The mTOR Pathway in Pluripotent Stem Cells: Lessons for Understanding Cancer Cell Dormancy

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The mTOR Pathway in Pluripotent Stem Cells: Lessons for Understanding Cancer Cell Dormancy. / Alhasan, Bashar; Gordeev, Sergey; Князева, Александра Романовна ; Александрова, Ксения Владимировна; Margulis, Boris; Guzhova, Irina; Suvorova, Irina.

In: Membranes, Vol. 11, No. 11, 858, 07.11.2021.

Research output: Contribution to journal › Review article › peer-review

BibTeX

@article{34bcac763dd549b1b3a894199d9aeb21,

title = "The mTOR Pathway in Pluripotent Stem Cells: Lessons for Understanding Cancer Cell Dormancy",

abstract = "Currently, the success of targeted anticancer therapies largely depends on the correct understanding of the dormant state of cancer cells, since it is increasingly regarded to fuel tumor recurrence. The concept of cancer cell dormancy is often considered as an adaptive response of cancer cells to stress, and, therefore, is limited. It is possible that the cancer dormant state is not a privilege of cancer cells but the same reproductive survival strategy as diapause used by embryonic stem cells (ESCs). Recent advances reveal that high autophagy and mTOR pathway reduction are key mechanisms contributing to dormancy and diapause. ESCs, sharing their main features with cancer stem cells, have a delicate balance between the mTOR pathway and autophagy activity permissive for diapause induction. In this review, we discuss the functioning of the mTOR signaling and autophagy in ESCs in detail that allows us to deepen our understanding of the biology of cancer cell dormancy.",

keywords = "Autophagy, Cancer cell dormancy, Embryonic diapause, Embryonic stem cells, MTOR, Pluripotency, Pluripotent stem cells, LONG-TERM, cancer cell dormancy, autophagy, ACTIVATED PROTEIN-KINASE, pluripotent stem cells, embryonic stem cells, MOUSE, SELF-RENEWAL, embryonic diapause, pluripotency, AUTOPHAGY, BREAST-CANCER, GROWTH, mTOR, TUMOR DORMANCY, CARDIOMYOCYTE DIFFERENTIATION, SUPPRESSOR GENE ARHI",

author = "Bashar Alhasan and Sergey Gordeev and Князева, {Александра Романовна} and Александрова, {Ксения Владимировна} and Boris Margulis and Irina Guzhova and Irina Suvorova",

note = "Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2021",

month = nov,

day = "7",

doi = "10.3390/membranes11110858",

language = "English",

volume = "11",

journal = "Membranes",

issn = "2077-0375",

publisher = "MDPI AG",

number = "11",

}

RIS

TY - JOUR

T1 - The mTOR Pathway in Pluripotent Stem Cells: Lessons for Understanding Cancer Cell Dormancy

AU - Alhasan, Bashar

AU - Gordeev, Sergey

AU - Князева, Александра Романовна

AU - Александрова, Ксения Владимировна

AU - Margulis, Boris

AU - Guzhova, Irina

AU - Suvorova, Irina

PY - 2021/11/7

Y1 - 2021/11/7

N2 - Currently, the success of targeted anticancer therapies largely depends on the correct understanding of the dormant state of cancer cells, since it is increasingly regarded to fuel tumor recurrence. The concept of cancer cell dormancy is often considered as an adaptive response of cancer cells to stress, and, therefore, is limited. It is possible that the cancer dormant state is not a privilege of cancer cells but the same reproductive survival strategy as diapause used by embryonic stem cells (ESCs). Recent advances reveal that high autophagy and mTOR pathway reduction are key mechanisms contributing to dormancy and diapause. ESCs, sharing their main features with cancer stem cells, have a delicate balance between the mTOR pathway and autophagy activity permissive for diapause induction. In this review, we discuss the functioning of the mTOR signaling and autophagy in ESCs in detail that allows us to deepen our understanding of the biology of cancer cell dormancy.

AB - Currently, the success of targeted anticancer therapies largely depends on the correct understanding of the dormant state of cancer cells, since it is increasingly regarded to fuel tumor recurrence. The concept of cancer cell dormancy is often considered as an adaptive response of cancer cells to stress, and, therefore, is limited. It is possible that the cancer dormant state is not a privilege of cancer cells but the same reproductive survival strategy as diapause used by embryonic stem cells (ESCs). Recent advances reveal that high autophagy and mTOR pathway reduction are key mechanisms contributing to dormancy and diapause. ESCs, sharing their main features with cancer stem cells, have a delicate balance between the mTOR pathway and autophagy activity permissive for diapause induction. In this review, we discuss the functioning of the mTOR signaling and autophagy in ESCs in detail that allows us to deepen our understanding of the biology of cancer cell dormancy.

KW - Autophagy

KW - Cancer cell dormancy

KW - Embryonic diapause

KW - Embryonic stem cells

KW - MTOR

KW - Pluripotency

KW - Pluripotent stem cells

KW - LONG-TERM

KW - cancer cell dormancy

KW - autophagy

KW - ACTIVATED PROTEIN-KINASE

KW - pluripotent stem cells

KW - embryonic stem cells

KW - MOUSE

KW - SELF-RENEWAL

KW - embryonic diapause

KW - pluripotency

KW - AUTOPHAGY

KW - BREAST-CANCER

KW - GROWTH

KW - mTOR

KW - TUMOR DORMANCY

KW - CARDIOMYOCYTE DIFFERENTIATION

KW - SUPPRESSOR GENE ARHI

UR - http://www.scopus.com/inward/record.url?scp=85119625385&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/8012816c-ce9d-3ba7-abce-22aef69ab2f6/

U2 - 10.3390/membranes11110858

DO - 10.3390/membranes11110858

M3 - Review article

C2 - 34832087

VL - 11

JO - Membranes

JF - Membranes

SN - 2077-0375

IS - 11

M1 - 858

ER -

ID: 88538457