Effects of dual inhibition of AKT and ERK1/2 pathways on endometrial pro-inflammatory, hormonal, and epigenetic microenvironment in endometriosis

Joe A Arosh; JeHoon Lee; Sakhila K Banu

doi:10.1016/j.mce.2021.111446

Effects of dual inhibition of AKT and ERK1/2 pathways on endometrial pro-inflammatory, hormonal, and epigenetic microenvironment in endometriosis

Joe A Arosh, JeHoon Lee, Sakhila K Banu

Molecular and cellular endocrinology · 2021 · vol. 539 , pp. 111446 · doi:10.1016/j.mce.2021.111446 · PMID:34478807 · W3198834199

article OA: closed CC0 ⤵ 8 in-corpus citations

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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study investigated how blocking AKT and ERK1/2 pathways impacts the pro-inflammatory, hormonal, and epigenetic environment within endometriosis lesions.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Butadienes Chromones Endometriosis MAP Kinase Signaling System Morpholines Nitriles Proto-Oncogene Proteins c-akt Animals Butadienes Butadienes Cell Line Cell Proliferation Cell Proliferation Cell Survival Cell Survival Chromones Chromones Cytokines Cytokines Disease Models, Animal

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References (66)

17β-Hydroxysteroid Dehydrogenase-2 Deficiency and Progesterone Resistance in Endometriosis via openalex
Aberrant expression of deoxyribonucleic acid methyltransferases DNMT1, DNMT3A, and DNMT3B in women with endometriosis via openalex
Activated AKT Pathway Promotes Establishment of Endometriosis via openalex
A Modified Baboon Model for Endometriosis via openalex
Co-operation between the AKT and ERK signaling pathways may support growth of deep endometriosis in a fibrotic microenvironment in vitro† via openalex
Cyclooxygenase-2 Regulates Survival, Migration, and Invasion of Human Endometriotic Cells through Multiple Mechanisms via openalex
Deficiency of Immunophilin FKBP52 Promotes Endometriosis via openalex
Differential regulation of Akt phosphorylation in endometriosis via openalex
Dual inhibition of ERK1/2 and AKT pathways is required to suppress the growth and survival of endometriotic cells and lesions via openalex
Endometriosis via openalex
Estrogen Receptor-β, Estrogen Receptor-α, and Progesterone Resistance in Endometriosis via openalex
Eutopic Endometrium in Women with Endometriosis: Ground Zero for the Study of Implantation Defects via openalex
Experimental Murine Endometriosis Induces DNA Methylation and Altered Gene Expression in Eutopic Endometrium1 via openalex
Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway Is Required for Endometrial Decidualization in Mice and Human via openalex
Gene Expression Analysis of Endometrium Reveals Progesterone Resistance and Candidate Susceptibility Genes in Women with Endometriosis via openalex
HOX gene expression is altered in the endometrium of women with endometriosis via openalex
Identification of an Invasive, N-Cadherin-Expressing Epithelial Cell Type in Endometriosis Using a New Cell Culture Model via openalex
Increased Activation of the PI3K/AKT Pathway Compromises Decidualization of Stromal Cells from Endometriosis via openalex
Increased Mitogen-Activated Protein Kinase Kinase/Extracellularly Regulated Kinase Activity in Human Endometrial Stromal Fibroblasts of Women with Endometriosis Reduces 3′,5′-Cyclic Adenosine 5′-Monophosphate Inhibition of Cyclin D1 via openalex
Influence of AKT on Progesterone Action in Endometrial Diseases via openalex
Integrins in the endometrium of women with endometriosis via openalex
Macrophages display proinflammatory phenotypes in the eutopic endometrium of women with endometriosis with relevance to an infectious etiology of the disease via openalex
Mechanisms of endometrial progesterone resistance via openalex
Molecular and preclinical basis to inhibit PGE <sub>2</sub> receptors EP2 and EP4 as a novel nonsteroidal therapy for endometriosis via openalex
Molecular, Cellular, and Epigenetic Signatures of Prostaglandin E2 in Endometriosis via openalex
Molecular Mechanisms of Treatment Resistance in Endometriosis: The Role of Progesterone–Hox Gene Interactions via openalex
Progesterone Action in Endometrial Cancer, Endometriosis, Uterine Fibroids, and Breast Cancer via openalex
Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Adenomyosis and Its Rectification by a Histone Deacetylase Inhibitor and a Demethylation Agent via openalex
Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Endometriosis via openalex
Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Induces Apoptosis of Human Endometriotic Cells through Suppression of ERK1/2, AKT, NFκB, and β-Catenin Pathways and Activation of Intrinsic Apoptotic Mechanisms via openalex
Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Inhibits Adhesion of Human Endometriotic Epithelial and Stromal Cells Through Suppression of Integrin-Mediated Mechanisms1 via openalex
Selective inhibition of prostaglandin E2 receptors EP2 and EP4 inhibits invasion of human immortalized endometriotic epithelial and stromal cells through suppression of metalloproteinases via openalex
Steroid receptor and aromatase expression in baboon endometriotic lesions via openalex
The Altered Distribution of the Steroid Hormone Receptors and the Chaperone Immunophilin FKBP52 in a Baboon Model of Endometriosis Is Associated With Progesterone Resistance During the Window of Uterine Receptivity via openalex
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Cited by (8)

Source provenance

europepmc: last seen: 2026-06-04T01:30:01.192114+00:00
openalex: last seen: 2026-06-10T17:14:06.276822+00:00
pubmed: last seen: 2026-05-13T22:24:20.309598+00:00

