microRNA-544 promoted human osteosarcoma cell proliferation by downregulating AXIN2 expression

Chen, Ming; Liu, Yongyi; Zheng, Min‐Qing; Wang, Xinliang; Gao, Xinghua; Chen, Lin; Zhang, Guang‐Ming

doi:10.3892/ol.2018.8218

Cited by 6 publications

(7 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have shown that miRNA expression is aberrant in ESCC, which suggests that miRNAs play an important role in ESCC progression (6,7). miR-544 was recently demonstrated to function either as a tumor suppressor or oncogene in different types of cancer (8–13,16). However, the expression, function and molecular mechanism of miR-544 in ESCC have not been well illustrated.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that miR-544 targets different genes in various cancer types. In osteosarcoma, miR-544 promotes cell proliferation by negatively regulating axin-2 (8). In hepatocellular carcinoma, it enhances immune escape through downregulation of natural cytotoxicity triggering receptor 1/NKp46 by targeting runt-related transcription factor 3 (9).…”

Section: Discussionmentioning

confidence: 99%

“…Accumulated evidence has illustrated that miRNAs play diverse roles in the regulation of cancer initiation and progression of ESCC (6,7). Certain studies have demonstrated that miR-544 serves as an oncogene in osteosarcoma, liver cancer, gastric cancer and colorectal cancer (8–11). However, miR-544 acts as a tumor suppressor and inhibits tumor progression in breast cancer and glioma (12,13); this contrast in function may be tissue-specific.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

MicroRNA‑544 inhibits esophageal squamous cell carcinoma cell proliferation and enhances sensitivity to cisplatin by repressing E2F transcription factor 5

Sun

Zhang

et al. 2019

Oncol Lett

View full text Add to dashboard Cite

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide. MicroRNA (miRNA)-544 is an important cancer-associated RNA that is downregulated in multiple types of cancer. However, the role of miR-544 in ESCC progression remains unknown. In the present study, miR-544 expression level was determined via RT-qPCR in 30 pairs of ESCC and adjacent normal tissues and in a panel of ESCC cell lines. Cell proliferation and cell apoptosis were assessed by MTT and flow cytometry assays. Luciferase reporter assay and western blot analysis were conducted to verify E2F transcription factor 5 (E2F5), an oncogene in ESCC, as a novel target gene of miR-544. The results illustrated that miR-544 is frequently downregulated in ESCC tissues and cell lines. Overexpression of miR-544 in ESCC cells resulted in decreased cell proliferation and increased cell apoptosis. Thus, E2F5 was identified as a target of miR-544, and its expression was negatively correlated with miR-544 expression in clinical ESCC tissues. More importantly, overexpression of miR-544 led to increased sensitivity of ESCC cells to cisplatin, an anticancer drug. Overall, these findings indicate that miR-544 serves as a tumor suppressor by targeting E2F5; thus, miR-544 may be a therapeutic target for the treatment of ESCC.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA‑544 inhibits esophageal squamous cell carcinoma cell proliferation and enhances sensitivity to cisplatin by repressing E2F transcription factor 5

Sun

Zhang

et al. 2019

Oncol Lett

View full text Add to dashboard Cite

show abstract

“…The association between miRNAs and the occurrence and development of tumors has also attracted increasing attention in life science research (14). Researchers have found that miRNAs can regulate the progression of OS (15-17). miR-9 is a member of the miRNA family, and it has been found to be abnormally expressed in a number of types of tumor cells, such as breast cancer, lung cancer, gastric cancer and OS (18-22).…”

