Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Feb;16(1):55–70. doi: 10.20892/j.issn.2095-3941.2018.0157

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright 2019 Cancer Biology & Medicine

This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

PMC Copyright notice

Insulin promotes ECC-1 cell progression via the estrogen receptor (ER) by activating the PI3K and MAPK pathways. (A) BrdU enzyme-linked immunosorbent assay (ELISA) of the effects of insulin stimulation on ECC-1 cell proliferation after knockdown of ER and/or insulin receptor (InsR). (B, C) Flow cytometry analysis of the effects of insulin stimulation on ECC-1 cell cycle distribution after knockdown of ER and/or InsR. (D, E) The percentage of apoptotic ECC-1 cells (after knockdown of ER and/or InsR) treated with insulin was determined by flow cytometry analysis using Annexin V-FITC antibodies. (F, G) Western blot analysis of the effects of insulin treatment on the ratios of phosphorylated (p)-ER/ER, p-Akt/Akt, p-MAPK/MAPK, and p-ERK/ERK in ECC-1 cells after knockdown of ER and/or InsR. *P < 0.05 for all experiments.