MiR-129-5p Suppresses Cell Proliferation of Human Osteosarcoma Cancer by Down-Regulating LncRNA Lnc712

Yu, Yifan; Zuo, Wenshan; Cai, Wei; Xu, Yong; Liu, Weidong; Zhao, Zhongwei

doi:10.2147/cmar.s284078

Cited by 5 publications

(5 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we show that miR-129-5p inhibits proliferation, attenuates migration and induces apoptosis in vitro and suppresses tumor growth in vivo in hepatocellular carcinoma. Similar tumor-suppressive effects of miR-129-5p have also been observed in osteosarcoma [ 46 ], prostate [ 47 ] and breast cancer [ 48 ].…”

Section: Discussionsupporting

confidence: 64%

MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functions in hepatocellular carcinoma by directly targeting hepatoma-derived growth factor HDGF

et al. 2022

View full text Add to dashboard Cite

Background In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis. Methods Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined. Results HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3′UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs. Conclusions This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis.

show abstract

Section: Discussionsupporting

confidence: 64%

MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functions in hepatocellular carcinoma by directly targeting hepatoma-derived growth factor HDGF

et al. 2022

View full text Add to dashboard Cite

show abstract

“…miRNAs were documented to play a critical role in cancers and so had been emerged as novel molecular markers for tumor diagnosis and prognostic assessment [ 19 ]. miR-129-5p was an important molecule involved in the regulation of cell proliferation, migration, apoptosis and signaling pathways [ 20 , 21 ]. miR-129-5p was identified to decreased in prostate cancer and may function as a tumor suppressor via repression of ETV1 [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

“…miR-129-5p was identified to decreased in prostate cancer and may function as a tumor suppressor via repression of ETV1 [ 22 ]. Besides, another study has demonstrated that miR-129-5p may suppress cell proliferation of osteosarcoma cancer by down-regulating Lnc712 [ 21 ]. Similarly, in this study, we found that miR-129-5p was lowly expressed while expression levels of TNFSF10 were highly expressed in BC than in normal uroepithelial cell line.…”

Section: Discussionmentioning

confidence: 99%

LncRNA XIST promotes bladder cancer progression by modulating miR-129-5p/TNFSF10 axis

Kong,

Wang,

Gao

et al. 2024

Discov Onc

View full text Add to dashboard Cite

Background The differential expression, biological function, and ceRNA regulatory mechanism of lncRNA XIST in bladder cancer (BC) were investigated, and its clinical values for the early diagnosis of bladder cancer patients were elucidated. Methods qRT-PCR was employed to detect the expression patterns of lncRNA XIST, miR-129-5p and TNFSF10. The biological functions were measured by CCK8 assay, wound healing assay and transwell assay. Bioinformatics analysis and Dual-Luciferase reporter assay were employed to evaluate the interactions between the lncRNA XIST, miR-129-5p and TNFSF10. Results LncRNA XIST and TNFSF10 were highly expressed and miR-129-5p was low expressed (P < 0.05) in bladder cancer cell line. The depletion of lncRNA XIST inhibited BC proliferation, migration and invasion. Mechanistically, lncRNA XIST could sponge miR-129-5p to regulate TNFSF10 expression in bladder cancer. Furthermore, compared with adjacent tissues, lncRNA XIST and miR-129-5p were lowly expressed (P < 0.01) in bladder cancer tissues, and TNFSF10 was highly expressed (P < 0.001). miR-129-5p and TNFSF10 were associated with the risk of bladder cancer (P < 0.05); the difference in AUC values for the diagnosis of bladder cancer by lncRNA XIST (AUC = 0.739), miR-129-5p (AUC = 0.850) and TNFSF10 (AUC = 0.753) was statistically significant (P < 0.01), and the three genes combined AUC was 0.900, 95%CI was 0.842–0.958 with a sensitivity of 83.3% and specificity of 86.7%. Conclusion XIST, an elevated lncRNA in bladder cancer, inhibition of which could suppress the progression of BC. LncRNA XIST and miR-129-5p could form ceRNA to regulate the expression of TNFSF10.

show abstract

“…In this study, we obtained 25 miRNAs closely associated with the prognostic signature and constructed the first FKBP11-related ceRNA network regulatory axis for OS. Bioinformatics analysis revealed that NBR2 and FKBP11 possess similar miR-129-5p-binding sites, and the miR-129-5p suppresses the progression of tumors, including OS [ 27 , 28 ]. The results of the luciferase reporter gene experiments showed that both NBR2 and FKBP11 were physically associated with miR-129-5p.…”

Section: Discussionmentioning

confidence: 99%

Machine learning and experimental validation to construct a metastasis-related gene signature and ceRNA network for predicting osteosarcoma prognosis

Liao¹,

Liu

Xiao

et al. 2022

J Orthop Surg Res

View full text Add to dashboard Cite

Objective Osteosarcoma (OS) is more common in adolescents and significantly harmful, and the survival rate is considerably low, especially in patients with metastatic OS. The identification of effective biomarkers and associated regulatory mechanisms, which predict OS occurrence and development as well as improve prognostic accuracy, will help develop more refined protocols for OS treatment. Methods In this study, genes showing differential expression in metastatic and non-metastatic types of OS were identified, and the ones affecting OS prognosis were screened from among these. Following this, the functions and pathways associated with the genes were explored via enrichment analysis, and an effective predictive signature was constructed using Cox regression based on the machine learning algorithm, least absolute shrinkage and selection operator (LASSO). Next, a correlative competing endogenous RNA (ceRNA) regulatory axis was constructed after verification by bioinformatics analysis and luciferase reporter gene experiments conducted based on the prognostic signature. Results Overall, 251 differentially expressed genes were identified and screened using bioinformatics and double luciferase reporter gene experiments. An effective prognostic signature was constructed based on 15 genes associated with OS metastasis, and upstream non-coding RNAs were identified to construct the “NBR2/miR-129-5p/FKBP11” regulatory axis based on the ceRNA networks, which helped identify candidate biomarkers for the OS clinical diagnosis and treatment, drug research, and prognostic prediction, among other applications. The findings of this study provide a novel strategy for determining the mechanism underlying OS occurrence and development and the appropriate treatment.

show abstract

MiR-129-5p Suppresses Cell Proliferation of Human Osteosarcoma Cancer by Down-Regulating LncRNA Lnc712

Cited by 5 publications

References 20 publications

MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functions in hepatocellular carcinoma by directly targeting hepatoma-derived growth factor HDGF

MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functions in hepatocellular carcinoma by directly targeting hepatoma-derived growth factor HDGF

LncRNA XIST promotes bladder cancer progression by modulating miR-129-5p/TNFSF10 axis

Machine learning and experimental validation to construct a metastasis-related gene signature and ceRNA network for predicting osteosarcoma prognosis

Contact Info

Product

Resources

About