Long noncoding RNA BSN-AS2 induced by E2F1 promotes spinal osteosarcoma progression by targeting miR-654-3p/SYTL2 axis

Zhou, Xiuping; Li, Jitian; Teng, Junyan; Liu, Yufeng; Zhang, Di; Liu, Linyun; Zhang, Wenming

doi:10.1186/s12935-020-01205-y

Cited by 15 publications

(13 citation statements)

References 31 publications

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“…To assess the molecular mechanism of hsa_circ_0079480 in AML, the miRNA targets were predicted using online tools (Circular RNA Interactome and circBank [ 17 – 20 ]), and two potential candidates (hsa-miR-346 and hsa-miR-654-3p) were identified ( Figure 4A ). Pull-down experiments validated the enrichment of hsa_circ_0079480 and miR-654-3p in both MOLM-13 and AML-193 cell lines ( Figure 4B ).…”

Section: Resultsmentioning

confidence: 99%

Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis

Chen

et al. 2020

Aging

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Circular RNAs (circRNAs) are newly-discovered endogenous non-coding RNAs that have vital functions in regulating gene expression in tumorigenesis. Nonetheless, the function of circRNAs in acute myeloid leukemia (AML) are not yet clarified. In this analysis, hsa_circ_0079480, a novel circRNA, has been identified as being highly expressed in AML. Loss-of-function assays showed that reduction of hsa_circ_0079480 decreased the growth and stimulated apoptosis of AML cells in vitro . Furthermore, miR-654-3p was sponged by hsa_circ_0079480, and hepatoma-derived growth factor (HDGF) was targeted by miR-654-3p with respect to the fundamental mechanism. Moreover, the influence on growth and apoptosis of AML cells stimulated by hsa_circ_0079480 inhibition can be rescued by miR-654-3p inhibitor or HDGF overexpression. In summary, hsa_circ_0079480 is highly expressed in AML and drives by tumor progression via regulation of hsa_circ_0079480/miR-654-3p/HDGF axis, indicating that hsa_circ_0079480 may function as a new treatment target for AML therapy.

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Section: Resultsmentioning

confidence: 99%

Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis

Chen

et al. 2020

Aging

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“…collectively, it can be concluded that MKLN1-AS increased HdGF expression in Hcc cells by acting as a ceRNA and competitively binding to miR-654-3p. miR-654-3p is downregulated in ovarian cancer (47), gastric cancer (48) and papillary thyroid cancer (49), but is upregulated in osteosarcoma (50). Moreover, miR-654-3p exerts cancer-inhibiting (47)(48)(49) or cancer-promoting roles (50), and is implicated in cancer oncogenesis and progression (47)(48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

“…miR-654-3p is downregulated in ovarian cancer ( 47 ), gastric cancer ( 48 ) and papillary thyroid cancer ( 49 ), but is upregulated in osteosarcoma ( 50 ). Moreover, miR-654-3p exerts cancer-inhibiting ( 47 – 49 ) or cancer-promoting roles ( 50 ), and is implicated in cancer oncogenesis and progression ( 47 – 50 ). A recent study reported that miR-654-3p expression was down-regulated in HCC, which was associated with poor patient prognosis, and that overexpression of miR-654-3p restricted cell proliferation, migration and invasion in HCC ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA MKLN1‑AS aggravates hepatocellular carcinoma progression by functioning as a molecular sponge for miR‑654‑3p, thereby promoting hepatoma‑derived growth factor expression

