The role of UPR‐related long noncoding RNAs in development of endocrine resistance in breast cancer

Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first‐line treatment. Most ER‐positive breast cancer patients initially respond to endocrine therapy, but up to 40% of patients develop resistance over time, and the main mechanism is aberrant activa...

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Veröffentlicht in:International journal of cancer Jg. 157; H. 12; S. 2434 - 2446
Hauptverfasser: Liu, Wen, Gupta, Sahil, Gupta, Sanjeev
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Hoboken, USA John Wiley & Sons, Inc 15.12.2025
Wiley Subscription Services, Inc
Schlagworte:
Animals
Antineoplastic Agents, Hormonal - pharmacology
Antineoplastic Agents, Hormonal - therapeutic use
Breast cancer
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cell fate
Drug Resistance, Neoplasm - genetics
endocrine resistance
Endocrine therapy
Endoplasmic reticulum
Endoplasmic Reticulum Stress - genetics
Estrogen receptors
Female
Gene Expression Regulation, Neoplastic
Humans
long noncoding RNA
Microenvironments
Non-coding RNA
Patients
Protein folding
RNA, Long Noncoding - genetics
Signal Transduction
unfolded protein response
Unfolded Protein Response - genetics
long noncoding RNA
unfolded protein response
breast cancer
endocrine resistance
ISSN:0020-7136, 1097-0215, 1097-0215
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Abstract Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first‐line treatment. Most ER‐positive breast cancer patients initially respond to endocrine therapy, but up to 40% of patients develop resistance over time, and the main mechanism is aberrant activation of ER signaling pathways. Recent research has shown that cancer's uncontrolled proliferative capacity and a hostile microenvironment can induce endoplasmic reticulum (EnR) stress and trigger unfolded protein response (UPR), which plays a crucial role in determining cell fate. Furthermore, increasing evidence suggests that noncoding ribonucleic acids (RNAs), which are involved during the crosstalk between the UPR and ER signaling pathways, play an essential role in endocrine resistance. In this review, we provide an overview of long noncoding RNA (lncRNA) that is involved both in endocrine resistance and UPR. We provide new insights into potential treatment strategies to overcome endocrine resistance in ER‐positive breast cancer patients by targeting the lncRNA that plays key roles in endocrine resistance and UPR signaling. Finally, we discuss the current state and future directions for targeting lncRNAs to improve clinical outcomes in endocrine‐resistant breast cancer patients.
AbstractList Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first‐line treatment. Most ER‐positive breast cancer patients initially respond to endocrine therapy, but up to 40% of patients develop resistance over time, and the main mechanism is aberrant activation of ER signaling pathways. Recent research has shown that cancer's uncontrolled proliferative capacity and a hostile microenvironment can induce endoplasmic reticulum (EnR) stress and trigger unfolded protein response (UPR), which plays a crucial role in determining cell fate. Furthermore, increasing evidence suggests that noncoding ribonucleic acids (RNAs), which are involved during the crosstalk between the UPR and ER signaling pathways, play an essential role in endocrine resistance. In this review, we provide an overview of long noncoding RNA (lncRNA) that is involved both in endocrine resistance and UPR. We provide new insights into potential treatment strategies to overcome endocrine resistance in ER‐positive breast cancer patients by targeting the lncRNA that plays key roles in endocrine resistance and UPR signaling. Finally, we discuss the current state and future directions for targeting lncRNAs to improve clinical outcomes in endocrine‐resistant breast cancer patients.
Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first-line treatment. Most ER-positive breast cancer patients initially respond to endocrine therapy, but up to 40% of patients develop resistance over time, and the main mechanism is aberrant activation of ER signaling pathways. Recent research has shown that cancer's uncontrolled proliferative capacity and a hostile microenvironment can induce endoplasmic reticulum (EnR) stress and trigger unfolded protein response (UPR), which plays a crucial role in determining cell fate. Furthermore, increasing evidence suggests that noncoding ribonucleic acids (RNAs), which are involved during the crosstalk between the UPR and ER signaling pathways, play an essential role in endocrine resistance. In this review, we provide an overview of long noncoding RNA (lncRNA) that is involved both in endocrine resistance and UPR. We provide new insights into potential treatment strategies to overcome endocrine resistance in ER-positive breast cancer patients by targeting the lncRNA that plays key roles in endocrine resistance and UPR signaling. Finally, we discuss the current state and future directions for targeting lncRNAs to improve clinical outcomes in endocrine-resistant breast cancer patients.Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first-line treatment. Most ER-positive breast cancer patients initially respond to endocrine therapy, but up to 40% of patients develop resistance over time, and the main mechanism is aberrant activation of ER signaling pathways. Recent research has shown that cancer's uncontrolled proliferative capacity and a hostile microenvironment can induce endoplasmic reticulum (EnR) stress and trigger unfolded protein response (UPR), which plays a crucial role in determining cell fate. Furthermore, increasing evidence suggests that noncoding ribonucleic acids (RNAs), which are involved during the crosstalk between the UPR and ER signaling pathways, play an essential role in endocrine resistance. In this review, we provide an overview of long noncoding RNA (lncRNA) that is involved both in endocrine resistance and UPR. We provide new insights into potential treatment strategies to overcome endocrine resistance in ER-positive breast cancer patients by targeting the lncRNA that plays key roles in endocrine resistance and UPR signaling. Finally, we discuss the current state and future directions for targeting lncRNAs to improve clinical outcomes in endocrine-resistant breast cancer patients.
Author Gupta, Sanjeev
Gupta, Sahil
Liu, Wen
Author_xml – sequence: 1
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  organization: University of Galway
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  fullname: Gupta, Sanjeev
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  organization: University of Galway
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Issue 12
Keywords long noncoding RNA
unfolded protein response
breast cancer
endocrine resistance
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Snippet Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first‐line treatment. Most ER‐positive breast cancer...
Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first‐line treatment. Most ER‐positive breast cancer...
Breast cancer patients who express estrogen receptor α (ER) typically receive endocrine therapy as a first-line treatment. Most ER-positive breast cancer...
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StartPage 2434
SubjectTerms Animals
Antineoplastic Agents, Hormonal - pharmacology
Antineoplastic Agents, Hormonal - therapeutic use
Breast cancer
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cell fate
Drug Resistance, Neoplasm - genetics
endocrine resistance
Endocrine therapy
Endoplasmic reticulum
Endoplasmic Reticulum Stress - genetics
Estrogen receptors
Female
Gene Expression Regulation, Neoplastic
Humans
long noncoding RNA
Microenvironments
Non-coding RNA
Patients
Protein folding
RNA, Long Noncoding - genetics
Signal Transduction
unfolded protein response
Unfolded Protein Response - genetics
Title The role of UPR‐related long noncoding RNAs in development of endocrine resistance in breast cancer
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fijc.70067
https://www.ncbi.nlm.nih.gov/pubmed/40749127
https://www.proquest.com/docview/3263645290
https://www.proquest.com/docview/3235723251
Volume 157
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