New insights into prostate cancer stem cells

Chen, Xin; Rycaj, Kiera; Liu, Xin; Tang, Dean G.

doi:10.4161/cc.23721

Cited by 67 publications

(73 citation statements)

References 100 publications

(119 reference statements)

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“…There is ongoing debate concerning the cell of origin for prostate cancer, but most evidence would suggest that it can arise from prostate stem cells or cells with stem-like features. It is very possible that cancers can arise from several different incompletely differentiated cells (Wang et al 2009b, Goldstein et al 2010, Taylor et al 2010, Chen et al 2013. For the sake of this discussion, these cells will be collectively called stem cells.…”

Section: Ar In Prostate Cancer Initiationmentioning

confidence: 99%

Androgens and androgen receptor signaling in prostate tumorigenesis

Zhou¹,

Bolton²,

Jones³

2014

Journal of Molecular Endocrinology

165

112

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Androgens and androgen receptor (AR) signaling are necessary for prostate development and homeostasis. AR signaling also drives the growth of nearly all prostate cancer cells. The role of androgens and AR signaling has been well characterized in metastatic prostate cancer, where it has been shown that prostate cancer cells are exquisitely adept at maintaining functional AR signaling to drive cancer growth. As androgens and AR signaling are so intimately involved in prostate development and the proliferation of advanced prostate cancer, it stands to reason that androgens and AR are also involved in prostate cancer initiation and the early stages of cancer growth, yet little is known of this process. In this review, we summarize the current state of knowledge concerning the role of androgens and AR signaling in prostate tissue, from development to metastatic, castration-resistant prostate cancer, and use that information to suggest potential roles for androgens and AR in prostate cancer initiation.

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Section: Ar In Prostate Cancer Initiationmentioning

confidence: 99%

Androgens and androgen receptor signaling in prostate tumorigenesis

Zhou¹,

Bolton²,

Jones³

2014

Journal of Molecular Endocrinology

165

112

View full text Add to dashboard Cite

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“…This concept was first demonstrated in leukemia and increasing evidence supports this model in various types of solid tumors including cervical cancer (19)(20)(21)(22)(23)(24). CSCs are thought to be involved in tumor recurrence and metastasis; failure to treat CSCs by surgery or chemotherapy would result in relapse (17).…”

Section: Introductionmentioning

confidence: 99%

Decreased expression of the plasminogen activator inhibitor type 1 is involved in degradation of extracellular matrix surrounding cervical cancer stem cells

Sato

Kawana

Adachi

et al. 2015

International Journal of Oncology

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Abstract. The plasminogen activator (PA) system consists of plasminogen activator inhibitor type 1 (PAI-1), urokinase-type plasminogen activator and its receptor (uPA and uPAR). PAI-1 inhibits the activation of uPA (which converts plasminogen to plasmin), and is involved in cancer invasion and metastasis, by remodeling the extracellular matrix (ECM) through regulating plasmin. Cancer stem cells (CSCs) are a small subset of cells within tumors, and are thought to be involved in tumor recurrence and metastasis. Considering these facts, we investigated the relationship between PAI-1 and cervical CSCs. We used ALDH1 as a marker of cervical CSCs. First, we demonstrated that culturing ALDH1-high cells and ALDH-low cells on collagen IV-coted plates increased their expression of active PAI-1 (ELISA), and these increases were suggested to be at mRNA expression levels (RT-qPCR). Secondly, we demonstrated PAI-1 was indeed involved in the ECM maintenance. With gelatin zymography assays, we found that ALDH1-high cells and ALDH-low cells expressed pro-matrix metalloproteinase-2 (pro-MMP-2) irrespective of their coatings. With gelatinase/collagenase assay kit, we confirmed that collagenase activity was increased when ALDH1-low cells were exposed to TM5275, a small molecule inhibitor of PAI-1. Putting the data together, we hypothesized that cancer cells adhered to basal membrane secrete abundant PAI-1, on the other hand, cancer cells (especially CSCs rather than non-CSCs) distant from basal membrane secrete less PAI-1, which makes the ECM surrounding CSCs more susceptible to degradation. Our study could be an explanation of conflicting reports, where some researchers found negative impacts of PAI-1 expression on clinical outcomes and others not, by considering the concept of CSCs.

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“…[92][93][94] However, rigorous studies are required to delineate the exact TIC markers that will differentiate this subpopulation for specific genomic studies as this relates to individualized prognosis. 95,96 Finally, subtumoural heterogeneity in cancer metabolism (e.g. both acute and chronic hypoxia co-exist within a tumour and lead to significant gradients of oxygen consumption) could also confound quantitation and summary statistics for assaying the fraction of tumour hypoxia from one patient to another.…”

Section: Hypoxia and Genomic Instability In Prostate Cancer: A Novel mentioning

confidence: 99%

An arranged marriage for precision medicine: hypoxia and genomic assays in localized prostate cancer radiotherapy

Bristow

Berlin²,

Pra

2014

BJR

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Prostate cancer (CaP) is the most commonly diagnosed malignancy in males in the Western world with one in six males diagnosed in their lifetime. Current clinical prognostication groupings use pathologic Gleason score, pre-treatment prostatic-specific antigen and Union for International Cancer Control-TNM staging to place patients with localized CaP into low-, intermediate-and high-risk categories. These categories represent an increasing risk of biochemical failure and CaP-specific mortality rates, they also reflect the need for increasing treatment intensity and justification for increased side effects. In this article, we point out that 30-50% of patients will still fail image-guided radiotherapy or surgery despite the judicious use of clinical risk categories owing to interpatient heterogeneity in treatment response. To improve treatment individualization, better predictors of prognosis and radiotherapy treatment response are needed to triage patients to bespoke and intensified CaP treatment protocols. These should include the use of pre-treatment genomic tests based on DNA or RNA indices and/or assays that reflect cancer metabolism, such as hypoxia assays, to define patient-specific CaP progression and aggression. More importantly, it is argued that these novel prognostic assays could be even more useful if combined together to drive forward precision cancer medicine for localized CaP.

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New insights into prostate cancer stem cells

Cited by 67 publications

References 100 publications

Androgens and androgen receptor signaling in prostate tumorigenesis

Androgens and androgen receptor signaling in prostate tumorigenesis

Decreased expression of the plasminogen activator inhibitor type 1 is involved in degradation of extracellular matrix surrounding cervical cancer stem cells

An arranged marriage for precision medicine: hypoxia and genomic assays in localized prostate cancer radiotherapy

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