<scp>CRM</scp>1 and chromosomal passenger complex component survivin are essential to normal mitosis progress and to preserve keratinocytes from mitotic abnormalities

Labarrade, F.; Botto, J.; Domloge, N.

doi:10.1111/ics.12311

Cited by 3 publications

(4 citation statements)

References 29 publications

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“…The involvement of hematopoietic adipocyte-derived stem cells (ASCs) in apoptotic resistance displayed by adipocyte tissue in obese subjects was correlated to upregulated survivin expression [40]. Keratinocyte Stem Cells (KSCs) show high expression of survivin, that plays a prominent role in preventing abnormal mitosis in these cells [41,42]. The suitability of the IAP as a marker for KSCs, which helps in maintaining skin homeostasis has been explored [43].…”

Section: Survivin In Stem Cellsmentioning

confidence: 99%

Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics

Warrier

Agarwal

Kumar

2020

Stem Cell Rev and Rep

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Survivin is one of the rare proteins that is differentially expressed in normal and cancer cells and is directly or indirectly involved in numerous pathways required for tumor maintenance. It is expressed in almost all cancers and its expression has been detected at early stages of cancer. These traits make survivin an exceptionally attractive target for cancer therapeutics. Even with these promising features to be an oncotherapeutic target, there has been limited success in the clinical trials targeting survivin. Only recently it has emerged that survivin was not being specifically targeted which could have resulted in the negative clinical outcome. Also, focus of research has now shifted from survivin expression in the overall heterogeneous tumor cell populations to survivin expression in cancer stem cells as these cells have proved to be the major drivers of tumors. Therefore, in this review we have analyzed the expression of survivin in normal and cancer cells with a particular focus on its expression in cancer stem cell compartment. We have discussed the major signaling pathways involved in regulation of survivin. We have explored the current development status of various types of interventions for inhibition of survivin. Furthermore, we have discussed the challenges involving the development of potent and specific survivin inhibitors for cancer therapeutics. Finally we have given insights for some of the promising future anticancer treatments.

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Section: Survivin In Stem Cellsmentioning

confidence: 99%

Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics

Warrier

Agarwal

Kumar

2020

Stem Cell Rev and Rep

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“…Recruitment of XPO1 to these sites is via phosphorylation by the CDK1/Cyclin B complex at the serine 391 site of XPO1, which is a different site than where it binds to various cargo NES [ 42 , 43 ]. One cargo, Survivin, which is upregulated during cellular development and is a member of the inhibitor of apoptosis family, complexes with XPO1 to facilitate normal cellular division through assembly of the chromosome passenger complex during mitosis [ 44 , 45 , 46 ]. Increased expression of Survivin is also associated with cancer cell survival; specifically, cytoplasmic Survivin is more abundant when XPO1 is overexpressed and promotes chemoresistance through inhibition of apoptosis [ 47 , 48 , 49 , 50 , 51 ].…”

Section: Xpo1 Biological Function and Relevancementioning

confidence: 99%

Therapeutic Targeting of Exportin-1 in Childhood Cancer

Galinski

Alexander

Mitchell

et al. 2021

Cancers

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Overexpression of Exportin-1 (XPO1), a key regulator of nuclear-to-cytoplasmic transport, is associated with inferior patient outcomes across a range of adult malignancies. Targeting XPO1 with selinexor has demonstrated promising results in clinical trials, leading to FDA approval of its use for multiple relapsed/refractory cancers. However, XPO1 biology and selinexor sensitivity in childhood cancer is only recently being explored. In this review, we will focus on the differential biology of childhood and adult cancers as it relates to XPO1 and key cargo proteins. We will further explore the current state of pre-clinical and clinical development of XPO1 inhibitors in childhood cancers. Finally, we will outline potentially promising future therapeutic strategies for, as well as potential challenges to, integrating XPO1 inhibition to improve outcomes for children with cancer.

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“…38,39 Survivin as member of the chromosomal passenger complex was characterized as playing a prominent role in preventing abnormal mitosis in keratinocyte. 40 In the epidermis, survivin was described as a marker of keratinocytes stem cell, 41 we hypothesized that miR-203 may play a critical role in survivin regulation, influencing re-epithelialization and epithelial stem cells features. Therefore, we designed the study to determine whether miR-203 could target survivin mRNA.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, survivin is the smallest member of inhibitor of apoptosis (IAP) protein family, linked as highly deregulated in cancer, 36,37 implicate in cell cycle progression when nuclear, and implicated in apoptosis inhibition when cytoplasmic 38,39 . Survivin as member of the chromosomal passenger complex was characterized as playing a prominent role in preventing abnormal mitosis in keratinocyte 40 . In the epidermis, survivin was described as a marker of keratinocytes stem cell, 41 we hypothesized that miR‐203 may play a critical role in survivin regulation, influencing re‐epithelialization and epithelial stem cells features.…”

Section: Introductionmentioning

confidence: 99%

miR‐203 represses keratinocyte stemness by targeting survivin

Labarrade

Botto

Imbert

2022

J of Cosmetic Dermatology

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Objective The epidermis possesses the capacity to replace dying cells and to heal wounds, thanks to resident stem cells, which have self‐renewal properties. In skin physiology, miRNAs have been shown to be involved in many processes, including skin and hair morphogenesis. Recently, differentiation of epidermal stem cells was shown to be promoted by the miR‐203. The miR‐203 is upregulated during epidermal differentiation and is of interest because of significant targets. Methods By utilizing a bioinformatic tool, we identified a target site for miR‐203 in the survivin mRNA. Silencing miR‐203 was managed with the use of antagomir; the silencing of survivin was performed with a siRNA. Survivin expression was determined by qPCR or immunofluorescence in cultured cells, and by immunohistochemistry in skin sections. Involucrin expression was used as marker of keratinocyte differentiation. A rice extract with previously demonstrated anti‐aging properties was evaluated on miR‐203 modulation. Results In this study, we identified a miR‐203/survivin axis, important for epidermal homeostasis. We report that differentiation of keratinocyte is dependent on the level of miR‐203 expression and that inhibition of miR‐203 can increase the expression of survivin, an epidermal marker of stemness. Conclusion In summary, our findings suggest that miR‐203 target 3′UTR region of survivin mRNA and directly represses survivin expression in the epidermis. The rice extract was identified as modulator of miR‐203 and pointed out as a promising microRNA‐based strategy in treating skin changes occurring with aging.

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CRM1 and chromosomal passenger complex component survivin are essential to normal mitosis progress and to preserve keratinocytes from mitotic abnormalities

Cited by 3 publications

References 29 publications

Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics

Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics

Therapeutic Targeting of Exportin-1 in Childhood Cancer

miR‐203 represses keratinocyte stemness by targeting survivin

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