MicroRNA-1294 inhibited oral squamous cell carcinoma growth by targeting c-Myc

Wang, Zuojun; Yan, Jinsheng; Zou, Tingqian; Gao, Hui

doi:10.3892/ol.2018.8967

Cited by 22 publications

(24 citation statements)

References 36 publications

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“…In glioma, miR-1294 inhibited cell proliferation and contributed to chemosensitivity via directing TPX2 [23]. Similarly, it was also down-regulated in oral squamous cell carcinoma tissues and cells and acted as a tumor suppressor via inhibiting proliferation and migration through regulating c-Myc [24]. Notably, previous study reported the correlation between the down-regulation of miR-1294 and the poor prognosis of esophageal squamous cell carcinoma [25].…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0004370 promotes esophageal cancer progression through miR-1294/LASP1 pathway

et al. 2019

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Circular RNAs (circRNAs) formed by back-splicing play multiple roles in the occurrence and development of cancer. Here, we found that hsa_circ_0004370 was up-regulated in both esophageal cancer (EC) tissues and cell lines. Loss function of hsa_circ_0004370 by si-RNA significantly suppressed proliferation and invasion and promoted apoptosis in both EC cell lines. The sponging of miR-1294 by hsa_circ_0004370 was bioinformatically predicted and subsequently verified by luciferase reporter assay and RNA immunoprecipitation assay. Further, hsa_circ_0004370 involved in the up-regulation of LASP1 by sponging miR-1294. Besides, the inhibition of the down-regulated hsa_circ_0004370 on cell malignant behaviors was rescued by miR-1294 inhibitor. Finally, this rescue effect was abrogated by suppressing the expression of LASP1. The results present here suggest that hsa_circ_0004370 functions as an oncogene on cell proliferation, apoptosis, and invasion via miR-1294/LASP1 axis.

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Section: Discussionmentioning

confidence: 99%

Hsa_circ_0004370 promotes esophageal cancer progression through miR-1294/LASP1 pathway

et al. 2019

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“…More importantly, we identified that PKM2, a new target gene of miR-1294, played key roles in miR-1294mediated actions in osteosarcoma cells. Moreover, the tumor-suppressing role of miR-1294 has been reported in other of tumors, such as gastric cancer, 8 esophageal squamous cell carcinoma, 19 epithelial ovarian cancer, 7 oral squamous cell carcinoma, 9 and glioma. 11 Uncontrolled growth, invasion, and metastasis are the main characteristics of tumor cells.…”

Section: Discussionmentioning

confidence: 96%

“…5 Increasing evidence shows that miRNAs play important roles in regulating cancer cell development. 6 Previous studies have demonstrated that miR-1294 is lowly expressed in multiple cancers, such as epithelial ovarian cancer, 7 gastric cancer, 8 oral squamous cell carcinoma, 9 osteosarcoma, 10 and glioma. 11 Forced expression of miR-1294 inhibits tumor cell growth and cisplatin resistance.…”

Section: Introductionmentioning

confidence: 99%

<p>Antitumor Effect of miR-1294/Pyruvate Kinase M2 Signaling Cascade in Osteosarcoma Cells</p>

Yuan¹,

Yu²,

Chen³

et al. 2020

OTT

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Background: MicroRNAs (miRNAs) can act as negative regulators of gene expression, and play a crucial role in cancer progression. The aim of this study was to investigate the role of miR-1294/pyruvate kinase M2 (PKM2) axis in osteosarcoma cells in vitro and in vivo. Methods: The function of miR-1294 and its association with PKM2 in osteosarcoma cells were studied by real-time PCR, CCK-8, Western blot, scratch test, transwell assay, flow cytometry, and dual-luciferase reporter assays. The effect of miR-1294 on tumor growth in vivo was evaluated in a subcutaneous xenograft model of osteosarcoma. Results: miR-1294 was downregulated in osteosarcoma cells. Forced overexpression of miR-1294 inhibited cell proliferation, migration, and invasion, and induced G0/G1 arrest and apoptosis. Consistently, protein expression levels of proliferating cell nuclear antigen, c-Myc, cyclin D1, active matrix metalloproteinase 2, and active matrix metalloproteinase 9 were decreased, and cleaved caspase 3 and cleaved PARP were increased following miR-1294 overexpression. Moreover, we demonstrated that PKM2 was a target of miR-1294 in osteosarcoma cells, and the effects caused by miR-1294 mimic were reversed by the overexpression of PKM2. Furthermore, we found that upregulation of miR-1294 inhibited tumorigenesis of osteosarcoma cells in vivo, which was accompanied by downregulation of PKM2. Conclusion: Our results revealed that miR-1294/PKM2 signaling cascade exerts important roles in the regulation of tumor progression, implying that this pathway may serve as a potential therapeutic target in osteosarcoma.

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“…MiR-1294 is considered a tumor suppressor in many cancers, such as clear cell renal cell carcinoma and oral squamous cell carcinoma. 14 , 15 Besides, miR-1294 can be sponged by circ_0005198 to participate in the mediation of circ_0005198 on the proliferation, apoptosis and metastasis of glioma. 16 In OS, Zhang et al found that miR-1294 could restrain the proliferation and invasion of OS cells, 17 which provided a basis for exploring the role of miR-1294 in OS.…”

Section: Introductionmentioning

confidence: 99%

<p>Circ_0000885 Enhances Osteosarcoma Progression by Increasing FGFR1 Expression via Sponging MiR-1294</p>

Chen

Zhang

Bai

et al. 2020

CMAR

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Background: As a malignant tumor, the progression of osteosarcoma (OS) is mediated by multiple regulators, including circular RNAs (circRNAs). However, the role of circ_0000885 in OS is unclear. Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of circ_0000885, miR-1294 and fibroblast growth factor receptor 1 (FGFR1). Cell proliferation was evaluated using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Flow cytometry and transwell assay were employed to determine the cell cycle distribution, cell migration and invasion, respectively. Moreover, the relationship between miR-1294 and circ_0000885 or FGFR1 was confirmed by dual-luciferase reporter assay. The protein level of FGFR1 was assessed via Western blot (WB) analysis. Animal experiments were used to verify the effect of circ_0000885 silencing on OS tumor growth in vivo. Results: Circ_0000885 level was increased in OS tissues and cells. Knockdown of circ_0000885 repressed the proliferation, migration, invasion and induced cell cycle arrest in OS cells. There was a binding relationship between miR-1294 and circ_0000885, and miR-1294 inhibitor could reverse the inhibitory effect of silenced circ_0000885 on OS progression. MiR-1294 could target FGFR1, and overexpressed FGFR1 could invert the suppression effect of miR-1294 mimic on OS progression. Silencing of circ_0000885 hindered FGFR1 expression, while this effect could be recovered by miR-1294 inhibitor. In addition, circ_0000885 knockdown reduced OS tumor growth via regulating the FGFR1 expression by sponging miR-1294 in vivo. Conclusion: Circ_0000885 played an active role in OS progression, indicating that it might be a potential target for OS therapy.

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MicroRNA-1294 inhibited oral squamous cell carcinoma growth by targeting c-Myc

Cited by 22 publications

References 36 publications

Hsa_circ_0004370 promotes esophageal cancer progression through miR-1294/LASP1 pathway

Hsa_circ_0004370 promotes esophageal cancer progression through miR-1294/LASP1 pathway

<p>Antitumor Effect of miR-1294/Pyruvate Kinase M2 Signaling Cascade in Osteosarcoma Cells</p>

<p>Circ_0000885 Enhances Osteosarcoma Progression by Increasing FGFR1 Expression via Sponging MiR-1294</p>

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