microRNA-143, down-regulated in osteosarcoma, promotes apoptosis and suppresses tumorigenicity by targeting Bcl-2

Zhang, Hao; Cai, Xiaobing; Wang, Yang; Tang, Haojun; Tong, Daki; Ji, Fang

doi:10.3892/or_00000994

Cited by 61 publications

(4 citation statements)

References 25 publications

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“…MicroRNAs have also been found to regulate the levels of BCL-2 family proteins. BCL-2 protein can be targeted by several microRNAs such as miR-143, whereby an overexpression of miR-143 in osteosarcoma promotes apoptosis by downregulating BCL-2 [108]. In rhabdomyosarcoma, STAT3 was observed to be constitutively activated to induce the expression of several target genes including anti-apoptotic BCL-2, BCL-XL, and Survivin, while transcription factors such as PAX3 and PAX3/FKHR were shown to induce BCL-XL mRNA expression, thus highlighting the involvement of BCL-2 family proteins in rhabdomyosarcoma tumorigenesis [69,109].…”

Section: Dysregulation Of Apoptosis and Apoptosis-targeted Therapimentioning

confidence: 99%

Destined to Die: Apoptosis and Pediatric Cancers

Choo

Loh

Chen

2019

Cancers

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Apoptosis (programmed cell death) is a systematic and coordinated cellular process that occurs in physiological and pathophysiological conditions. Sidestepping or resisting apoptosis is a distinct characteristic of human cancers including childhood malignancies. This review dissects the apoptosis pathways implicated in pediatric tumors. Understanding these pathways not only unraveled key molecules that may serve as potential targets for drug discovery, but also molecular nodes that integrate with other signaling networks involved in processes such as development. This review presents current knowledge of the complex regulatory system that governs apoptosis with respect to other processes in pediatric cancers, so that fresh insights may be derived regarding treatment resistance or for more effective treatment options.

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Section: Dysregulation Of Apoptosis and Apoptosis-targeted Therapimentioning

confidence: 99%

Destined to Die: Apoptosis and Pediatric Cancers

Choo

Loh

Chen

2019

Cancers

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“…MiR-143 has been proved to have an anti-cancer effect by targeting multiple genes related to cell proliferation, apoptosis and migration, such as Bcl-2 (13), MYO6 (14), ELK1 (15), and ERK5 (16). Extracellular signal-regulated kinase 5 (ERK5), a mitogen-activated protein kinase (MAPK), is commonly reported as a target gene of miR-143 (17,18).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-143 inhibits cell growth by targeting ERK5 and MAP3K7 in breast cancer

Zhou

Dong

Huang

et al. 2017

Braz J Med Biol Res

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This study aimed to investigate the function and mechanism of microRNA-143 (miR-143) in the occurrence and development of breast cancer (BC). A total of 30 BC tissues, 30 corresponding noncancerous tissues, and 10 normal control (NC) breast tissues were obtained to detect the levels of miR-143, extracellular signal-regulated kinase 5 (ERK5) and mitogen-activated protein 3 kinase 7 (MAP3K7) using RT-qPCR, western blotting or immunohistochemistry. The correlation of miR-143 with ERK5 or MAP3K7 was evaluated using Pearson correlation analysis. MCF-7 cells were transiently transfected with miR-143 mimic, miR-143 inhibitor, miR-143 mimic/inhibitor + si-ERK5, si-MAP3K7 or si-cyclin D1. Then, cell growth was evaluated by MTT assay and the expressions of phospho-ERK5 (p-ERK5), ERK5, p-MAP3K7, MAP3K7 and cyclin D1 were detected by western blotting. Results showed that, compared with noncancerous tissues or NC breast tissues, miR-143 level was decreased, while p-ERK5, ERK5, p-MAP3K7 and MAP3K7 expressions were increased in BC tissues (all P<0.01). The miR-143 level was negatively correlated with the mRNA level of ERK5 or MAP3K7 (r=-4.231 or r=-4.280, P<0.01). In addition, up-regulated miR-143 significantly decreased the expressions of p-ERK5, ERK5, p-MAP3K7, MAP3K7 and cyclin D1 (all P<0.01), as well as cell viability in MCF-7 cells (all P<0.05) while the effect of down-regulated miR-143 was the opposite. In conclusion, both ERK5 and MAP3K7 may be the target genes of miR-143. Increased expression of miR-143 can inhibit cell growth, which may be associated with ERK5 and MAP3K7 expressions in BC.

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“…Nearly 90% of all OS cases have shown micrometastasis at the diagnosis stage, indicating systematic chemotherapy as the first therapy option (Adhikari et al, 2010). Specifically, for patients who have not presented with any signs of metastatic diseases when diagnosed, the survival rate is between 60%-70% over a 5-year span, but for those who have presented with metastatic diseases, their clinical outcomes are much more severe (H. Zhang et al, 2010). The neoadjuvant chemotherapy combined with surgery has done well to increase the long-term survival rate of the OS-afflicted patients as well as common anticancer drugs of OS including doxorubicin and methotrexate (Huang et al, 2012).…”

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confidence: 99%

Retracted: Effects of FOSL1 silencing on osteosarcoma cell proliferation, invasion and migration through the ERK/AP‐1 signaling pathway

Han

Zhao

Sun

et al. 2018

Journal Cellular Physiology

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Osteosarcoma (OS), as the most frequent primary malignancy of bone, is characterized by the presence of malignant mesenchymal cells. In the current study, our aim was to explore the possible effects Fos-like antigen-1 (FOSL1) had on the silencing regarding OS cell proliferation, invasion, and migration through the activation of the extracellular-signal-regulated kinase (ERK)/activator protein-1 (AP-1) signaling pathway. After the collection of OS on top of already having the adjacent normal tissue samples, the protein positive expression rate of FOSL1 was then measured by implementing the use of immunohistochemistry and discovered that FOSL1 was robustly expressed in OS. Later, to better grasp the impact FOSL1 projects on OS and its underlying mechanism, we determined the OS related genes as well as the ERK/AP-1 signaling pathway related genes expression by using a reversetranscription quantitative polymerase chain reaction and western blot assay techniques. The results of the aforementioned two experiments revealed that the FOSL1 depletion had downregulated the expression of OS related genes by simultaneously downregulating the ERK/AP-1 signaling pathway. Moreover, cell proliferation, cycle, apoptosis, invasion, and migration of FOS1 were all tested by using a cell counting kit-8 assay, flow cytometry, Transwell assay, and scratch test, and these results presented that silencing of the FOSL1 gene inhibited OS cell proliferation, invasion, and migration. Our findings revealed a novel mechanism by which FOSL1 depletion played a significantly negative role in the OS progression through the regulation of the ERK/AP-1 signaling pathway. Functional suppression of FOSL1 might be a future therapeutic strategy regarding OS.

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microRNA-143, down-regulated in osteosarcoma, promotes apoptosis and suppresses tumorigenicity by targeting Bcl-2

Cited by 61 publications

References 25 publications

Destined to Die: Apoptosis and Pediatric Cancers

Destined to Die: Apoptosis and Pediatric Cancers

MicroRNA-143 inhibits cell growth by targeting ERK5 and MAP3K7 in breast cancer

Retracted: Effects of FOSL1 silencing on osteosarcoma cell proliferation, invasion and migration through the ERK/AP‐1 signaling pathway

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