miR‑15a represses cancer cell migration and invasion under conditions of hypoxia by targeting and downregulating Bcl‑2 expression in human osteosarcoma cells

Leng, Jiali; Song, Qingxu; Zhao, Yuguang; Wang, Zhenyu

doi:10.3892/ijo.2018.4285

Cited by 22 publications

(25 citation statements)

References 38 publications

(33 reference statements)

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“…Previously, Bcl-2 was reported to promote EMT and metastasis (13,37). Furthermore, Bcl-2 was also involved in cell metastasis in hypoxia (38,39). In the present study, it was demonstrated that the expression of STC1 was positively associated with that of Bcl-2, N-cadherin and MMP2, but negatively associated with the level of E-cadherin.…”

Section: Discussionsupporting

confidence: 60%

Stanniocalcin‑1 promotes cell proliferation, chemoresistance and metastasis in hypoxic gastric cancer cells via Bcl‑2

Wang

Zhou

et al. 2019

Oncol Rep

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Gastric cancer (GC) is one of the most lethal diseases worldwide, but the mechanism of GC development remains elusive. In the present study, the roles of stanniocalcin-1 (STC1) in GC were investigated. It was demonstrated that overexpression of STC1 mRNA and protein were associated with poor survival of patients with GC. The expression of STC1 was enhanced in hypoxic GC cells and overexpression of STC1 facilitated cell proliferation in hypoxia but not in normoxia. Furthermore, STC1 promoted chemoresistance, migration and invasion in hypoxia. Upregulating the expression of STC1 enhanced the expression of B cell lymphoma (Bcl)-2, neural-cadherin and matrix metalloproteinase-2, whereas it reduced the levels of cytochrome c, cleaved-caspase-9, cleaved-caspase-3 and epithelial-cadherin. However, downregulation of STC1 altered the expression of these proteins in the opposite direction. Furthermore, disturbing the expression of Bcl-2 partly reversed the changes to these proteins and also the pro-proliferation, anti-apoptosis and pro-invasion potential of STC1. In vivo experiments indicated that enhanced expression of STC1 promoted tumor growth and metastasis in mice. Collectively, the results indicated that STC1 may serve an oncogenic role in hypoxic GC via dysregulating Bcl-2, indicating that STC1 may be a potential therapeutic target in the treatment of GC.

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Section: Discussionsupporting

confidence: 60%

Stanniocalcin‑1 promotes cell proliferation, chemoresistance and metastasis in hypoxic gastric cancer cells via Bcl‑2

Wang

Zhou

et al. 2019

Oncol Rep

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“…miR-15A is antiangiogenic and decreases osteosarcoma cell invasiveness [ 29 ] and is upregulated by tetrac at αvβ3. The same miR also acts to reduce metastasis by inhibiting multiple components of the TGFβ pathway [ 30 ], which is discussed in more detail in a later section.…”

Section: Cancer Metastasis-relevant Molecular Mechanisms Of Thyroimentioning

confidence: 99%

Contributions of Thyroid Hormone to Cancer Metastasis

et al. 2018

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Acting at a cell surface receptor on the extracellular domain of integrin αvβ3, thyroid hormone analogues regulate downstream the expression of a large panel of genes relevant to cancer cell proliferation, to cancer cell survival pathways, and to tumor-linked angiogenesis. Because αvβ3 is involved in the cancer cell metastatic process, we examine here the possibility that thyroid hormone as l-thyroxine (T4) and the thyroid hormone antagonist, tetraiodothyroacetic acid (tetrac), may respectively promote and inhibit metastasis. Actions of T4 and tetrac that are relevant to cancer metastasis include the multitude of synergistic effects on molecular levels such as expression of matrix metalloproteinase genes, angiogenesis support genes, receptor tyrosine kinase (EGFR/ERBB2) genes, specific microRNAs, the epithelial–mesenchymal transition (EMT) process; and on the cellular level are exemplified by effects on macrophages. We conclude that the thyroid hormone-αvβ3 interaction is mechanistically linked to cancer metastasis and that modified tetrac molecules have antimetastatic activity with feasible therapeutic potential.

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“…Studies by Cai et al (2012), Tian et al (2015), and Leng et al (2018) have demonstrated that miR-15a induces cell cycle arrest and promotes apoptosis in OS by downregulating the expression of CCND1, 51 and attenuates the growth of OS cells by targeting TNFAIP1 18 or Bcl-2. 52 In this study, we observed that miR-15a-5p inhibited the proliferation, migration, and invasion of OS cells, and the inhibition of miR-15a-5p reversed the anti-tumor effect of LINC00662 knockdown in OS cells. These results indicated that LINC00662 knockdown can inhibit tumorigenesis by upregulating miR-15a-5p in OS cells.…”

Section: Discussionmentioning

confidence: 59%

<p>LINC00662 Long Non-Coding RNA Knockdown Attenuates the Proliferation, Migration, and Invasion of Osteosarcoma Cells by Regulating the microRNA-15a-5p/Notch2 Axis</p>

Liu¹,

Meng²

2020

OTT

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Purpose: Osteosarcoma (OS) is a frequently occurring malignancy in children and adolescents. In this study, we aimed to investigate the effects of the long non-coding RNA (lncRNA) LINC00662 (LINC00662) in OS and the underlying molecular mechanism. Methods: The expression of LINC00662, microRNA-15a-5p (miR-15a-5p), and Notch2 in OS was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration, and invasion of OS cells were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and transwell assay. The interactions among LINC00662, miR-15a-5p, and Notch2 were determined by dual-luciferase reporter assays. A tumor xenograft model was established in mice for evaluating tumor growth in vivo. Results: The expression of LINC00662 and Notch2 was found to be upregulated in OS, but the expression of miR-15a-5p was downregulated. The results demonstrated that LINC00662 knockdown attenuated the proliferation, migration, and invasion of OS cells and suppressed tumor growth in mice. The study further demonstrated that LINC00662 directly interacted with miR-15a-5p, and that Notch2 was a target of miR-15a-5p. The inhibition of miR-15a-5p or Notch2 overexpression markedly reversed the suppressive effect of sh-LINC00662 on the proliferation, migration, and invasion of OS cells. Conclusion: The study demonstrated that LINC00662 could be a potential biomarker for OS therapy, and LINC00662 knockdown suppressed the proliferation, migration, and invasion of OS cells by regulating the miR-15a-5p/Notch2 axis.

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miR‑15a represses cancer cell migration and invasion under conditions of hypoxia by targeting and downregulating Bcl‑2 expression in human osteosarcoma cells

Cited by 22 publications

References 38 publications

Stanniocalcin‑1 promotes cell proliferation, chemoresistance and metastasis in hypoxic gastric cancer cells via Bcl‑2

Stanniocalcin‑1 promotes cell proliferation, chemoresistance and metastasis in hypoxic gastric cancer cells via Bcl‑2

Contributions of Thyroid Hormone to Cancer Metastasis

<p>LINC00662 Long Non-Coding RNA Knockdown Attenuates the Proliferation, Migration, and Invasion of Osteosarcoma Cells by Regulating the microRNA-15a-5p/Notch2 Axis</p>

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