Section: Introductionmentioning

confidence: 99%

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

et al. 2019

View full text Add to dashboard Cite

Osteosarcoma (OS) is a common primary malignancy in adolescents and children. MicroRNAs (miRNAs or miRs) can regulate the progression of OS. Herein, we explored the target genes and effects of miR-9 in OS. Cell growth, colony formation and cell cycle were respectively examined using a cell counting kit-8 (CCK-8), crystal violet staining and flow cytometry. The target gene of miR-9 was predicted according to the MicroRNA.org website. Luciferase activity was examined using a dual luciferase reporter gene assay kit. The corresponding factors levels were analyzed by carrying out reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. A mouse model of OS was also established and the volume and weight of the tumors of the mice with OS were measured. The levels of p16 in the mice with OS were detected by immunohistochemistry (IHC). The data revealed a high expression of miR-9 and a low expression of p16 in the OS tissue. p16 was found to be the target gene for miR-9 in OS. miR-9 depletion decreased the proliferation and colony formation of Saos-2 cells by arresting the cells at the G1 phase, accompanied by the downregulation of cyclin A, cyclin D1 and c-Myc expression levels. Moreover, miR-9 depletion inhibited the phosphorylation of p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK). In vivo , miR-9 depletion decreased the tumor volume and weight and increased p16 expression in the mouse tumor tissues. Nevertheless, p16 silencing reversed the suppressive effects of miR-9 inhibitors on OS cells. On the whole, the findings of this study substantiate that miR-9 depletion suppresses cell proliferation by targeting p16 in OS and by mediating the activation of the ERK/p38/JNK pathway.

show abstract

“…For example, Chen et al [10] reported that miR-183 could regulate bladder cancer cells growth and apoptosis via targeting AXIN2. A recent report by Chen et al pointed out that down regulating AXIN2 expression could promote human osteosarcoma cell proliferation [11]. Another paper showed that targeting AXIN2 axis could suppress tumor growth and metastasis in colorectal cancer [12].…”

Section: Introductionmentioning

confidence: 99%

New insights of the correlation between AXIN2 polymorphism and cancer risk and susceptibility: evidence from 72 studies

Liu

et al. 2021

BMC Cancer

View full text Add to dashboard Cite

Background Numerous studies have reported the correlation between AXIN2 polymorphism and cancer risk, but the results seem not consistent. In order to get an overall, accurate and updated results about AXIN2 polymorphism and cancer risk, we conducted this study. Methods An updated analysis was performed to analyze the correlation between AXIN2 polymorphisms and cancer risk. Linkage disequilibrium (LD) analysis was also used to show the associations. Results Seventy-two case-control studies were involved in the study, including 22,087 cases and 18,846 controls. The overall results showed rs11079571 had significant association with cancer risk (allele contrast model: OR = 0.539, 95%CI = 0.478–0.609, PAdjust = 0.025; homozygote model: OR = 0.22, 95% CI = 0.164–0.295, PAdjust< 0.001; heterozygote model: OR = 0.292, 95% CI = 0.216–0.394, PAdjust< 0.001; dominant model: OR = 0.249, 95% CI = 0.189–0.33, PAdjust< 0.001). The same results were obtained with rs1133683 in homozygote and recessive models (PAdjust< 0.05), and in rs35285779 in heterozygote and dominant models (PAdjust< 0.05). LD analysis revealed significant correlation between rs7210356 and rs9915936 in the populations of CEU, CHB&CHS, ESN and JPT (CEU: r2 = 0.91; CHB&CHS: r2 = 0.74; ESN: r2 = 0.62, JPT: r2 = 0.57), and a significant correlation between rs9915936 and rs7224837 in the populations of CHB&CHS, ESN and JPT (r2>0.5), between rs7224837 and rs7210356 in the populations of CEU, CHB&CHS, JPT (r2>0.5), between rs35435678 and rs35285779 in the populations of CEU, CHB&CHS and JPT (r2>0.5). Conclusions AXIN2 rs11079571, rs1133683 and rs35285779 polymorphisms have significant correlations with overall cancer risk. What’s more, two or more polymorphisms such as rs7210356 and rs9915936, rs9915936 and rs7224837, rs7224837 and rs7210356, rs35435678 and rs35285779 have significant correlation with cancer susceptibility in different populations.

show abstract

microRNA-544 promoted human osteosarcoma cell proliferation by downregulating AXIN2 expression

Cited by 6 publications

References 27 publications

MicroRNA‑544 inhibits esophageal squamous cell carcinoma cell proliferation and enhances sensitivity to cisplatin by repressing E2F transcription factor 5

MicroRNA‑544 inhibits esophageal squamous cell carcinoma cell proliferation and enhances sensitivity to cisplatin by repressing E2F transcription factor 5

miR‑9 depletion suppresses the proliferation of osteosarcoma cells by targeting p16

New insights of the correlation between AXIN2 polymorphism and cancer risk and susceptibility: evidence from 72 studies

Contact Info

Product

Resources

About