Progesterone receptor expression during prostate cancer progression suggests a role of this receptor in stromal cell differentiation

Yu, Yue; Ou, Yang; Fazli, Ladan; Rennie, Paul S.; Gleave, Martin; Dong, Xuesen

doi:10.1002/pros.22988

Cited by 33 publications

(34 citation statements)

References 17 publications

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“…Microfilaments are the smallest of the three skeleton structures, are composed of actin and exist in the form of free and globular actin G-actin or F-actin (23). Previous data indicate that the changes in actin polymerization/depolymerization, namely actin skeleton reconstruction, serve important regulatory roles in phenotypes of malignant cells (24). It has been suggested that intervention in cellular skeleton microfilament actin reconstruction may be a functional target of anticancer drugs, and may be regarded as a basis for developing novel antineoplastic drugs (25).…”

Section: Discussionmentioning

confidence: 99%

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Huang

Wang

2018

Oncol Lett

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Abstract. It is widely considered that endoplasmic reticulum stress may rapidly induce apoptosis. The aim of the present study was to investigate the effect of thapsigargin on the induction of apoptosis in prostate cancer cells, and to explore its possible mechanism. A Cell Counting Kit-8 was selected to determine the effect of thapsigargin (0, 1, 10 and 100 nM) on the proliferation of PC3 cells. Cell proliferation of the prostate cancer cells was effectively inhibited by treatment with thapsigargin, and thapsigargin significantly increased the rate of apoptosis and caspase-3/9 activities in prostate cancer cells. The protein expression of phosphorylated (p)-RAC-α serine threonine-protein kinase, p-mechanistic target of rapamycin, F-actin and paxillin were significantly decreased, and cofilin-1 protein expression was significantly increased by treatment with thapsigargin in prostate cancer cells. Overall, the data of the present study revealed that thapsigargin induced apoptosis in prostate cancer cells through cofilin-1 and paxillin.

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Section: Discussionmentioning

confidence: 99%

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Huang

Wang

2018

Oncol Lett

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“…Ligand-activation of PR plays a critical role in female mammary gland development/homeostasis and other female reproductive organs [10]. Additionally, PR is expressed in prostate tissue and plays an essential role in tissue microenvironment and stromal cell differentiation [17]. PR has two isoforms which have differential roles in normal organ functioning and the balanced expression of both isoforms is critical for normal tissue function [10,18].…”

Section: Class I: the Progesterone Receptor Structural And Functionamentioning

confidence: 99%

“…HMGB1/2 is a protein that increases DNA-protein binding interactions indirectly through increasing the number of contacts of the PR to DNA through dynamic conformational change [21][22][23]. Furthermore, recent evidence suggests a role of PR in prostate cancer progression, specifically through its role in regulating smooth actin muscle (SMAα) in stromal cells [17,24]. PR levels were upregulated after castration in patients with prostate cancer, which could contribute to treatment resistance due to its role in stromal cell differentiation and mobility [17,24].…”

Section: Class I: the Progesterone Receptor Structural And Functionamentioning

confidence: 99%

“…Furthermore, recent evidence suggests a role of PR in prostate cancer progression, specifically through its role in regulating smooth actin muscle (SMAα) in stromal cells [17,24]. PR levels were upregulated after castration in patients with prostate cancer, which could contribute to treatment resistance due to its role in stromal cell differentiation and mobility [17,24]. Until recently, the role of PR in prostate cancer was not evaluated but maybe a key player in understanding current mechanisms of treatment resistance.…”

Section: Class I: the Progesterone Receptor Structural And Functionamentioning

confidence: 99%

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Structure and Function of the Nuclear Receptor Superfamily and Current Targeted Therapies of Prostate Cancer

Porter

Ortiz

Bratslavsky

et al. 2019

Cancers

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The nuclear receptor superfamily comprises a large group of proteins with functions essential for cell signaling, survival, and proliferation. There are multiple distinctions between nuclear superfamily classes defined by hallmark differences in function, ligand binding, tissue specificity, and DNA binding. In this review, we utilize the initial classification system, which defines subfamilies based on structure and functional difference. The defining feature of the nuclear receptor superfamily is that these proteins function as transcription factors. The loss of transcriptional regulation or gain of functioning of these receptors is a hallmark in numerous diseases. For example, in prostate cancer, the androgen receptor is a primary target for current prostate cancer therapies. Targeted cancer therapies for nuclear hormone receptors have been more feasible to develop than others due to the ligand availability and cell permeability of hormones. To better target these receptors, it is critical to understand their structural and functional regulation. Given that late-stage cancers often develop hormone insensitivity, we will explore the strengths and pitfalls of targeting other transcription factors outside of the nuclear receptor superfamily such as the signal transducer and activator of transcription (STAT).

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“…Androgen-growth factors interactions are disordered in androgen-independent PCa and cause sensitization of cancerous cells to low level of androgens in their microenvironment. It was shown that progesterone receptor (PR) signaling plays an active role in changing PCa-associated stromal cell phenotype during the disease progression [57].…”

Section: Prostate Cancermentioning

confidence: 99%

Hormonal Impact on Tumor Growth and Progression

Reznikov¹

2015

Exp. Onc.

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In this review, current knowledge of hormones impact on prostate, breast and endometrium cancer growth and transition to hormone therapy resistant phenotype is summarized. A special consideration is given to genetic alterations and hormone responsive signa ling pathways. Estrogen, androgen and progesterone are the key drivers in these cancer variants. Hormone receptors and their interplay with plenty of growth factors generated by the tumor microenvironment contribute greatly to carcinogenesis and cancer cell proliferation. The tumor cell plasticity that could explain a loss of responsiveness to hormone deprivation therapy and aggressive course of the diseases has been addressed.

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Progesterone receptor expression during prostate cancer progression suggests a role of this receptor in stromal cell differentiation

Abstract: These results suggest that PR plays an active role in regulating stromal cell phenotypes during prostate cancer progression.

Cited by 33 publications

References 17 publications

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Structure and Function of the Nuclear Receptor Superfamily and Current Targeted Therapies of Prostate Cancer

Hormonal Impact on Tumor Growth and Progression

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