Akt regulates progesterone receptor B-dependent transcription and angiogenesis in endometrial cancer cells

Lee, Irene I.; Maniar, Kruti P.; Lydon, John P.; Kim, Julie

doi:10.1038/onc.2016.56

Cited by 37 publications

(35 citation statements)

References 43 publications

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“…The elucidation of molecular and cellular mechanisms responsible for the tumorigenesis and progression of endometrial cancer is critical to the development of novel diagnostic and therapeutic strategies for patients with endometrial cancer (18,19). miRNAs are considered to be novel candidate therapeutic agents for endometrial cancer due to their involvement in cancer initiation and progression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑409 may function as a tumor suppressor in endometrial carcinoma cells by targeting Smad2

Zhang¹,

Wang

Wu³

2018

Mol Med Report

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MicroRNAs (miRNAs) are frequently dysregulated in human cancer and can act as either potent oncogenes or tumor suppressor genes. The aberrant expression of miRNA-409 (miR-409) has been found in certain types of cancer, however, its expression and potential biological role in endometrial cancer remain to be fully elucidated. In the present study, a total of 16 pairs of tissue samples from 16 patients with endometrial cancer were used in the present study, each of which consisted of human endometrial cancer tissue and matched adjacent normal tissue from the same patient. The expression of miR-409 of the tissue were detected and its associations with Ishikawa and HEC-1B human endometrial cancer cell lines were studied. The results of the present study demonstrated that miR-409 was downregulated in human endometrial cancer, and it suppressed the growth of Ishikawa and HEC-1B human endometrial cancer cell lines. Bioinformatics analysis indicated that small mothers against decapentaplegic 2 (Smad2) was a putative target of miR-409. In a luciferase reporter system, it was confirmed that Smad2 was a direct target gene of miR-409. It was also demonstrated that Smad2 was upregulated in human endometrial cancer tissues, and this was inversely correlated with the expression of miR-409. These findings indicated that miR-409 targeted the Smad2 transcript and suppressed endometrial cancer cell growth, suggesting that miR-409 has a tumor suppressive role in the pathogenesis of human endometrial cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑409 may function as a tumor suppressor in endometrial carcinoma cells by targeting Smad2

Zhang¹,

Wang

Wu³

2018

Mol Med Report

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“…The AKT pathway may also impact progesterone action; AKT can downregulate PR protein expression of PR in breast cancer and endometrial cancer cells, and in stromal cells derived from endometriosis (125-127). AKT has been shown to attenuate PR action in endometrial cancer cells by affecting recruitment of coregulators to PR on chromatin (128). AKT inhibitors increased cellular PR and decreased cell survival and increased apoptosis in endometriosis (127).…”

Section: Endometriosis and Infertility: Role Of Eutopic Endometriummentioning

confidence: 99%

Endometrial receptivity in the eutopic endometrium of women with endometriosis: it is affected, and let me show you why

Lessey¹,

Kim²

2017

Fertility and Sterility

206

155

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The endometrium maintains complex controls on proliferation and apoptosis as part of repetitive menstrual cycles that prepare the endometrium for the window of implantation and pregnancy. The reliance on inflammatory mechanisms for both implantation and menstruation, creates the opportunity in the setting of endometriosis for the establishment of chronic inflammation that is disruptive to endometrial receptivity, causing both infertility and abnormal bleeding. Clinically, there can be little doubt that the endometrium of women with endometriosis is less receptive to embryo implantation, and strong evidence exists to suggests that endometrial changes are associated with decreased cycle fecundity as a result of this disease. Here we provide unifying concepts regarding those changes and how they are coordinated to promote progesterone resistance and estrogen dominance through aberrant cell signaling pathways and reduced expression of key homeostatic proteins in eutopic endometrium of women with endometriosis.

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“…The PR expression was closely related to the level of the growth factor/PI3K/AKT/mTOR system activation. Lee (2016) revealed the significant connections between the AKT activity, PTEN loss, and PR receptor level (Lee et al, 2016;. We found that the prostate cancer malignization in high PR expression (> 0.1 RLU) was associated with the rise in PTEN mRNA level, and the decline in NF-κB p50 expression.…”

Section: Discussionmentioning

confidence: 81%

“…But its level didn't differ in patients with the benign and cancer prostate pathology, remaining elevated in transformed and non-transformed cells. It is known that the associations between the transcriptional activity of AR and PR could affect the disorders of hormone reception and lead to PCa development (Quayle et al, 2007;Chen et al, 2017;Lee et al, 2016). The PR expression was found to be associated with the expression of both AR and its regulatory peptides (Brn-3α and TRIM16) in patients with BH.…”

Section: Discussionmentioning

confidence: 97%

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Progesterone Receptor Expression in the Benign Prostatic Hyperplasia and Prostate Cancer Tissues, Relation with Transcription, Growth Factors, Hormone Reception and Components of the AKT/mTOR Signaling Pathway

Спирина

Kovaleva

Усынин

et al. 2020

Asian Pac J Cancer Prev

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Background: Progesterone receptor (PR) is a critical regulator in reproductive tissues that controls a variety of cellular processes. The objective of the study was to study the PR expression in patients with benign prostatic hyperplasia and prostate cancers in connection with the transcription, growth factors, AR, ERα, ERβ, and components of the AKT/ mTOR signaling pathway expression. Materials and methods: Ninety-seven patients with prostate pathology were enrolled in the study. Forty-two patients had benign prostatic hyperplasia (BH). Fifty-five patients had locally advanced prostate cancer (PCa). The PSA level and the amount of testosterone in the serum were measured using an ELISA assay. The expression level of NF-κB p65, NF-κB p50, HIF-1, HIF-2, growth factor VEGF, VEGFR2, CAIX, as well as AR, ERα, ERβ, PR, Brn-3α, TRIM16 were quantified by RT-PCR. The protein level of Brn-3α, TRIM16 was detected by Western Blotting. Results: Growth in PR expression was observed in PCa tissues compared to BH ones without changes in the clinical and pathological features of the patients. An increase in PR expression was detected in patients with PCa compared to BH. Its mRNA level depended on the expression of AR, Brn-3α, and TRIM16, components of the AKT/mTOR signaling pathway, transcription, and growth factors. An increase in the TRIM16 expression in the PCa tissues was noted in the case of a low PR level. We revealed the growth in PR expression was accompanied by the suppression of the signaling cascade activity, AR, Brn-3α mRNA level, and the enhanced PTEN expression in PCa tissues. The increase in PR expression in PCa led to a decrease in the level of mRNA of NF-κB, HIF-1, VEGF, and VEGFR2. Conclusion: In general, the data indicated the significance of the PR expression in the development of the prostate pathology that affected the cross-talk between the steroid hormone reception and signal transduction.

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Akt regulates progesterone receptor B-dependent transcription and angiogenesis in endometrial cancer cells

Cited by 37 publications

References 43 publications

MicroRNA‑409 may function as a tumor suppressor in endometrial carcinoma cells by targeting Smad2

MicroRNA‑409 may function as a tumor suppressor in endometrial carcinoma cells by targeting Smad2

Endometrial receptivity in the eutopic endometrium of women with endometriosis: it is affected, and let me show you why

Progesterone Receptor Expression in the Benign Prostatic Hyperplasia and Prostate Cancer Tissues, Relation with Transcription, Growth Factors, Hormone Reception and Components of the AKT/mTOR Signaling Pathway

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