Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming

Raquel Buj; Chi Wei Chen; Erika S. Dahl; Kelly E. Leon; Rostislav Kuskovsky; Natella Maglakelidze; Maithili Navaratnarajah; Gao Zhang; Mary T. Doan; Helen Jiang; Michael Zaleski; Lydia Kutzler; Holly Lacko; Yiling Lu; Gordon B. Mills; Raghavendra Gowda; Gavin P. Robertson; Joshua I. Warrick; Meenhard Herlyn; Yuka Imamura; Scot R. Kimball; David J. DeGraff; Nathaniel W. Snyder; Katherine M. Aird

doi:10.1016/j.celrep.2019.07.084

Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming

Raquel Buj
, Chi Wei Chen
, Erika S. Dahl
, Kelly E. Leon
, Rostislav Kuskovsky
, Natella Maglakelidze
, Maithili Navaratnarajah
, Gao Zhang
, Mary T. Doan
, Helen Jiang
, Michael Zaleski
, Lydia Kutzler
, Holly Lacko
, Yiling Lu
, Gordon B. Mills
, Raghavendra Gowda
, Gavin P. Robertson
, Joshua I. Warrick
, Meenhard Herlyn
, Yuka Imamura

Scot R. Kimball, David J. DeGraff, Nathaniel W. Snyder, Katherine M. Aird

Research output: Contribution to journal › Article › peer-review

49 Scopus citations

Abstract

Senescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.

Original language	English (US)
Pages (from-to)	1971-1980.e8
Journal	Cell Reports
Volume	28
Issue number	8
DOIs	https://doi.org/10.1016/j.celrep.2019.07.084
State	Published - Aug 20 2019

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

General Biochemistry, Genetics and Molecular Biology

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10.1016/j.celrep.2019.07.084

Cite this

Buj, R., Chen, C. W., Dahl, E. S., Leon, K. E., Kuskovsky, R., Maglakelidze, N., Navaratnarajah, M., Zhang, G., Doan, M. T., Jiang, H., Zaleski, M., Kutzler, L., Lacko, H., Lu, Y., Mills, G. B., Gowda, R., Robertson, G. P., Warrick, J. I., Herlyn, M., ... Aird, K. M. (2019). Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming. Cell Reports, 28(8), 1971-1980.e8. https://doi.org/10.1016/j.celrep.2019.07.084

@article{8517143331184256a9707102008e603f,

title = "Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming",

abstract = "Senescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.",

author = "Raquel Buj and Chen, \{Chi Wei\} and Dahl, \{Erika S.\} and Leon, \{Kelly E.\} and Rostislav Kuskovsky and Natella Maglakelidze and Maithili Navaratnarajah and Gao Zhang and Doan, \{Mary T.\} and Helen Jiang and Michael Zaleski and Lydia Kutzler and Holly Lacko and Yiling Lu and Mills, \{Gordon B.\} and Raghavendra Gowda and Robertson, \{Gavin P.\} and Warrick, \{Joshua I.\} and Meenhard Herlyn and Yuka Imamura and Kimball, \{Scot R.\} and DeGraff, \{David J.\} and Snyder, \{Nathaniel W.\} and Aird, \{Katherine M.\}",

note = "Publisher Copyright: {\textcopyright} 2019 The Author(s)",

year = "2019",

month = aug,

day = "20",

doi = "10.1016/j.celrep.2019.07.084",

language = "English (US)",

volume = "28",

pages = "1971--1980.e8",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Elsevier BV",

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Buj, R, Chen, CW, Dahl, ES, Leon, KE, Kuskovsky, R, Maglakelidze, N, Navaratnarajah, M, Zhang, G, Doan, MT, Jiang, H, Zaleski, M, Kutzler, L, Lacko, H, Lu, Y, Mills, GB, Gowda, R, Robertson, GP, Warrick, JI, Herlyn, M, Imamura, Y, Kimball, SR, DeGraff, DJ, Snyder, NW & Aird, KM 2019, 'Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming', Cell Reports, vol. 28, no. 8, pp. 1971-1980.e8. https://doi.org/10.1016/j.celrep.2019.07.084

TY - JOUR

T1 - Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming

AU - Buj, Raquel

AU - Chen, Chi Wei

AU - Dahl, Erika S.

AU - Leon, Kelly E.

AU - Kuskovsky, Rostislav

AU - Maglakelidze, Natella

AU - Navaratnarajah, Maithili

AU - Zhang, Gao

AU - Doan, Mary T.

AU - Jiang, Helen

AU - Zaleski, Michael

AU - Kutzler, Lydia

AU - Lacko, Holly

AU - Lu, Yiling

AU - Mills, Gordon B.

AU - Gowda, Raghavendra

AU - Robertson, Gavin P.

AU - Warrick, Joshua I.

AU - Herlyn, Meenhard

AU - Imamura, Yuka

AU - Kimball, Scot R.

AU - DeGraff, David J.

AU - Snyder, Nathaniel W.

AU - Aird, Katherine M.

PY - 2019/8/20

Y1 - 2019/8/20

N2 - Senescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.

AB - Senescence bypass through p16 loss predisposes to transformation and tumorigenesis. Buj et al. found that the loss of p16 upregulates nucleotide metabolism through increased mTORC1-mediated translation of RPIA to bypass senescence in an RB-independent manner. Thus, the mTORC1-RPIA axis is a metabolic vulnerability for p16-null cancers.

UR - https://www.scopus.com/pages/publications/85070554726

UR - https://www.scopus.com/pages/publications/85070554726#tab=citedBy

U2 - 10.1016/j.celrep.2019.07.084

DO - 10.1016/j.celrep.2019.07.084

M3 - Article

C2 - 31433975

AN - SCOPUS:85070554726

SN - 2211-1247

VL - 28

SP - 1971-1980.e8

JO - Cell Reports

JF - Cell Reports

IS - 8

ER -

Suppression of p16 Induces mTORC1-Mediated Nucleotide Metabolic Reprogramming

Abstract

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