ArticleBMC medical genomics2019
Medroxyprogesterone acetate causes the alterations of endoplasmic reticulum related mRNAs and lncRNAs in endometrial cancer cells.
Article in BMC medical genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Role of Endoplasmic Reticulum Stress-Associated Genes in Septic Neonatal Foals.Antioxidants (Basel, Switzerland) · 2025Article
- Comprehensive analyses of mitophagy-related genes and mitophagy-related lncRNAs for patients with ovarian cancer.BMC women's health · 2024Article
- Identification of a mBMC pulmonary medicine · 2023Article
- The Role of Autophagy and Apoptosis in the Combined Action of Plasma-Treated Saline, Doxorubicin, and Medroxyprogesterone Acetate on K562 Myeloid Leukaemia Cells.International journal of molecular sciences · 2023Article
- Construction of the systemic anticancer immune environment in tumour-bearing humanized mouse by using liposome-encapsulated anti-programmed death ligand 1 antibody-conjugated progesterone.Frontiers in immunology · 2023Article
- Calcium and calcium-related proteins in endometrial cancer: opportunities for pharmacological intervention.International journal of biological sciences · 2022Review
- FBXL16 Promotes Endometrial Progesterone Resistance via PP2AJournal of immunology research · 2022Article
- Contemporary Fertility-Sparing Management Options of Early Stage Endometrioid Endometrial Cancer in Young Nulliparous Patients.Journal of clinical medicine · 2021Review
- Progestins as Anticancer Drugs and Chemosensitizers, New Targets and Applications.Pharmaceutics · 2021Review
- Hsa_Circ_0001860 Promotes Smad7 to Enhance MPA Resistance in Endometrial CancerFrontiers in cell and developmental biology · 2021Article
- Clinical Use of Progestins and Their Mechanisms of Action: Present and Future (Review).Sovremennye tekhnologii v meditsine · 2021Review
- Psychological Stress and Functional Endometrial Disorders: Update of Mechanism Insights.Frontiers in endocrinology · 2021Review
- Effects of homocysteine-induced endoplasmic reticulum protein on endoplasmic reticulum stress, autophagy, and neuronal apoptosis following intracerebral hemorrhage.IBRO reports · 2020Article
- Development of a nine-lncRNA signature as a novel prognostic marker of estrogen receptor-negative breast cancer.Oncology letters · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProgestin is effective to promote endometrial cancer (EC) cells apoptosis, however, continuous progestin administration causes low level of progestin receptor B (PRB), further resulting in progestin resistance. Here, we performed microarray analysis on Ishikawa cells (PRB+) treated with medroxyprogesterone acetate (MPA) to explore the molecular mechanism underlying the inhibitory influence of MPA on PRB+ EC cells.
methodsMicroarray analysis was performed by using Ishikawa cells (PRB+) treated with MPA. Differentially expressed mRNA and long noncoding RNAs (lncRNAs) were identified. Furthermore, the functions of these mRNAs and lncRNAs were predicted by functional enrichment analysis. QRT-PCR was further performed to verify the microarray data.
resultsA total of 358 differentially expressed genes and 292 lncRNAs were identified in Ishikawa cells (PRB+) treated with MPA. QRT-PCR verified these data. Functional enrichment analysis identified endoplasmic reticulum (ER) stress as the key pathway involved in the inhibitory effect of MPA on EC cells. And the ER stress apoptotic molecule CHOP and ER stress related molecule HERPUD1 were both highly expressed in Ishikawa cells (PRB+) treated with MPA. Co-expression analysis showed lnc-CETP-3 was highly correlated with CHOP and HERPUD1, suggesting it might participate in ER stress pathway-related EC cell apoptosis caused by MPA. In addition, compared with untreated cells, lnc-CETP-3, CHOP and HERPUD1 were significantly up-regulated in Ishikawa cells (PRB+) treated with MPA, whereas they have no statistical significance in KLE cells (PRB-).
conclusionsMPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+. Lnc-CETP-3 might be involved in this process. These findings may provide therapeutic targets for EC patients with PRB-, and resistance-related targets to increase the sensitivity of MPA on EC cells.
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