Literature DB >> 29620049

Oncogene-induced senescence: a double edged sword in cancer.

Xue-Ling Liu1, Jian Ding2, Ling-Hua Meng3.   

Abstract

Oncogene-induced cellular senescence (OIS) is a complex program that is triggered in response to aberrant activation of oncogenic signaling. Initially, OIS was thought to be a barrier to malignant transformation because of its suppression on cell proliferation. Later studies showed that senescence induced by oncogenes can also promote the initiation and development of cancer. The opposing effects of OIS occur through different combinations of downstream effectors as well as the interplay of senescent cells and the microenvironment, such as senescence-associated inflammation. Here, we review the common features and molecular mechanisms underlying OIS and the interaction between senescent cells and the microenvironment. We propose that targeting senescent cells may have a beneficial therapeutic effect during the treatment of cancer.

Entities:  

Keywords:  SASP; cancer therapy; cellular senescence; oncogene; tumor microenvironment

Mesh:

Year:  2018        PMID: 29620049      PMCID: PMC6289471          DOI: 10.1038/aps.2017.198

Source DB:  PubMed          Journal:  Acta Pharmacol Sin        ISSN: 1671-4083            Impact factor:   6.150


  58 in total

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2.  Chromatin remodeling underlies the senescence-associated secretory phenotype of tumor stromal fibroblasts that supports cancer progression.

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Journal:  Cancer Res       Date:  2012-03-15       Impact factor: 12.701

Review 3.  Oncogenic functions of tumour suppressor p21(Waf1/Cip1/Sdi1): association with cell senescence and tumour-promoting activities of stromal fibroblasts.

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Journal:  N Engl J Med       Date:  2006-06-15       Impact factor: 91.245

5.  Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

Authors:  M Serrano; A W Lin; M E McCurrach; D Beach; S W Lowe
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Review 7.  Autophagy and aging.

Authors:  David C Rubinsztein; Guillermo Mariño; Guido Kroemer
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Review 8.  Inside and out: the activities of senescence in cancer.

Authors:  Pedro A Pérez-Mancera; Andrew R J Young; Masashi Narita
Journal:  Nat Rev Cancer       Date:  2014-07-17       Impact factor: 60.716

9.  Identification of senescent cell surface targetable protein DPP4.

Authors:  Kyoung Mi Kim; Ji Heon Noh; Monica Bodogai; Jennifer L Martindale; Xiaoling Yang; Fred E Indig; Sandip K Basu; Kei Ohnuma; Chikao Morimoto; Peter F Johnson; Arya Biragyn; Kotb Abdelmohsen; Myriam Gorospe
Journal:  Genes Dev       Date:  2017-09-06       Impact factor: 11.361

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Journal:  Nat Cell Biol       Date:  2013-06-16       Impact factor: 28.824

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  31 in total

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Authors:  Akshaya Chandrasekaran; May Y Lee; Xuexin Zhang; Shaheen Hasan; Habben Desta; Scott A Tenenbaum; J Andrés Melendez
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2.  GREB1 regulates PI3K/Akt signaling to control hormone-sensitive breast cancer proliferation.

Authors:  Corinne N Haines; Hope D Klingensmith; Makanko Komara; Craig J Burd
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3.  Chronic WNT/β-catenin signaling induces cellular senescence in lung epithelial cells.

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Review 4.  Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence.

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Review 5.  The Bone Marrow Niche in B-Cell Acute Lymphoblastic Leukemia: The Role of Microenvironment from Pre-Leukemia to Overt Leukemia.

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6.  Overexpression of oncogenic H-Ras in hTERT-immortalized and SV40-transformed human cells targets replicative and specialized DNA polymerases for depletion.

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Journal:  PLoS One       Date:  2021-05-07       Impact factor: 3.240

7.  Monoallelic IDH1 R132H Mutation Mediates Glioma Cell Response to Anticancer Therapies via Induction of Senescence.

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Review 8.  Mutations and mechanisms of WNT pathway tumour suppressors in cancer.

Authors:  Jeroen M Bugter; Nicola Fenderico; Madelon M Maurice
Journal:  Nat Rev Cancer       Date:  2020-10-23       Impact factor: 60.716

9.  A risk signature of four aging-related genes has clinical prognostic value and is associated with a tumor immune microenvironment in glioma.

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Journal:  Aging (Albany NY)       Date:  2021-06-10       Impact factor: 5.682

10.  Inactivation of the Euchromatic Histone-Lysine N-Methyltransferase 2 Pathway in Pancreatic Epithelial Cells Antagonizes Cancer Initiation and Pancreatitis-Associated Promotion by Altering Growth and Immune Gene Expression Networks.

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Journal:  Front Cell Dev Biol       Date:  2021-06-23
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