasion were analyzed using Cell Counting Kit-8 assay, flow cytometry and transwell assay, respectively. The interaction between miR-218-5p and circSAMD4A or KLF8 was verified using dual-luciferase reporter assay or RNA immunoprecipitation assay. In vivo experiments were performed using murine xenograft models. CircSAMD4A and KLF8 were elevated in osteosarcoma, and knockdown of circSAMD4A or KLF8 sensitized osteosarcoma cells to DXR by mediating resistant cell viability, migration and invasion inhibition, and cell cycle arrest in vitro. miR-218-5p was decreased in osteosarcoma, and miR-218-5p inhibition enhanced DXR resistance. Besides, miR-218-5p was found to bind to circSAMD4A or KLF8, and subsequent rescue experiments indicated that miR-218-5p inhibition reversed the inhibitory effects of circSAMD4A silencing on DXR resistance, and silencing miR-218-5p enhanced DXR resistance by targeting KLF8 in osteosarcoma cells. Moreover, circSAMD4A could indirectly regulate KLF8 via miR-218-5p. Additionally, circSAMD4A knockdown enhanced the cytotoxicity of DXR in osteosarcoma in vivo via regulating miR-218-5p and KLF8. In all, circSAMD4A enhanced cell DXR resistance in osteosarcoma by regulating the miR-218-5p/KLF8 axis, suggesting a novel therapeutic target for therapy-resistant osteosarcoma.

scholarly journals LINC01116 Promotes Doxorubicin Resistance in Osteosarcoma by Epigenetically Silencing miR-424-5p and Inducing Epithelial-Mesenchymal Transition

2021 ◽  
Vol 12 ◽  
Author(s):  
Ran Li ◽  
Qing Ruan ◽  
Jia Zheng ◽  
Butian Zhang ◽  
Hongliang Yang
Keyword(s):  
Cell Viability ◽  
Western Blotting ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Mesenchymal Transition ◽  
Doxorubicin Resistance ◽  
Specific Pcr ◽  
E Cadherin

Background: Development of resistance to doxorubicin-based chemotherapy limits its curative effect in osteosarcoma. In the current study, we focused on investigating the mechanisms underlying the development of doxorubicin resistance in osteosarcoma.Methods: The human osteosarcoma cell line MG-63 and doxorubicin-resistant MG-63/Dox cells were used in this study. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of the long non-coding RNA LINC01116 in the two cell lines. Then, the specific shRNA for LINC01116 was employed to suppress LINC01116 expression in MG-63/Dox cells. Cell viability was assessed by the CCK-8 and colony formation assays. Cell migration and invasion were evaluated by the transwell assay. Moreover, the epithelial-mesenchymal transition (EMT)-related proteins, E-cadherin, vimentin, and N-cadherin were evaluated by Western blotting. The regulation of LINC01116 on miR-424-5p expression was examined using methylation-specific PCR, RNA immunoprecipitation, and Western blotting assay. The potential targeting of HMGA2 by miR-424-5p was predicted using the bioinformatics databases TargetScan and miRanda and verified by a dual-luciferase reporter assay.Results: LINC01116 was more highly expressed in MG-63/Dox cells than in MG-63 cells. Inhibition of LINC01116 suppressed cell viability, migration, and invasion, along with upregulating the expression of E-cadherin, downregulating vimentin, and attenuating doxorubicin resistance in MG-63/Dox cells. Further mechanism-related investigations indicated that LINC01116 regulated HMGA2 expression via the EZH2-associated silencing of miR-424-5p.Conclusion: LINC01116 exerts regulatory effects on doxorubicin resistance through the miR-424-5p axis, providing a potential approach to overcoming chemoresistance in osteosarcoma.

scholarly journals Silencing Herg1 by shRNA inhibits the proliferation and invasion of osteosarcoma in vivo and in vitro

2021 ◽  
Author(s):  
Zhida Chen ◽  
Chao Song ◽  
Yunping Chen ◽  
Lili Xiao ◽  
Yuanjie Jiang ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Affinity Purification ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Nude Mouse Model ◽  
Proliferation And Invasion

Abstract Background: Osteosarcoma is the most common malignant bone tumor of childhood, and improvements in the survival rates have reached a plateau phase. This study was aimed to explore the the importance of the human ether-a-go-go-related potassium channel (Herg1) in the proliferation and invasion of osteosarcoma.Methods: The effects of Herg1 silenced on osteosarcoma cell proliferation and invasion were detected by were detected by CCK-8 assay, wound healing assay and transwell assay, respectively. Tandem affinity purification, mass spectrometry and Dual luciferase reporter assay were used to find out possible molecules responsible for the action of Herg1 on osteosarcoma cells. Nude mouse model was used to investigate the in vivo functions of Herg1. Results: Herg1 silencing by shRNA significantly suppressed the proliferation and invasion of osteosarcoma cells in vitro as well as tumorigenicity and metastasis in nude mice. Moreover, Herg1 promoted osteosarcoma progression via turning off Hippo signaling pathway, leading to the activation of Yes-associated protein (YAP). Mechanistically, Herg1 co-localized and interacted with NF2 (also called Merlin), and this interaction probably caused the de-phosphorylation of MST1/2 and LATS1/2, which drove YAP nuclear translocation and transcriptional activation. Conclusion: Herg1 acts as an oncogene in osteosarcoma and may therefore serve as a useful therapeutic target for osteosarcoma patients.

