scholarly journals Primary cell cultures as models of prostate cancer development

2005 ◽  
Vol 12 (1) ◽  
pp. 19-47 ◽  
Author(s):  
D M Peehl
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Biological Activities ◽  
Primary Cultures ◽  
Neuroendocrine Cells ◽  
Biological Behavior ◽  
Full Potential ◽  
Cell Surface Antigens

This review focuses on primary cultures of human prostatic epithelial cells and their applications as models of normal and malignant biological behavior. Current abilities to culture cells from normal tissues, from premalignant dysplastic lesions (prostatic intraepithelial neoplasia), from primary adenocarcinomas, and from metastases are described. Evidence for representation of the interrelated cells of the normal prostatic epithelium — stem cells, basal epithelial cells, secretory epithelial cells, transit amplifying cells and neuroendocrine cells — in primary cultures is presented. Comparisons between normal and cancer-derived primary cultures are made regarding biological activities relevant to carcinogenesis, such as proliferation, apoptosis, differentiation, senescence, adhesion, migration, invasion, steroid hormone metabolism, other metabolic pathways and angiogenesis. Analyses of tumor suppressor activity, differential gene expression and cytogenetics in primary cultures have revealed changes relevant to prostate cancer progression. Preclinical studies with primary cultures have provided information useful for designing new strategies for chemoprevention, chemotherapy, cytotoxin therapy, radiation therapy, gene therapy and imaging. While the behavior of normal primary cultures is often used as a basis for comparison with established, immortal prostate cancer cell lines, the most informative studies are performed with donor-matched pairs of normal and malignant primary cultures, grown under identical conditions. Challenges that remain to be addressed if the full potential of primary cultures as a model system is to be realized include isolation, culture and characterization of stem cells, improved methodology to induce or maintain a fully differentiated, androgen-responsive phenotype, and identification of cell surface antigens or other markers with which to purify pure populations of live cancer or premalignant cells apart from non-malignant epithelial cells prior to culture.

Lineage potential, plasticity and environmental reprogramming of epithelial stem/progenitor cells

2014 ◽  
Vol 42 (3) ◽  
pp. 637-644 ◽  
Author(s):  
Alessandro W. Amici ◽  
Fatai O. Onikoyi ◽  
Paola Bonfanti
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Cell Therapy ◽  
Hair Follicle ◽  
Progenitor Cells ◽  
Environmental Cues ◽  
Full Potential ◽  
Thymic Epithelium ◽  
Differentiated Cells ◽  
Stratified Epithelia

Recent evidence supports and reinforces the concept that environmental cues may reprogramme somatic cells and change their natural fate. In the present review, we concentrate on environmental reprogramming and fate potency of different epithelial cells. These include stratified epithelia, such as the epidermis, hair follicle, cornea and oesophagus, as well as the thymic epithelium, which stands alone among simple and stratified epithelia, and has been shown recently to contain stem cells. In addition, we briefly discuss the pancreas as an example of plasticity of intrinsic progenitors and even differentiated cells. Of relevance, examples of plasticity and fate change characterize pathologies such as oesophageal metaplasia, whose possible cell origin is still debated, but has important implications as a pre-neoplastic event. Although much work remains to be done in order to unravel the full potential and plasticity of epithelial cells, exploitation of this phenomenon has already entered the clinical arena, and might provide new avenues for future cell therapy of these tissues.

scholarly journals Use of Bone Marrow‐Derived Mesenchymal Stem Cells in Prostate Cancer Could Increase the Risk of Cancer Progression

2019 ◽  
Author(s):  
A. Thirumal Raj ◽  
Supriya Kheur ◽  
Ramesh Bhonde ◽  
Archana A. Gupta ◽  
Vikrant R. Patil ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Progression ◽  
Risk Of Cancer

Embryo co-culture with bovine amniotic membrane stem cells can enhance the cryo-survival of IVF-derived bovine blastocysts comparable with co-culture with bovine oviduct epithelial cells

Zygote ◽  
2020 ◽  
pp. 1-6
Author(s):  
Shayan Nejat-Dehkordi ◽  
Ebrahim Ahmadi ◽  
Abolfazl Shirazi ◽  
Hassan Nazari ◽  
Naser Shams-Esfandabadi
Keyword(s):  
Stem Cells ◽  
Growth Factors ◽  
Epithelial Cells ◽  
Embryonic Development ◽  
Amniotic Membrane ◽  
Biological Activities ◽  
Survival Rates ◽  
Blastocyst Stage ◽  
Oviduct Epithelial Cells

Summary Culture conditions have a profound effect on the quality of in vitro-produced embryos. Co-culturing embryos with somatic cells has some beneficial effects on embryonic development. Considering the ability of stem cells to secrete a broad range of growth factors with different biological activities, we hypothesized that bovine amniotic membrane stem cells (bAMSCs) might be superior to bovine oviduct epithelial cells (BOECs) in supporting embryonic development and enhancing their cryo-survival. Bovine abattoir-derived oocytes were matured and fertilized in vitro. The resultant presumptive zygotes were then cultured up to the blastocyst stage in the following groups: (i) co-culture with bAMSCs, (ii) co-culture with BOECs, and (iii) cell-free culture (Con). Embryos that reached the blastocyst stage were vitrified and warmed, and their post-warming re-expansion, survival and hatching rates were evaluated after 72 h culture. Results showed that the cleavage, blastocyst, and 2 h post-warming re-expansion rates of embryos did not differ between groups. However, their survival rates in BOEC and bAMSC groups were significantly higher compared with the control (72.7, 75.6 and 37.5%, respectively, P < 0.05). In conclusion, our results showed that the cryo-survivability of IVF-derived bovine embryos could be improved through co-culturing with bAMSCs. Moreover, considering the possibility to provide multiple passages from bAMSCs compared with BOECs, due to their stemness properties and their ability to produce growth factors, the use of bAMSCs is a good alternative to BOECs in embryo co-culture systems.

