Effects of extracellular vesicle-derived noncoding RNAs on pre-metastatic niche and tumor progression

Chen, Zhuang; Wang, Qiming; Wang, Zhibin; Wang, Wenkang; Yuan, Weitang; Liu, Yang; Sun, Zhenqiang; Wang, Chengzeng

doi:10.1016/j.gendis.2022.12.011

Cited by 3 publications

(2 citation statements)

References 133 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the past decade, growing evidence has emphasized that miRNAs packaged within EVs could regulate cell‐cell communication to affect cell function. For instance, highly abundant miRNAs (such as miR‐21‐5p) in EVs could promote the formation of premetastatic niche and tumor progression 25 . To investigate whether miRNAs in 143B EVs could control the migration of MNNG cells, total RNA were extracted from 143B EVs, 143B, and MNNG cells, and detected by miRNA microarray.…”

Section: Resultsmentioning

confidence: 99%

“…For instance, highly abundant miRNAs (such as miR‐21‐5p) in EVs could promote the formation of premetastatic niche and tumor progression. 25 To investigate whether miRNAs in 143B EVs could control the migration of MNNG cells, total RNA were extracted from 143B EVs, 143B, and MNNG cells, and detected by miRNA microarray. The top 10 miRNAs within 143B EVs were miR‐4281, miR‐720, miR‐21, miR‐1225‐5p, miR‐451, miR‐1246, miR‐1207‐5p, miR‐1202, miR‐638, and miR‐2861 (Figure 2A ).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

miR‐1246 promotes osteosarcoma cell migration via NamiRNA‐enhancer network dependent on Argonaute 2

Yang,

Zou,

Liang

et al. 2024

MedComm

View full text Add to dashboard Cite

High metastatic propensity of osteosarcoma leads to its therapeutic failure and poor prognosis. Although nuclear activation miRNAs (NamiRNAs) are reported to activate gene transcription via targeting enhancer and further promote tumor metastasis, it remains uncertain whether NamiRNAs regulate osteosarcoma metastasis and their exact mechanism. Here, we found that extracellular vesicles of the malignant osteosarcoma cells (143B) remarkably increased the migratory abilities of MNNG cells representing the benign osteosarcoma cells by two folds, which attributed to their high miR‐1246 levels. Specially, miR‐1246 located in nucleus could activate the migration gene expression (such as MMP1) to accelerate MNNG cell migration through elevating the enhancer activities via increasing H3K27ac enrichment. Instead, MMP1 expression was dramatically inhibited after Argonaute 2 (AGO2) knockdown. Notably, in vitro assays demonstrated that AGO2 recognized the hybrids of miR‐1246 and its enhancer DNA via PAZ domains to prevent their degradation from RNase H and these protective roles of AGO2 may favor the gene activation by miR‐1246 in vivo. Collectively, our findings suggest that miR‐1246 could facilitate osteosarcoma metastasis through interacting with enhancer to activate gene expression dependent on AGO2, highlighting the nuclear AGO2 as a guardian for NamiRNA‐targeted gene activation and the potential of miR‐1246 for osteosarcoma metastasis therapy.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%