Gao¹,

Chen²,

Chi³

et al. 2020

Int J Mol Med

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Long non-coding RNAs (lncRNAs) have recently gained attention due to their important roles in human cancer types, such as breast and gastric cancer. The present study measured alterations in muskelin 1 antisense RNA (MKLN1-AS) expression in hepatocellular carcinoma (Hcc) and evaluated its clinical value in patients with Hcc. Additionally, the current study investigated the effects of MKLN1-AS on the malignant features of Hcc cells. The detailed molecular mechanisms underlying the cancer-promoting activities of MKLN1-AS in Hcc cells were also elucidated. MKLN1-AS expression in Hcc tissues and cell lines was detected using reverse-transcription quantitative PCR (RT-qPCR). Cell Counting Kit-8 assays and flow cytometry were used to determine the roles of MKLN1-AS in Hcc cell proliferation and apoptosis. Migration and invasion assays, as well as tumor xenograft experiments were conducted to analyze migration and invasion in vitro and tumor growth in vivo, respectively. The interaction among microRNA-654-3p (miR-654-3p), MKLN1-AS and hepatoma-derived growth factor (HdGF) in Hcc was investigated using luciferase reporter assay, RNA immunoprecipitation assay, RT-qPcR, western blotting and rescue experiments. MKLN1-AS was upregulated in Hcc tissues and cell lines, and a high MKLN1-AS expression was associated with shorter overall survival and disease-free survival in patients with Hcc. Functionally, the knockdown of MKLN1-AS impaired Hcc cell proliferation, migration and invasion, as well as induced cell apoptosis in vitro. Knockdown of MKLN1-AS expression also inhibited cell proliferation in vivo. The results indicated that MKLN1-AS functioned as a competing endogenous RNA by sponging miR-654-3p in Hcc cells. Additionally, miR-654-3p targeting of HdGF was positively modulated by MKLN1-AS, and miR-654-3p knockdown partially abrogated this effect. Rescue experiments demonstrated that knockdown of miR-654-3p and overexpression of HdGF both abolished MKLN1-AS knockdown-induced cellular processes in Hcc. In summary, MKLN1-AS induced pro-oncogenic effects during Hcc progression by serving as a molecular sponge for miR-654-3p to increase HdGF expression. Therefore, the MKLN1-AS/miR-654-3p/HdGF axis may offer a novel target for the diagnosis, prognosis, prevention and treatment of Hcc.

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“…Emerging research evidence posits that noncoding RNAs, including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs serve signi cant roles in modulating pathogenesis, detection, and prognosis of OS [7,8]. LncRNAs function as crucial OS biosignatures and drug targets by serving as competitive endogenous RNAs (ceRNAs) for miRNAs to repress mRNA expression [9].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA FEZF1-AS1 Inhibits metastasis of Osteosarcoma Cells by miR-4456/GALNT10

Zhou

Shen

et al. 2020

Preprint

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Background: Osteosarcoma (OS) is among the malignant tumors with high mortality and low survival, especially in children and adolescents. Research shows that LncRNA FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) enhances osteosarcoma progression. Nevertheless, the function and mechanism of FEZF1-AS1 in metastasis of OS remains unclear.Methods: We used qRT-PCR to assay for the expression of FEZF1-AS1, miR-4456, and GALNT10 in OS tissue specimens and cell lines. We also investigated the progression of OS through metastasis using the wound healing and Transwell assays. Moreover, we used the dual-luciferase reporter test, RIP assays, and western blot to validate whether FEZF1-AS1 serves as a competing endogenous RNA (ceRNA), modulating the expression of GALNT10 through sponging miR-4456 in OS.Results: FEZF1-AS1 was up modulated in OS tissues. Silencing FEZF1-AS1 repressed OS cell migration and invasion. microRNA-4456 (miR-4456) was involved in FEZF1-AS1-induced migration and invasion. miR-4456 was down modulated in OS tissue specimens and cell lines. Functionally, the up modulation of miR-4456 reversed the facilitative influence of FEZF1-AS1 on OS cell infiltration and migration. Mechanically, FEZF1-AS1 interacted with miR-4456 in a reciprocal suppressed manner. Moreover, miR-4456 targets GALNT10 via the Luciferase assay. Besides, the up modulation of GALNT10 reversed the migration and invasion inhibited by FEZF1-AS1 knockdown. Silencing of FEZF1-AS1 inhibits OS cell infiltration and migration through miR-4456 /GALNT10 sponging.Conclusion: Herein, we demonstrated that FEZF1-AS1 is a prospective bio signature of metastasis in OS patients. Mechanistically, we showed that the FEZF1-AS1/miR-4456/GALNT10 axis is a target for novel therapeutic development for OS.

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Long noncoding RNA BSN-AS2 induced by E2F1 promotes spinal osteosarcoma progression by targeting miR-654-3p/SYTL2 axis

Cited by 15 publications

References 31 publications

Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis

Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis

Long non‑coding RNA MKLN1‑AS aggravates hepatocellular carcinoma progression by functioning as a molecular sponge for miR‑654‑3p, thereby promoting hepatoma‑derived growth factor expression

Knockdown of lncRNA FEZF1-AS1 Inhibits metastasis of Osteosarcoma Cells by miR-4456/GALNT10

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