Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29563806
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
MicroRNA 302b-3p/302c-3p/302d-3p inhibits epithelial-mesenchymal transition and
promotes apoptosis in human endometrial carcinoma cells
#MMPMID29563806
Li Y
; Huo J
; Pan X
; Wang C
; Ma X
Onco Targets Ther
2018[]; 11
(?): 1275-1284
PMID29563806
show ga
BACKGROUND: Studies have shown that the microRNA miR-302 can affect the
proliferation, migration and cell cycle progression of endometrial carcinoma
(EC). miR-302 clusters have been shown to play an important role in the
proliferation and differentiation of cancer cells and in their tumorigenicity.
SUBJECTS AND METHODS: In this study, we detected the expression of genes through
quantitative reverse transcription polymerase chain reaction (qRT-PCR). We
detected the expression of proteins through Western blot. The Annexin
V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining assay
were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect the cell
apoptosis. The CCK-8 were used to detect the ability of
miR-302b-3p/302c-3p/302d-3p to affect the cell proliferation. The Cell cycle
analysis were used to detect the ability of miR-302b-3p/302c-3p/302d-3p to affect
the cell cycle. Finally, the wound healing assay was used to detect the ability
of miR-302b-3p/302c-3p/302d-3p to impact cell migration. RESULTS: We found that
miR-302b-3p/302c-3p/302d-3p of the miR-302 cluster was downregulated in EC, and
it altered the epithelial-mesenchymal transition (EMT) process in the EC cell
lines Ishikawa and HEC-1A. Western blot and the Annexin V- FITC/PI
double-staining assay were used to detect the ability of
miR-302b-3p/302c-3p/302d-3p to promote the apoptosis of Ishikawa and HEC-1A
cells. In addition, qRT-PCR results showed that overexpression of
miR-302b-3p/302c-3p/302d-3p significantly inhibited the expression of ZEB1,
suppressed the expression of Bcl-2 and promoted the expression of BAX. The
overexpression of miR-302b-3p/302c-3p/302d-3p inhibited the proliferation and
migration of Ishikawa and HEC-1A cells. Cell cycle analysis showed that
miR-302b-3p/302c-3p/302d-3p arrested cell cycle progression in the G0/G1 phase.
CONCLUSION: All results showed that miR-302b-3p/302c-3p/302d-3p can be used as a
tumor suppressor in EC and is expected to be a new target for the treatment of
EC.
free
free
free
