Prostate Cancer Stem Cells and Nanotechnology: A Focus on Wnt Signaling

Qin, Wei; Zheng, Yu; Qian, Bin‐Zhi; Zhao, Meng

doi:10.3389/fphar.2017.00153

Cited by 26 publications

(25 citation statements)

References 162 publications

(186 reference statements)

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“…Androgen receptors activate multiple extranuclear signaling pathways involved in prostate cancer progression, including WNT/β-catenin pathway [reviewed by (41)]. In the nucleus, β-catenin requires interaction with TCF/LEF transcription factors and other co-activators, such as CBP or p300, and activates the transcription of the target genes involved in cell proliferation, migration and invasion of different cancer cells [reviewed by (41)(42)(43)], including prostate cancer (25,32,44). After androgen-deprivation, the interaction of β-catenin with TCF4 is enhanced and partly involved with androgenindependent growth of prostate cancer cells [(45); reviewed by (46)].…”

Section: Discussionmentioning

confidence: 99%

Estrogen Receptors Promote Migration, Invasion and Colony Formation of the Androgen-Independent Prostate Cancer Cells PC-3 Through β-Catenin Pathway

2020

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Prostate cancer is initially dependent on the androgen, gradually evolves into an androgen-independent form of the disease, also known as castration-resistant prostate cancer (CRPC). At this stage, current therapies scantily improve survival of the patient. Androgens and estrogens are involved in normal prostate and prostate cancer development. The mechanisms by which estrogens/estrogen receptors (ERs) induce prostate cancer and promote prostate cancer progression have not yet been fully identified. Our laboratory has shown that androgen-independent prostate cancer cells PC-3 express both ERα and ERβ. The activation of ERβ increases the expression of β-catenin and proliferation of PC-3 cells. We now report that the activation of ERβ promotes the increase of migration, invasion and anchorage-independent growth of PC-3 cells. Furthermore, the activation of ERα also plays a role in invasion and anchorageindependent growth of PC-3 cells. These effects are blocked by pretreatment with PKF 118-310, compound that disrupts the complex β-catenin/TCF/LEF, suggesting that ERs/β-catenin are involved in all cellular characteristics of tumor development in vitro. Furthermore, PKF 118-310 also inhibited the upregulation of vascular endothelial growth factor A (VEGFA) induced by activation of ERs. VEGF also is involved on invasion of PC-3 cells. In conclusion, this study provides novel insights into the signatures and molecular mechanisms of ERβ in androgen-independent prostate cancer cells PC-3. ERα also plays a role on invasion and colony formation of PC-3 cells.

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Section: Discussionmentioning

confidence: 99%

Estrogen Receptors Promote Migration, Invasion and Colony Formation of the Androgen-Independent Prostate Cancer Cells PC-3 Through β-Catenin Pathway

2020

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“…CRPC likely develops from the prostate cancer stem cells (PCSCs), a subset of cells within the tumor which regulate initiation, but importantly also recurrence [145]. PCSCs were successfully isolated from patient tissue samples on the basis of their α 2 β 1 hi CD133 + CD44 + phenotype [146,147,148,149]. PCSCs have a high proliferation rate and increased ability of colony formation in 3D cultures, as well as an ability to form prostate-like structures when injected in immunocompromised mice compared to CD44 − and CD133 − cells [146,147,148,149].…”

Section: The Hippo Pathway’s Role In Prostate Cancer Stem Cellsmentioning

confidence: 99%

The Hippo Pathway in Prostate Cancer

Salem

Hansen

2019

Cells

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Despite recent efforts, prostate cancer (PCa) remains one of the most common cancers in men. Currently, there is no effective treatment for castration-resistant prostate cancer (CRPC). There is, therefore, an urgent need to identify new therapeutic targets. The Hippo pathway and its downstream effectors—the transcriptional co-activators, Yes-associated protein (YAP) and its paralog, transcriptional co-activator with PDZ-binding motif (TAZ)—are foremost regulators of stem cells and cancer biology. Defective Hippo pathway signaling and YAP/TAZ hyperactivation are common across various cancers. Here, we draw on insights learned from other types of cancers and review the latest advances linking the Hippo pathway and YAP/TAZ to PCa onset and progression. We examine the regulatory interaction between Hippo-YAP/TAZ and the androgen receptor (AR), as main regulators of PCa development, and how uncontrolled expression of YAP/TAZ drives castration resistance by inducing cellular stemness. Finally, we survey the potential therapeutic targeting of the Hippo pathway and YAP/TAZ to overcome PCa.

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“…To this end several markers including CD44, ALDH1 and CD133 have been identified in different cancers. Novel strategies including the use of nanotechnology aim to detect, characterize and eliminate CSCs with enhanced efficacy than current methods [ 420 , 421 ]. Currently, several chemotherapeutic agents targeting CSCs are under investigation and some included in clinical trials.…”

Section: Discussionmentioning

confidence: 99%

Advances in Therapeutic Targeting of Cancer Stem Cells within the Tumor Microenvironment: An Updated Review

Dzobo

Senthebane

Ganz

et al. 2020

Cells

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Despite great strides being achieved in improving cancer patients’ outcomes through better therapies and combinatorial treatment, several hurdles still remain due to therapy resistance, cancer recurrence and metastasis. Drug resistance culminating in relapse continues to be associated with fatal disease. The cancer stem cell theory posits that tumors are driven by specialized cancer cells called cancer stem cells (CSCs). CSCs are a subpopulation of cancer cells known to be resistant to therapy and cause metastasis. Whilst the debate on whether CSCs are the origins of the primary tumor rages on, CSCs have been further characterized in many cancers with data illustrating that CSCs display great abilities to self-renew, resist therapies due to enhanced epithelial to mesenchymal (EMT) properties, enhanced expression of ATP-binding cassette (ABC) membrane transporters, activation of several survival signaling pathways and increased immune evasion as well as DNA repair mechanisms. CSCs also display great heterogeneity with the consequential lack of specific CSC markers presenting a great challenge to their targeting. In this updated review we revisit CSCs within the tumor microenvironment (TME) and present novel treatment strategies targeting CSCs. These promising strategies include targeting CSCs-specific properties using small molecule inhibitors, immunotherapy, microRNA mediated inhibitors, epigenetic methods as well as targeting CSC niche-microenvironmental factors and differentiation. Lastly, we present recent clinical trials undertaken to try to turn the tide against cancer by targeting CSC-associated drug resistance and metastasis.

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Prostate Cancer Stem Cells and Nanotechnology: A Focus on Wnt Signaling

Cited by 26 publications

References 162 publications

Estrogen Receptors Promote Migration, Invasion and Colony Formation of the Androgen-Independent Prostate Cancer Cells PC-3 Through β-Catenin Pathway

Estrogen Receptors Promote Migration, Invasion and Colony Formation of the Androgen-Independent Prostate Cancer Cells PC-3 Through β-Catenin Pathway

The Hippo Pathway in Prostate Cancer

Advances in Therapeutic Targeting of Cancer Stem Cells within the Tumor Microenvironment: An Updated Review

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