scholarly journals Mechanisms of castration resistant prostate cancer formation and progression through neuroendocrine differentiation

2021 ◽  
Keyword(s):  
Prostate Cancer ◽  
Smooth Muscle ◽  
Epithelial Cells ◽  
Neuroendocrine Differentiation ◽  
Underlying Mechanism ◽  
Neuroendocrine Cells ◽  
Basal Cells ◽  
Castration Resistant Prostate Cancer ◽  
Normal Prostate ◽  
Castration Resistant

Normal prostate tissues consist mainly of epithelial cells, including secretory epithelial cells, basal cells, and neuroendocrine cells, and of mesenchymal cells, including smooth muscle cells and fibroblasts. The mechanisms leading to castration resistant prostate cancer (CRPC) are complex and diverse, but most involve neuroendocrine differentiation. In fact, during the development of prostate cancer, some of the tumor cells transform into neuroendocrine-like cells. This transition is a main underlying mechanism of CRPC formation.

scholarly journals The Role of Androgen Receptor in Cross Talk Between Stromal Cells and Prostate Cancer Epithelial Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Qianyao Tang ◽  
Bo Cheng ◽  
Rongyang Dai ◽  
Ronghao Wang
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Tumor Microenvironment ◽  
Epithelial Cells ◽  
Cross Talk ◽  
Cell Invasion ◽  
Stromal Cells ◽  
Neuroendocrine Cells ◽  
Stromal Fibroblasts ◽  
Biological Regulation

Prostate cancer (PCa) lists as the second most lethal cancer for men in western countries, and androgen receptor (AR) plays a central role in its initiation and progression, which prompts the development of androgen deprivation therapy (ADT) as the standard treatment. Prostate tumor microenvironment, consisting of stromal cells and extracellular matrix (ECM), has dynamic interactions with PCa epithelial cells and affects their growth and invasiveness. Studies have shown that both genomic and non-genomic AR signaling pathways are involved in the biological regulation of PCa epithelial cells. In addition, AR signaling in prostate stroma is also involved in PCa carcinogenesis and progression. Loss of AR in PCa stroma is clinically observed as PCa progresses to advanced stage. Especially, downregulation of AR in stromal fibroblasts dysregulates the expression levels of ECM proteins, thus creating a suitable environment for PCa cells to metastasize. Importantly, ADT treatment enhances this reciprocal interaction and predisposes stromal cells to promote cell invasion of PCa cells. During this process, AR in PCa epithelium actively responds to various stimuli derived from the surrounding stromal cells and undergoes enhanced degradation while elevating the expression of certain genes such as MMP9 responsible for cell invasion. AR reduction in epithelial cells also accelerates these cells to differentiate into cancer stem-like cells and neuroendocrine cells, which are AR-negative PCa cells and inherently resistant to ADT treatments. Overall, understanding of the cross talk between tumor microenvironment and PCa at the molecular level may assist the development of novel therapeutic strategies against this disease. This review will provide a snapshot of AR’s action when the interaction of stromal cells and PCa cells occurs.

scholarly journals Reducing Selenoprotein F Promotes the Transformation of Immortalized Prostate Epithelial Cells

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1809-1809
Author(s):  
Lenny Hong ◽  
Mostafa Elhodaky ◽  
Shrinidhi Kadkol ◽  
Alan Diamond
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Tca Cycle ◽  
Soft Agar ◽  
Metabolic Shift ◽  
Normal Prostate ◽  
Funding Sources ◽  
Prostate Cells ◽  
Prostate Epithelial Cells

Abstract Objectives Selenoprotein F (SELENOF) levels are responsive to available dietary selenium and found in high levels in benign prostate cells. It is implicated in prostate cancer (PCa) mortality due to associations between polymorphisms in the corresponding gene and death from the disease. SELENOF levels are dramatically lower in prostate cancer compared to adjacent benign tissue. The objective of this study was to determine whether reducing SELENOF levels in human, non-transformed RWPE-1 prostate epithelial cells alters their phenotype to implicate SELENOF loss in PCa progression. Methods SELENOF levels were reduced in RWPE-1 cells that express high levels of SELENOF using a SELENOF shRNA construct. Proliferation was determined by quantifying DNA using fluorometric dsDNA quantitation. Growth in soft agar and cell mobility of cells in culture (wound healing assay) were imaged using an Evos FL microscope and quantified using Image J software. The oxygen consumption rate (OCR) was measured using a Seahorse XFe24 Analyzer. Results SELENOF levels were reduced in RWPE-1 and these cells exhibited decreased contact inhibition in culture (n = 3, P &lt; 0.001) when compared to controls. Normal prostate epithelial cells are atypical in that they rely on glycolysis for energy production, have a truncated TCA cycle, and a metabolic shift from glycolysis to oxidative phosphorylation (OXPHOS) occurs in PCa. Reducing SELENOF in RWPE-1 cells resulted in higher OCR compared to controls, indicating that SELENOF can impact the sources and pathways used in cellular energy metabolism. Conclusions Reduced SELENOF levels in RWPE-1 prostate cells resulted in properties consistent with a transformed phenotype and an increase in OCR, and indicating that the reduction in SELENOF may contribute a metabolic shift towards a PCa cancer-like metabolism. Together, these results indicate that SELENOF loss likely contributes to cancer progression. Funding Sources This work was supported by a grant from the Department of Defense to AMD and a Pre-Doctoral Education for Clinical and Translational Scientists Fellowship to LKH.

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