scholarly journals LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972095309
Author(s):  
Jianmin Liu ◽  
Ming Chen ◽  
Longyang Ma ◽  
Xingbo Dang ◽  
Gongliang Du
Keyword(s):  
Cell Proliferation ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Luciferase Reporter Gene ◽  
Nude Mouse Model ◽  
Cell Functions ◽  
Proliferation And Invasion

Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.

scholarly journals The lncRNA NEAT1 promotes the epithelial-mesenchymal transition and metastasis of osteosarcoma cells by sponging miR-483 to upregulate STAT3 expression

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yan Chen ◽  
Jun Li ◽  
Jia-Kun Xiao ◽  
Lei Xiao ◽  
Bin-Wu Xu ◽  
...  
Keyword(s):  
Nude Mice ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Aberrant Expression ◽  
Mesenchymal Transition ◽  
U2os Cells ◽  
Lncrna Neat1

Abstract Background Osteosarcoma is one of the most prevalent primary bone tumours in adolescents. Accumulating evidence shows that aberrant expression of the long non-coding RNA (lncRNA) NEAT1 and microRNA-483 (miR-483) contribute to the epithelial-mesenchymal transition (EMT), invasion and metastasis of tumour cells. However, the potential regulatory effects of NEAT1 and miR-483 on the EMT of osteosarcoma remain elusive. Methods The expression of the NEAT1, miR-483, signal transducer and activator of transcription-1 (STAT1), STAT3, and EMT-associated markers was measured using qRT-PCR or western blotting. NEAT1 overexpression or knockdown was induced by lentivirus-mediated transfection. A luciferase reporter assay was employed to confirm the association between NEAT1/miR-483 and miR-483/STAT3. RNA immunoprecipitation (RIP) was also performed to verify the NEAT1 and miR-483 interaction. Wound healing and transwell assays were implemented to assess the migration and invasion of U2OS cells. Unilateral subcutaneous injection of U2OS into nude mice was performed to investigate tumour metastasis in vivo. Results The expression of miR-483 was downregulated in both osteosarcoma cell lines and osteosarcoma tissues. The overexpression of miR-483 suppressed the migration, invasion, and expression of EMT-associated proteins in U2OS cells, while simultaneous overexpression of STAT3 partially relieved this suppression. Mechanistically, miR-483 specifically targeted the 3′ untranslated region (3′UTR) of STAT3 and repressed its expression. However, NEAT1 sponged miR-438, increased STAT3 expression, and repressed STAT1 expression, subsequently increasing the EMT of osteosarcoma cells. The knockdown of NEAT1 in transplanted U2OS cells impaired the liver and lung metastases of osteosarcoma in nude mice. Moreover, NEAT1 silencing inhibited the mesenchymal- epithelial transition (MET) of osteosarcoma at metastasis sites. Conclusions The lncRNA NEAT1/miR-483/STAT3 axis plays a crucial role in regulating the metastasis of osteosarcoma and potentially represents one appealing therapeutic target for osteosarcoma treatment in the future.

scholarly journals Silencing long intergenic non-protein coding RNA 00987 inhibits proliferation, migration, and invasion of osteosarcoma cells by sponging miR-376a-5p to regulate FNBP1 expression

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Riliang Cao ◽  
Jianli Shao ◽  
Wencai Zhang ◽  
Yongxin Lin ◽  
Zerong Huang ◽  
...  
Keyword(s):  
Biological Function ◽  
Cancer Cell Line ◽  
Underlying Mechanism ◽  
Bioinformatic Analysis ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Protein Coding

AbstractHigh expression of long intergenic non-protein coding RNA 987 (LINC00987) is strongly associated with low overall survival of osteosarcoma; however, its role in osteosarcoma remains unclear. This study explored the biological function and underlying mechanism of LINC00987 in osteosarcoma. In this study, LINC00987 expression in osteosarcoma cells was analyzed using Cancer Cell Line Encyclopedia and qRT-PCR. The proliferation and migration and invasion in osteosarcoma cells were evaluated using Cell Counting Kit-8 and Transwell assays, respectively. Bioinformatic analysis was used to predict the LINC00987-bound miRNAs and miR-376a-5p-bound mRNAs. Dual-luciferase reporter assays were used to assess the interaction between miR-376a-5p, LINC00987, and forming-binding protein 1 (FNBP1). FNBP1 expression was measured by western blotting. LINC00987 was found to be upregulated in osteosarcoma cells. LINC00987 silencing suppressed proliferation, migration, and invasion of osteosarcoma cells. Additionally, miR-376a-5p expression was downregulated in osteosarcoma cells. miR-376a-5p knockdown reversed the effect of LINC00987 silencing on the biological function of osteosarcoma cell. miR-376a-5p was found to target LINC00987 and FNBP1. FNBP1protein level was increased in osteosarcoma cells; however, it was inhibited by silencing LINC00987 and enhanced by silencing miR-376a-5p. In conclusions, this study suggests LINC00987 silencing inhibits osteosarcoma cell proliferation, migration, and invasion by sponging miR-376a-5p to regulate FNBP1 expression. LINC00987 as a potential therapeutic target for osteosarcoma.

Sign in / Sign up

Export Citation Format

Share Document