License: CC0 · commercial use OK

[1] 17β-Hydroxysteroid Dehydrogenase-2 Deficiency and Progesterone Resistance in Endometriosis via openalex

[2] Aberrant expression of deoxyribonucleic acid methyltransferases DNMT1, DNMT3A, and DNMT3B in women with endometriosis via openalex

[3] Activated AKT Pathway Promotes Establishment of Endometriosis via openalex

[4] A Modified Baboon Model for Endometriosis via openalex

[5] Co-operation between the AKT and ERK signaling pathways may support growth of deep endometriosis in a fibrotic microenvironment in vitro† via openalex

[6] Cyclooxygenase-2 Regulates Survival, Migration, and Invasion of Human Endometriotic Cells through Multiple Mechanisms via openalex

[7] Deficiency of Immunophilin FKBP52 Promotes Endometriosis via openalex

[8] Differential regulation of Akt phosphorylation in endometriosis via openalex

[9] Dual inhibition of ERK1/2 and AKT pathways is required to suppress the growth and survival of endometriotic cells and lesions via openalex

[10] Endometriosis via openalex

[11] Estrogen Receptor-β, Estrogen Receptor-α, and Progesterone Resistance in Endometriosis via openalex

[12] Eutopic Endometrium in Women with Endometriosis: Ground Zero for the Study of Implantation Defects via openalex

[13] Experimental Murine Endometriosis Induces DNA Methylation and Altered Gene Expression in Eutopic Endometrium1 via openalex

[14] Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway Is Required for Endometrial Decidualization in Mice and Human via openalex

[15] Gene Expression Analysis of Endometrium Reveals Progesterone Resistance and Candidate Susceptibility Genes in Women with Endometriosis via openalex

[16] HOX gene expression is altered in the endometrium of women with endometriosis via openalex

[17] Identification of an Invasive, N-Cadherin-Expressing Epithelial Cell Type in Endometriosis Using a New Cell Culture Model via openalex

[18] Increased Activation of the PI3K/AKT Pathway Compromises Decidualization of Stromal Cells from Endometriosis via openalex

[19] Increased Mitogen-Activated Protein Kinase Kinase/Extracellularly Regulated Kinase Activity in Human Endometrial Stromal Fibroblasts of Women with Endometriosis Reduces 3′,5′-Cyclic Adenosine 5′-Monophosphate Inhibition of Cyclin D1 via openalex

[20] Influence of AKT on Progesterone Action in Endometrial Diseases via openalex

[21] Integrins in the endometrium of women with endometriosis via openalex

[22] Macrophages display proinflammatory phenotypes in the eutopic endometrium of women with endometriosis with relevance to an infectious etiology of the disease via openalex

[23] Mechanisms of endometrial progesterone resistance via openalex

[24] Molecular and preclinical basis to inhibit PGE <sub>2</sub> receptors EP2 and EP4 as a novel nonsteroidal therapy for endometriosis via openalex

[25] Molecular, Cellular, and Epigenetic Signatures of Prostaglandin E2 in Endometriosis via openalex

[26] Molecular Mechanisms of Treatment Resistance in Endometriosis: The Role of Progesterone–Hox Gene Interactions via openalex

[27] Progesterone Action in Endometrial Cancer, Endometriosis, Uterine Fibroids, and Breast Cancer via openalex

[28] Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Adenomyosis and Its Rectification by a Histone Deacetylase Inhibitor and a Demethylation Agent via openalex

[29] Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Endometriosis via openalex

[30] Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Induces Apoptosis of Human Endometriotic Cells through Suppression of ERK1/2, AKT, NFκB, and β-Catenin Pathways and Activation of Intrinsic Apoptotic Mechanisms via openalex

[31] Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Inhibits Adhesion of Human Endometriotic Epithelial and Stromal Cells Through Suppression of Integrin-Mediated Mechanisms1 via openalex

[32] Selective inhibition of prostaglandin E2 receptors EP2 and EP4 inhibits invasion of human immortalized endometriotic epithelial and stromal cells through suppression of metalloproteinases via openalex

[33] Steroid receptor and aromatase expression in baboon endometriotic lesions via openalex

[34] The Altered Distribution of the Steroid Hormone Receptors and the Chaperone Immunophilin FKBP52 in a Baboon Model of Endometriosis Is Associated With Progesterone Resistance During the Window of Uterine Receptivity via openalex

[35] The endometrial immune environment of women with endometriosis via openalex

[36] The Pains of Endometriosis via openalex

[37] W6662945580 via openalex

[38] W1848470479 via openalex

[39] W1984801458 via openalex

[40] W1991667131 via openalex

[41] W1995070589 via openalex

[42] W1998052292 via openalex

[43] W2037405213 via openalex

[44] W2044866500 via openalex

[45] W2051340861 via openalex

[46] W2053421436 via openalex

[47] W2070143104 via openalex

[48] W2072526299 via openalex

[49] W2083063093 via openalex

[50] W2089605820 via openalex

[51] W2097767970 via openalex

[52] W2110838173 via openalex

[53] W2130808015 via openalex

[54] W2137799669 via openalex

[55] W2138892400 via openalex

[56] W2143115887 via openalex

[57] W2148558073 via openalex

[58] W2152497434 via openalex

[59] W2154719999 via openalex

[60] W2155238754 via openalex

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[64] W2767360570 via openalex

[65] W4211081176 via openalex

[66] W1548219170 via openalex