miR-206 is down-regulated in breast cancer and inhibits cell proliferation through the up-regulation of cyclinD2

Zhou, Jing; Tian, Ye; Li, Juan; Lu, Binfeng; Sun, Ming; Zou, Yanfen; Kong, Rong; Luo, Yanhong; Shi, Yuting; Wang, Ke‐Ming; Ji, Guozhong

doi:10.1016/j.bbrc.2013.02.084

Cited by 88 publications

(74 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many studies have shown that miRNAs may function as either tumorigenic or tumor-suppressing genes [25,26]. In our study, we found that in cervical cancer cells, miR-7 suppressed cell viability, colony formation and promoted apoptosis in cervical cancer cells through downregulating the expression of XIAP by targeting the 3 0 UTR of XIAP.…”

Section: Discussionsupporting

confidence: 51%

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

et al. 2013

View full text Add to dashboard Cite

Edited by Tamas DalmayKeywords: microRNA microRNA-7 X-linked inhibitor of apoptosis protein Cell apoptosis Cervical cancer a b s t r a c t Our study demonstrated the functions of microRNA-7 (miR-7) in cervical cancer. The overexpression of miR-7 in the cervical cancer cell lines HeLa and C-33A suppressed cell viability and promoted cell apoptosis, whereas the inhibition of miR-7 had opposite effects. Furthermore, an oncogene, Xlinked inhibitor of apoptosis protein (XIAP), was identified as a new target of miR-7, and the ectopic expression of XIAP rescued the effects induced by miR-7 in HeLa and C-33A cells. These results indicate that miR-7 targeted and downregulated the oncogene XIAP to regulate the effect of miR-7 on apoptosis and malignant behaviors of HeLa and C-33A cells.

show abstract

Section: Discussionsupporting

confidence: 51%

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

et al. 2013

View full text Add to dashboard Cite

show abstract

“…For example, miR-206 was downregulated in breast cancer, and suppressed cell proliferation by targeting cyclinD2 (13). Moreover, miR-206 also mediated cardiac hypotrophy (14) and oxidative stress (15). Study has proved that miR-206 mediated in the osteogenic differentiation in steroid-induced avascular necrosis of femoral head.…”

Section: Introductionmentioning

confidence: 99%

Downregulated SOX9 mediated by miR‑206 promoted cell apoptosis in Legg-Calvï¿½-Perthes disease

Luo

Han

et al. 2017

Oncol Lett

View full text Add to dashboard Cite

Abstract. Legg-Calvé-Perthes disease (LCPD) commonly onsets in adolescents, and threatens their health. However, the potential mechanism underlying LCPD remains unclear. MicroRNA (miR)-206 and SRY-box 9 (SOX9) serve an important role in chondrocytes; however, their role in LCPD remains ambiguous. In the present study, whether miR-206 and SOX9 mediated cell apoptosis in dexamethasone (DEX)-induced LCPD was investigated. The chondrocytes of the LCPD and normal control group were isolated from clinical tissues. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the expression of miR-206 and SOX9 mRNA. Western blotting was used to measure the protein level of SOX9. A combination of Annexin V-fluorescein isothiocyanate flow cytometry was used to assess cell apoptosis. The association between miR-206 and SOX9 was detected using a luciferase reporter assay. miR-206 was overexpressed while SOX9 was downregulated in chondrocytes treated with DEX obtained from patients with LCPD. miR-206 targeted SOX9 to regulate its expression. Overexpression of miR-206 promoted cell apoptosis in TC28, while it was reversed by SOX9 overexpression. TC28 cells pretreated with DEX significantly promoted cell apoptosis, while cells transfected with miR-206 inhibitor significantly reversed the effect; however, downregulated SOX9 abolished the effects of miR-206 inhibitor. SOX9 mediated by miR-206 possibly contributed to the pathogenesis of LCPD. The results of the present study suggest that miR-206 and SOX9 function as important therapeutic targets for the future of clinical therapy.

show abstract

“…MiR-206 acts as a positive regulator of skeletal muscle differentiation, and a negative regulator of osteoblasts differentiation (2). Accumulating evidence also suggests a tumor suppressor function for miR-206, as it is frequently downregulated in many human malignancies (3). Several oncogenes (such as estrogen receptor 1, cyclinD2) and osteogenesis regulators (such as connexin 43) have been identified and confirmed as targets of miR-206 (3,4).…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating evidence also suggests a tumor suppressor function for miR-206, as it is frequently downregulated in many human malignancies (3). Several oncogenes (such as estrogen receptor 1, cyclinD2) and osteogenesis regulators (such as connexin 43) have been identified and confirmed as targets of miR-206 (3,4). However, its exact regulatory mechanisms during carcinogenesis and osteogenesis remain to be explored further.…”

Section: Introductionmentioning

confidence: 99%

Quantitative proteomics and protein network analysis of A549 lung cancer cells affected by miR-206

et al. 2013

View full text Add to dashboard Cite

miR-206 is down-regulated in breast cancer and inhibits cell proliferation through the up-regulation of cyclinD2

Cited by 88 publications

References 25 publications

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

Downregulated SOX9 mediated by miR‑206 promoted cell apoptosis in Legg-Calvï¿½-Perthes disease

Quantitative proteomics and protein network analysis of A549 lung cancer cells affected by miR-206

Contact Info

Product

Resources

About