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

letter

. 2023 Nov 7;19(6):1934–1939. doi: 10.5114/aoms/171308

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

Copyright: © 2023 Termedia & Banach

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

PMC Copyright notice

A – mRNA level of progesterone receptor in the EP group was much lower than that in the control group. B – MiR-320b expression in the EP group was much lower than that in the control group. C – mRNA level of MCL1 in the EP group was much lower than that in the control group. D – A negative regulatory relationship with a correlation coefficient of –0.5000 was confirmed between miR-320b and MCL1 expression. E – The protein level of MCL1 in the EP group was much higher than that in the control group. F – 0.5 μM of progesterone exerted no effect on the expression of miR-320b, while 1 and 2 μM of progesterone increased miR-320b expression in RL95-2 cells in a dose-dependent manner. G – 0.5 μM of progesterone exerted no effect on the expression of miR-320b, while 1 and 2 μM of progesterone increased miR-320b expression in HEC-1-A cells in a dose-dependent manner. H – 0.5 μM of progesterone exerted no effect on the expression of MCL1 mRNA, while 1 and 2 μM of progesterone decreased MCL1 mRNA expression in RL95-2 cells in a dose-dependent manner. I – 0.5 μM of progesterone exerted no effect on the expression of MCL1 mRNA, while 1 and 2 μM of progesterone decreased MCL1 mRNA expression in HEC-1-A cells in a dose-dependent manner. J – 0.5 μM of progesterone exerted no effect on the expression of MCL1 protein, while 1 and 2 μM of progesterone decreased MCL1 protein expression in RL95-2 cells in a dose-dependent manner. K – 0.5 μM of progesterone exerted no effect on the expression of MCL1 protein, while 1 and 2 μM of progesterone decreased MCL1 protein expression in HEC-1-A cells in a dose-dependent manner. L – Progesterone (1, 2 μM) dose-dependently inhibited the proliferation of RL95-2 cells. M – Progesterone (1, 2 μM) dose-dependently inhibited the proliferation of HEC-1-A cells. N – Progesterone (1, 2 μM) dose-dependently promoted the apoptosis of RL95-2 cells. O – Progesterone (1, 2 μM) dose-dependently promoted the apoptosis of HEC-1-A cells. P – MCL1 was identified as a target gene of miR-320b with a ‘seed sequence’ located in the 3’UTR of MCL1. Q – Luciferase activity of RL95-2 cells co-transfected with miR-320b mimics and wild-type MCL1 3’UTR was much lower than that of the cells co-transfected with miR-320b mimics and a scramble control. R – Luciferase activity of HEC-1-A cells co-transfected with miR-320b mimics and wild-type MCL1 3’UTR was much lower than that of the cells co-transfected with miR-320b mimics and a scramble control

A – mRNA level of progesterone receptor in the EP group was much lower than that in the control group. B – MiR-320b expression in the EP group was much lower than that in the control group. C – mRNA level of MCL1 in the EP group was much lower than that in the control group. D – A negative regulatory relationship with a correlation coefficient of –0.5000 was confirmed between miR-320b and MCL1 expression. E – The protein level of MCL1 in the EP group was much higher than that in the control group. F – 0.5 μM of progesterone exerted no effect on the expression of miR-320b, while 1 and 2 μM of progesterone increased miR-320b expression in RL95-2 cells in a dose-dependent manner. G – 0.5 μM of progesterone exerted no effect on the expression of miR-320b, while 1 and 2 μM of progesterone increased miR-320b expression in HEC-1-A cells in a dose-dependent manner. H – 0.5 μM of progesterone exerted no effect on the expression of MCL1 mRNA, while 1 and 2 μM of progesterone decreased MCL1 mRNA expression in RL95-2 cells in a dose-dependent manner. I – 0.5 μM of progesterone exerted no effect on the expression of MCL1 mRNA, while 1 and 2 μM of progesterone decreased MCL1 mRNA expression in HEC-1-A cells in a dose-dependent manner. J – 0.5 μM of progesterone exerted no effect on the expression of MCL1 protein, while 1 and 2 μM of progesterone decreased MCL1 protein expression in RL95-2 cells in a dose-dependent manner. K – 0.5 μM of progesterone exerted no effect on the expression of MCL1 protein, while 1 and 2 μM of progesterone decreased MCL1 protein expression in HEC-1-A cells in a dose-dependent manner. L – Progesterone (1, 2 μM) dose-dependently inhibited the proliferation of RL95-2 cells. M – Progesterone (1, 2 μM) dose-dependently inhibited the proliferation of HEC-1-A cells. N – Progesterone (1, 2 μM) dose-dependently promoted the apoptosis of RL95-2 cells. O – Progesterone (1, 2 μM) dose-dependently promoted the apoptosis of HEC-1-A cells. P – MCL1 was identified as a target gene of miR-320b with a ‘seed sequence’ located in the 3’UTR of MCL1. Q – Luciferase activity of RL95-2 cells co-transfected with miR-320b mimics and wild-type MCL1 3’UTR was much lower than that of the cells co-transfected with miR-320b mimics and a scramble control. R – Luciferase activity of HEC-1-A cells co-transfected with miR-320b mimics and wild-type MCL1 3’UTR was much lower than that of the cells co-transfected with miR-320b mimics and a scramble control