PMID- 37772550
OWN - NLM
STAT- MEDLINE
DCOM- 20231002
LR  - 20231002
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 43
IP  - 10
DP  - 2023 Oct
TI  - Estrogen Effects Differ Between Medium Maintenance and Replacement from 
      Transcriptional and Clinical Perspectives in T47D Breast Cancer Cells.
PG  - 4447-4469
LID - 10.21873/anticanres.16640 [doi]
AB  - BACKGROUND/AIM: Our most recent study revealed that the responsiveness of hormone 
      receptor-positive breast cancer (HR+ BC) cells to estrogen or endocrine therapy 
      can be altered by certain cell culture or ambient environmental conditions. 
      Nevertheless, we were unable to investigate the relevant molecular mechanism and 
      clinical relevance. Therefore, this study was planned as a follow-up. MATERIALS 
      AND METHODS: RNA sequencing was mainly used with T47D cells treated with or 
      without 17beta-estradiol (E2) under medium maintenance (MTN; conventional culture 
      method) and medium exchange (EXC; daily replacing the existing medium with fresh 
      medium). RESULTS: The role of E2 in transcription differed between MTN and EXC, 
      and E2 played more important roles in transcription in terms of cancer 
      development under EXC than under MTN, consistent with the previous functional 
      effects of EXC. The novel concept of the "estrogen-responsive and 
      proliferation-related gene (ERPG)" was introduced. The expression of ERPGs, which 
      were distinguished from typical estrogen-responsive genes, was correlated with 
      that of prognostic and predictive factors for HR+ BC. The transcriptional 
      induction of ERPGs and typical estrogen-responsive genes regardless of E2 
      treatment under MTN was reminiscent of constitutive estrogen receptor (ER) 
      activation. Additionally, phosphatidylinositol 3-kinase (PI3K)/protein kinase B 
      (AKT)/mammalian target of rapamycin (mTOR) inhibitors were more effective under 
      EXC than under MTN. CONCLUSION: This study, demonstrating the more important 
      roles of estrogen in terms of cancer development under EXC than under MTN, 
      supports the use of our research model in future studies to overcome endocrine 
      resistance in HR+ BC.
CI  - Copyright (c) 2023 International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Jang, Seok-Hoon
AU  - Jang SH
AD  - Department of Surgery, College of Medicine, Ewha Womans University, Seoul, 
      Republic of Korea.
AD  - Laboratory of Developmental Biology and Genomics, College of Veterinary Medicine, 
      Seoul National University, Seoul, Republic of Korea.
FAU - Paek, Se Hyun
AU  - Paek SH
AD  - Department of Surgery, Ewha Womans University Seoul Hospital, Seoul, Republic of 
      Korea.
FAU - Kim, Jong-Kyu
AU  - Kim JK
AD  - Department of Surgery, Ewha Womans University Seoul Hospital, Seoul, Republic of 
      Korea.
FAU - Seong, Je Kyung
AU  - Seong JK
AD  - Laboratory of Developmental Biology and Genomics, College of Veterinary Medicine, 
      Seoul National University, Seoul, Republic of Korea.
FAU - Lim, Woosung
AU  - Lim W
AD  - Department of Surgery, College of Medicine, Ewha Womans University, Seoul, 
      Republic of Korea; limw@ewha.ac.kr.
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Estrogens)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 4TI98Z838E (Estradiol)
RN  - 0 (Receptors, Estrogen)
SB  - IM
MH  - Humans
MH  - Female
MH  - *Estrogens/pharmacology
MH  - *Breast Neoplasms/drug therapy
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Estradiol/pharmacology/therapeutic use
MH  - Receptors, Estrogen/genetics/metabolism
MH  - Cell Line, Tumor
OTO - NOTNLM
OT  - Breast cancer
OT  - RNA sequencing
OT  - autocrine factor
OT  - endocrine resistance
OT  - estrogen-responsive gene
OT  - medium replacement
EDAT- 2023/09/29 12:43
MHDA- 2023/10/02 06:42
CRDT- 2023/09/29 07:31
PHST- 2023/07/28 00:00 [received]
PHST- 2023/09/03 00:00 [revised]
PHST- 2023/09/04 00:00 [accepted]
PHST- 2023/10/02 06:42 [medline]
PHST- 2023/09/29 12:43 [pubmed]
PHST- 2023/09/29 07:31 [entrez]
AID - 43/10/4447 [pii]
AID - 10.21873/anticanres.16640 [doi]
PST - ppublish
SO  - Anticancer Res. 2023 Oct;43(10):4447-4469. doi: 10.21873/anticanres.16640.