Erratum: Stearoyl-CoA-desaturase 1 regulates lung cancer stemness via stabilization and nuclear localization of YAP/TAZ

Noto, Alessia; Vitis, Claudia De; Pisanu, Maria Elena; Roscilli, G; Ricci, G; Catizone, A; Sorrentino, G; Chianese, G; Taglialatela‐Scafati, Orazio; Trisciuoglio, D; Bufalo, D Del; Martile, M Di; Napoli, A Di; Ruco, L; Costantini, Susan; Budillon, Alfredo; Melino, Gerry; Sal, G Del; Ciliberto, Gennaro; Mancini, Rita

doi:10.1038/onc.2017.212

Cited by 30 publications

(17 citation statements)

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“…Specifically, stearoyl coenzyme A desaturase 1 (SCD1), an enzyme involved in the conversion of saturated into unsaturated fatty acids, mediates the release of YAP/TAZ from the β-catenin destruction complex. The data from lung adenocarcinoma samples revealed that SCD1 co-expresses with nuclear YAP/TAZ suggesting a clear correlation between expression and activity of these genes, and thus with the desaturation index of the cell 85 – 87 . Although this link between YAP/TAZ-dependent unsaturation index of the cell and ferroptosis sensitivity has still not been investigated, studies showing that E-cadherin-dependent YAP/TAZ nuclear extrusion decreases the accumulation of lipid peroxides 69 – 71 , 73 suggest that this is something that deserves further and more in depth analysis.…”

Section: Cell-to-cell Contactmentioning

confidence: 99%

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

et al. 2020

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Contextualisation of the new type of cell death called “ferroptosis” opened a completely new avenue for the development of anti-cancer therapies. Cumulative fundamental research dating back to the mid-20th century, crowned by the extraordinary work of the group led by Dr. Stockwell from Columbia University in 2012, finally got its candidature to be applied in the clinical settings. Although the potential for clinical importance is undoubtedly growing every day, as showed by the increasing number of papers dealing with ferroptosis and its applications, long experience of cancer research and treatment taught us that caution is still necessary. The plasticity of the tumour cells, particularly acute, along with its involvement in the resistance mechanisms, that have been seen, to greater or lesser extent, for almost all currently used therapies, represents the biggest fascinations in biomedical research field and also the biggest challenge to achieving cures in cancer patients. Accordingly, the main features of fundamental research have to be vigilance and anticipation. In this review, we tried to summarize the literature data, accumulated in the past couple of years, which point out the pitfalls in which “ferroptosis inducers” can fall if used prematurely in the clinical settings, but at the same time can provide a great advantage in the exhausting battle with cancer resistance. This is the first comprehensive review focusing on the effects of the cell-to-cell contact/interplay in the development of resistance to ferroptosis, while the contribution of cell-born factors has been summarized previously so here we just listed them.

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Section: Cell-to-cell Contactmentioning

confidence: 99%

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

et al. 2020

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“…This latter induces the activation of Wnt/ β -catenin signaling, and this axis, in turn, regulates the nuclear localization (activation) of YAP/TAZ, effectors involved in the Hippo pathway ( Figure 5 ). Such a correlation was also associated with poor prognosis in test samples of human lung adenocarcinoma [ 186 ]. Actually, YAP/TAZ are inducers of stem cell proliferation and survival and, in several cancers, their expression sustains tumor growth and invasion [ 187 , 188 ].…”

Section: Lipid Droplets In Cancer Stem Cellsmentioning

confidence: 99%

An Overview of Lipid Droplets in Cancer and Cancer Stem Cells

Tirinato

Pagliari

Limongi

et al. 2017

Stem Cells International

182

141

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For decades, lipid droplets have been considered as the main cellular organelles involved in the fat storage, because of their lipid composition. However, in recent years, some new and totally unexpected roles have been discovered for them: (i) they are active sites for synthesis and storage of inflammatory mediators, and (ii) they are key players in cancer cells and tissues, especially in cancer stem cells. In this review, we summarize the main concepts related to the lipid droplet structure and function and their involvement in inflammatory and cancer processes.

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“…Next, in order to further confirm our observations, we evaluated the ability of VPA/SIM to affect YAP nuclear localization and activation, in 22Rv1 transiently transfected with either wild-type YAP (wt-YAP) or with the constitutively active mutated form YAP5SA [ 35 ] (Fig. 4 a).…”

Section: Resultsmentioning

confidence: 94%

“…Adherent 22Rv1 and 22Rv1 R_39 cells were transfected with YAP wild-type and YAP5SA plasmids as previously described by Noto A. et al [ 35 ] using Lipofectamine 2000 Reagents (Invitrogen, Carlsbad, CA, USA), according to the manufacturer’s recommendation. After 48 h from transfection, cells were collected and western blotting, real-time PCR and immunofluorescent experiments were performed as described before.…”

Section: Methodsmentioning

confidence: 99%

Synergistic antitumor interaction of valproic acid and simvastatin sensitizes prostate cancer to docetaxel by targeting CSCs compartment via YAP inhibition

Iannelli

Roca

Lombardi

et al. 2020

J Exp Clin Cancer Res

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Background Despite the introduction of several novel therapeutic approaches that improved survival, metastatic castration-resistant prostate cancer (mCRPC) remains an incurable disease. Herein we report the synergistic antitumor interaction between two well-known drugs used for years in clinical practice, the antiepileptic agent with histone deacetylase inhibitory activity valproic acid and the cholesterol lowering agent simvastatin, in mCRPC models. Methods Synergistic anti-tumor effect was assessed on PC3, 22Rv1, DU145, DU145R80, LNCaP prostate cancer cell lines and EPN normal prostate epithelial cells, by calculating combination index (CI), caspase 3/7 activation and colony formation assays as well as on tumor spheroids and microtissues scored with luminescence 3D-cell viability assay. Cancer stem cells (CSC) compartment was studied evaluating specific markers by RT-PCR, western blotting and flow cytometry as well as by limiting dilution assay. Cholesterol content was evaluated by 1H-NMR. Overexpression of wild-type YAP and constitutively active YAP5SA were obtained by lipofectamine-based transfection and evaluated by immunofluorescence, western blotting and RT-PCR. 22Rv1 R_39 docetaxel resistant cells were selected by stepwise exposure to increasing drug concentrations. In vivo experiments were performed on xenograft models of DU145R80, 22Rv1 parental and docetaxel resistant cells, in athymic mice. Results We demonstrated the capacity of the combined approach to target CSC compartment by a novel molecular mechanism based on the inhibition of YAP oncogene via concurrent modulation of mevalonate pathway and AMPK. Because both CSCs and YAP activation have been associated with chemo-resistance, we tested if the combined approach can potentiate docetaxel, a standard of care in mCRCP treatment. Indeed, we demonstrated, both in vitro and in vivo models, the ability of valproic acid/simvastatin combination to sensitize mCRPC cells to docetaxel and to revert docetaxel-resistance, by mevalonate pathway/YAP axis modulation. Conclusion Overall, mCRPC progression and therapeutic resistance driven by CSCs via YAP, can be tackled by the combined repurposing of two generic and safe drugs, an approach that warrants further clinical development in this disease.

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Erratum: Stearoyl-CoA-desaturase 1 regulates lung cancer stemness via stabilization and nuclear localization of YAP/TAZ

Cited by 30 publications

References 0 publications

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis

An Overview of Lipid Droplets in Cancer and Cancer Stem Cells

Synergistic antitumor interaction of valproic acid and simvastatin sensitizes prostate cancer to docetaxel by targeting CSCs compartment via YAP inhibition

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