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

. 2023 Aug 26;21:575. doi: 10.1186/s12967-023-04432-9

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

© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 2 — Effect of GPX3 knockdown on cell proliferation, cell cycle, cell apoptosis, mitochondrial membrane potential and MAPK signaling pathway in BPH-1 and WPMY-1 cells. Knockdown efficiency of GPX3 at the mRNA (A) and protein (B) levels with three different siRNA sequences in BPH-1 and WPMY -1 cells. C The cell viability of BPH-1 and WPMY -1 after knockdown of GPX3 at different time points by CCK-8 assay, and downregulation of GPX3 accelerated cell proliferation. ^*: si-con vs. si-GPX3-1; ^#: si-con vs. si-GPX3-3. D Flow cytometry analysis of cell cycle. E Histogram showing percentage of cell populations at different stages of the cell cycle (%), and G0/G1 phase was shortened in si-GPX3 transfected prostate cells with a corresponding increase of G2 phase but no significant change of S phase. F Relative densitometric quantification of Cyclin D1, CDK4, CDK6, Cyclin B1 and CDK1 protein in BPH-1 and WPMY-1 after knockdown of GPX3, and Cyclin D1, CDK4 and CDK6 underwent increase, while Cyclin B1 and CDK1 were no significant difference in prostate cells treated with si-GPX3. G Flow cytometry analysis of cell apoptosis. H Statistical analysis of apoptotic rate (%) showed GPX3 silencing inhibited the apoptosis of prostatic cells. I The mitochondrial membrane potential level of BPH-1 and WPMY-1 cells was examined by JC-1 staining. The scatter plot of the flow cytometry analysis shows the distribution of JC-1 aggregates (Orange) and JC-1 monomer (Blue) cell population. J Histogram calculated the relative ratio of Orange against Blue fluorescence, and silencing GPX3 contributed to more agminated MMP in prostate cells. K Relative densitometric quantification of Cyto-C protein in mitochondria or cytoplasm in BPH-1 and WPMY-1 after silence of GPX3, and GPX3 silencing led to a decrease in mitochondrial Cyto-C release. L Relative densitometric quantification of Cleaved-Caspase 9, Cleaved-Caspase 3, Bcl-2 and BAX protein in BPH-1 and WPMY-1 after knockdown of GPX3, and knockdown of GPX3 resulted in an increase in anti-apoptotic protein and a decrease in pro-apoptotic proteins. M Relative densitometric quantification of MAPK signaling pathway proteins in BPH-1 and WPMY-1 after knockdown of GPX3, and knockdown of GPX3 significantly inhibited the ERK1/2 pathway. ^*/#p < 0.05, ^**/##p < 0.01, ^***/###p < 0.001 and ns means no significant difference