Cancer stem cell-like cells-derived exosomal lncRNA promotes biological characteristics in thyroid cancer via miR-122-5p/P4HA1 axis.
1/5 보강
[INTRODUCTION] Here, the discussion focused on the function and possible mechanism of cancer stem cell-like cells (CSCs)-derived exosomal in thyroid cancer.
APA
Wu Q, He Y, et al. (2023). Cancer stem cell-like cells-derived exosomal lncRNA promotes biological characteristics in thyroid cancer via miR-122-5p/P4HA1 axis.. Regenerative therapy, 22, 19-29. https://doi.org/10.1016/j.reth.2022.11.005
MLA
Wu Q, et al.. "Cancer stem cell-like cells-derived exosomal lncRNA promotes biological characteristics in thyroid cancer via miR-122-5p/P4HA1 axis.." Regenerative therapy, vol. 22, 2023, pp. 19-29.
PMID
36582605 ↗
Abstract 한글 요약
[INTRODUCTION] Here, the discussion focused on the function and possible mechanism of cancer stem cell-like cells (CSCs)-derived exosomal in thyroid cancer.
[METHODS] Specifically, the bioinformatics analysis, dual-luciferase reporter assay and RT-qPCR were conducted to obtain the expression and regulation of , and the downstream miR-122-5p/P4HA1 axis. Exosomes were identified by transmission electron microscopy. The uptake of exosome by recipient cells was observed by PKH67 labeling. Functional experiments and western blot were adopted to detect the effects of exosomal /miR-122-5p/P4HA1 axis on thyroid cancer cells. Tumor xenograft and metastasis model combined with RT-qPCR, western blot and hematoxylin-eosin staining verified the role of .
[RESULTS] Exosomal up-regulated P4HA1 expression through miR-122-5p. and P4HA1 expressions were up-regulated, and miR-122-5p expression was down-regulated in thyroid cancer. Silent reduced cell viability and stemness. was found to be abundant in CSCs and CSCs-derived exosomes. Exosomal silencing could transfer to thyroid cancer cells to elevate E-cadherin level, and diminish P4HA1, N-cadherin and Vimentin levels, thus impeding cell migration and invasion. MiR-122-5p inhibitor reversed the function of exosomal , while P4HA1 silencing attenuated the effect of miR-122-5p inhibitor. Exosomal affected the growth and metastasis of thyroid cancer through the miR-122-5p/P4HA1 axis.
[CONCLUSION] CSCs-derived exosomal acts as an oncogene in thyroid cancer through miR-122-5p/P4HA1 axis.
[METHODS] Specifically, the bioinformatics analysis, dual-luciferase reporter assay and RT-qPCR were conducted to obtain the expression and regulation of , and the downstream miR-122-5p/P4HA1 axis. Exosomes were identified by transmission electron microscopy. The uptake of exosome by recipient cells was observed by PKH67 labeling. Functional experiments and western blot were adopted to detect the effects of exosomal /miR-122-5p/P4HA1 axis on thyroid cancer cells. Tumor xenograft and metastasis model combined with RT-qPCR, western blot and hematoxylin-eosin staining verified the role of .
[RESULTS] Exosomal up-regulated P4HA1 expression through miR-122-5p. and P4HA1 expressions were up-regulated, and miR-122-5p expression was down-regulated in thyroid cancer. Silent reduced cell viability and stemness. was found to be abundant in CSCs and CSCs-derived exosomes. Exosomal silencing could transfer to thyroid cancer cells to elevate E-cadherin level, and diminish P4HA1, N-cadherin and Vimentin levels, thus impeding cell migration and invasion. MiR-122-5p inhibitor reversed the function of exosomal , while P4HA1 silencing attenuated the effect of miR-122-5p inhibitor. Exosomal affected the growth and metastasis of thyroid cancer through the miR-122-5p/P4HA1 axis.
[CONCLUSION] CSCs-derived exosomal acts as an oncogene in thyroid cancer through miR-122-5p/P4HA1 axis.
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