Prostate Cancer Stem Cells: Research Advances

Jaworska, Dagmara; Król, Wojciech; Szliszka, Ewelina

doi:10.3390/ijms161126036

Cited by 51 publications

(45 citation statements)

References 132 publications

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“…After initial responses, patients almost always acquire resistance to taxane drugs, likely in part because of CSCs [10, 43]. As compared to bulk tumor cells, CSCs are resistant to most chemotherapeutic agents so treatment with taxanes likely enriches for CSCs.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting G protein βγ signaling blocks prostate cancer progression and enhances the efficacy of paclitaxel

et al. 2017

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Aberrant activation of G protein-coupled receptors (GPCRs) is implicated in prostate cancer progression, but targeting them has been challenging because multiple GPCRs are involved in cancer progression. In this study, we tested the effect of blocking signaling via a hub through which multiple GPCRs converge — the G-protein Gβγ subunits. Inhibiting Gβγ signaling in several castration-resistant prostate cancer cell lines (i.e. PC3, DU145 and 22Rv1), impaired cell growth and migration in vitro, and halted tumor growth and metastasis in nude mice. The blockade of Gβγ signaling also diminished prostate cancer stem cell-like activities, by reducing tumorsphere formation in vitro and tumor formation in a limiting dilution assay in nude mice. Furthermore, Gβγ blockade enhanced the sensitivity of prostate cancer cells to paclitaxel treatment, both in vitro and in vivo. Together, our results identify a novel function of Gβγ in regulating prostate cancer stem-cell-like activities, and demonstrate that targeting Gβγ signaling is an effective approach in blocking prostate cancer progression and augmenting response to chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Inhibiting G protein βγ signaling blocks prostate cancer progression and enhances the efficacy of paclitaxel

et al. 2017

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“…ALCAM is considered as a stem cell marker in colorectal [28][29][30][31][32] prostate [33,34] and glioblastoma cancer [35]. Cancer stem cells are a small subset of cancer cells that have considerable ability in selfrenewal and differentiation [36][37][38][39][40][41][42][43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Cloning and Expression of C2 and V Domains of ALCAM Protein in E. coli BL21 (DE3)

Dana¹,

Mazraeh²,

Chalbatani³

et al. 2017

Clin Microbiol

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Introduction: ALCAM as a glycoprotein is a member of the immunoglobulin family and plays an important role in cell growth, survival and motility. This protein also contributes to the development of tumour invasion in colorectal and breast cancers and is typically considered as a cancer stem cell marker. ALCAM as a cell-surface antigen, with high expression in some cancers as colorectal and breast, has the potential to diagnose and treat these cancers.

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“…Because tumor-initiating/cancer stem cells have been suspected to play a role in androgen ablation and chemotherapy resistance as well as post-treatment prostate cancer relapse [27], we also analyzed whether the enhanced treatment recovery displayed by TROP2 high cells was associated with high self-renewal ability. However we did not find any difference between the self-renewal ability of TROP2 high , TROP2 low and ungated cells from the LNCaP and 22Rv1 cell lines, suggesting that the androgen-sensitive cells that emerge post-treatment may not necessarily bear intrinsic cancer stem cell characteristics.…”

Section: Discussionmentioning

confidence: 99%

High expression of TROP2 characterizes different cell subpopulations in androgen-sensitive and androgen-independent prostate cancer cells

et al. 2016

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Progression of castration-resistant tumors is frequent in prostate cancer. Current systemic treatments for castration-resistant prostate cancer only produce modest increases in survival time and self-renewing Tumor-Initiating Cells (TICs) are suspected to play an important role in resistance to these treatments. However it remains unclear whether the same TICs display both chemo-resistance and self-renewing abilities throughout progression from early stage lesions to late, castration resistant tumors. Here, we found that treatment of mice bearing LNCaP-derived xenograft tumors with cytotoxic (docetaxel) and anti-androgen (flutamide) compounds enriched for cells that express TROP2, a putative TIC marker. Consistent with a tumor-initiating role, TROP2high cells from androgen-sensitive prostate cancer cell lines displayed an enhanced ability to re-grow in culture following treatment with taxane-based chemotherapy with or without androgen blockade. TROP2 down-regulation in these cells reduced their ability to recur after treatment with docetaxel, in the presence or absence of flutamide. Accordingly, in silico analysis of published clinical data revealed that prostate cancer patients with poor prognosis exhibit significantly elevated TROP2 expression level compared to low-risk patients, particularly in the case of patients diagnosed with early stage tumors. In contrast, in androgen-independent prostate cancer cell lines, TROP2high cells did not exhibit a differential treatment response but were characterized by their high self-renewal ability. Based on these findings we propose that high TROP2 expression identifies distinct cell sub-populations in androgen-sensitive and androgen-independent prostate tumors and that it may be a predictive biomarker for prostate cancer treatment response in androgen-sensitive tumors.

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Prostate Cancer Stem Cells: Research Advances

Cited by 51 publications

References 132 publications

Inhibiting G protein βγ signaling blocks prostate cancer progression and enhances the efficacy of paclitaxel

Inhibiting G protein βγ signaling blocks prostate cancer progression and enhances the efficacy of paclitaxel

Cloning and Expression of C2 and V Domains of ALCAM Protein in E. coli BL21 (DE3)

High expression of TROP2 characterizes different cell subpopulations in androgen-sensitive and androgen-independent prostate cancer cells

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