MiR‐492 regulates metastatic properties of hepatoblastoma via <scp>CD</scp>44

Frowein, Julia von; Hauck, Stefanie M.; Kappler, Roland; Pagel, Philipp; Fleischmann, Katrin K.; Magg, Thomas; Cairo, Stefano; Roscher, Adelbert A.; Schweinitz, Dietrich von; Schmid, Irene

doi:10.1111/liv.13687

Cited by 35 publications

(36 citation statements)

References 49 publications

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“…By contrast, miR-492 is highly expressed in hepatoblastoma tissues and cell lines. Retinal cells in patients with hepatoblastoma who present with high miR-492 levels exhibit more high-risk or aggressive behaviours than those with low miR-492 levels (26,27). miR-492 is also upregulated in hepatic cancer, and this upregulation is strongly associated with poor survival (23).…”

Section: Discussionmentioning

confidence: 99%

“…In clear cell renal cell carcinoma, miR-492 restoration restricts cell proliferation and invasion, induces cell apoptosis and promotes cell adhesion (22). Nonetheless, miR-492 serves oncogenic roles in hepatoblastoma by promoting cell proliferation, anchorage-independent growth and metastasis (26). In breast cancer, ectopic miR-492 expression significantly promotes cell proliferation and anchorage-independent growth (24).…”

Section: Discussionmentioning

confidence: 99%

“…Researchers have identified numerous target genes of miR-492, including TIMP2 (20) in cervical cancer, PAK7 (21) in osteosarcoma, CD44 (26) in hepatoblastoma, SOX7 (24) in breast cancer and PTEN (23) in hepatic cancer. LATS2, which is a member of the serine/threonine AGC kinase family, was validated as a direct target of miR-492 in RB.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Sun

Zhang

2018

Mol Med Report

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Numerous studies have demonstrated that microRNAs (miRNAs) are upregulated or downregulated in retinoblastoma (RB), and that this phenomenon is associated with the modulation of various malignant behaviours during RB occurrence and development. Therefore, the mechanisms that associate deregulated miRNAs with RB initiation and progression must be understood to identify effective therapeutic techniques for patients with RB. In the present study, miR-492 expression was upregulated in RB tissues and cell lines. The effects of miR-492 inhibition on the proliferation and invasion of RB cells were examined using Cell Counting kit-8 and invasion assays. The results revealed that miR-492 downregulation significantly decreased the proliferation and invasion of RB cells. Bioinformatics analysis predicted that large tumour-suppressor kinase 2 (LATS2) was a putative target of miR-492. Luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction and western blot analysis demonstrated that LATS2 was a direct target gene of miR-492 in RB cells. In addition, LATS2 expression was downregulated in RB tissues, and its downregulation was inversely correlated with miR-492 level. Furthermore, LATS2-knockdown abrogated the effects of miR-492 downregulation in RB cells. In conclusion, miR-492 inhibition may impede the malignant behaviour of RB by directly targeting LATS2. Therefore, targeting this miRNA may be an effective therapeutic method for treating patients with RB.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Sun

Zhang

2018

Mol Med Report

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“…No previous studies have reported on the regulatory roles of miR-1224-5p, miR-492, or miR-135b-5p in chondrosarcoma cells, 23,[25][26] yet some published documents have shown that miR-1224-5p, miR-492, and miR-135b-5p may play important roles in the proliferation, invasion, and metastasis of nonchondrosarcoma tumors. [13][14][15][16][17][18][19][20][21][22] To the best of our best knowledge, miR-6839-5p has not been reported in the literature. In the current study, we hypothesized that miR-1224-5p, miR-492, miR-135b-5p, and miR-6839-5p might play vital roles in how SW1353 cells respond to irradiation with 125 I seeds.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11][12] Some studies have demonstrated that miRNAs play an important role in the proliferation, invasion, and metastasis of cancer. [13][14][15][16][17][18][19][20][21][22] In recent years, several studies have assessed the roles of miRNAs in chondrosarcoma, yet none of the findings have focused on the effects of 125 I seeds irradiation exposure on the miRNAs expression profiles of conventional chondrosarcoma cells. 12,[23][24][25][26][27] In the current study, we developed a new in vitro 125 I seed irradiation model to study the effects of 125 I seed irradiation on the proliferation of grade II chondrosarcoma SW1353 cells.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Cells Proliferation and MicroRNAs Expression Profile in Human Chondrosarcoma SW1353 Cells Exposed to Iodine-125 Seeds Irradiation

Zhu

et al. 2020

Dose-Response

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Chondrosarcoma is the second most common bone malignancy in adults, and it is often resistant to traditional chemotherapy and radiation therapy. Permanent implantation of iodine-125 (125I) seeds has been explored for the treatment of many types of cancer. In this study, the aim was to investigate the proliferative and microRNA (miRNA) effects of 125I seeds irradiation on human chondrosarcoma SW1353 cells. First, a new in vitro 125I seed irradiation model was established, and cell viability and miRNA microarray assays were performed before and after exposure to the 125I seeds. Cell proliferation was inhibited, and miRNA expression was substantially altered by irradiation exposure. The inhibition of cell proliferation was positively correlated with increased radiation doses, with cells showing the highest total radiation dose 7 days after irradiation. A total of 2549 miRNAs were detected in the SW1353 cells after exposure to 6 Gy of radiation, which included 189 differentially expressed miRNAs (98 upregulated and 91 downregulated). Four miRNAs were found to play important roles in the inhibition of cell proliferation after irradiation exposure, including miR-1224-5p, miR-492, miR-135b-5p, and miR-6839-5p. The target genes of the associated miRNAs mentioned were vascular endothelial growth factor A ( VEGFA), C-X-C motif chemokine 12 ( CXCL12), mitogen-activated protein kinase kinase kinase kinase 3 ( MAP4K3), and apoptosis facilitator Bcl-2-like protein 14 ( BCL2L14). Hence, the mitogen-activated protein kinase signaling pathway may be involved in how chondrosarcoma cells respond to 125I seed irradiation.

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Resveratrol-induced apoptosis is associated with regulating the miR-492/CD147 pathway in malignant melanoma cells

Tang

Chen

et al. 2020

Naunyn-Schmiedeberg's Arch Pharmacol

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MiR‐492 regulates metastatic properties of hepatoblastoma via CD44

Abstract: We identified miR-492 and its target CD44 as regulators of a number of biological features important for malignancy and metastasis. Furthermore, we demonstrated the diagnostic and prognostic potential of miR-492, a promising novel therapeutic target and biomarker for hepatoblastoma.

Cited by 35 publications

References 49 publications

Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Inhibition of microRNA‑492 attenuates cell proliferation and invasion in retinoblastoma via directly targeting LATS2

Analysis of Cells Proliferation and MicroRNAs Expression Profile in Human Chondrosarcoma SW1353 Cells Exposed to Iodine-125 Seeds Irradiation

Resveratrol-induced apoptosis is associated with regulating the miR-492/CD147 pathway in malignant melanoma cells

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