Literature DB >> 28741506

SASP: Tumor Suppressor or Promoter? Yes!

Sonia G Rao1, James G Jackson2.   

Abstract

Cellular senescence is a permanent growth arrest in cells with damage or stress that could lead to transformation. Some tumor cells also undergo senescence in response to chemotherapy. Senescent cells secrete cytokines and other factors of the senescence-associated secretory phenotype (SASP) that contribute to tumor suppression by enforcing arrest and recruiting immune cells that remove these damaged or oncogene-expressing cells from organisms. However, some cells can develop a SASP comprising factors that are immunosuppressive and protumorigenic by paracrine mechanisms. Likewise, the SASP in treated cancers can either contribute to durable responses or drive relapse. Here, we discuss the studies that have demonstrated a complex and often conflicting role for the SASP in tumorigenesis and treatment response.
Copyright © 2016 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  SASP; chemotherapy response; immune response; p53; senescence; tumor suppression

Mesh:

Year:  2016        PMID: 28741506     DOI: 10.1016/j.trecan.2016.10.001

Source DB:  PubMed          Journal:  Trends Cancer        ISSN: 2405-8025


  66 in total

Review 1.  Cellular senescence: a view throughout organismal life.

Authors:  Cayetano von Kobbe
Journal:  Cell Mol Life Sci       Date:  2018-07-20       Impact factor: 9.261

2.  A previously identified apoptosis inhibitor iASPP confers resistance to chemotherapeutic drugs by suppressing senescence in cancer cells.

Authors:  Huayi Li; Wenxin Zhang; Kunming Zhao; Dong Zhao; Shanliang Zheng; Ying Hu
Journal:  J Biol Chem       Date:  2020-01-31       Impact factor: 5.157

Review 3.  Oncogene-induced senescence: a double edged sword in cancer.

Authors:  Xue-Ling Liu; Jian Ding; Ling-Hua Meng
Journal:  Acta Pharmacol Sin       Date:  2018-04-05       Impact factor: 6.150

Review 4.  Growth hormone in the tumor microenvironment.

Authors:  Vera Chesnokova; Shlomo Melmed
Journal:  Arch Endocrinol Metab       Date:  2019 Nov-Dec       Impact factor: 2.309

5.  BH3 mimetics selectively eliminate chemotherapy-induced senescent cells and improve response in TP53 wild-type breast cancer.

Authors:  Ashkan Shahbandi; Sonia G Rao; Ashlyn Y Anderson; Wesley D Frey; Joy O Olayiwola; Nathan A Ungerleider; James G Jackson
Journal:  Cell Death Differ       Date:  2020-05-26       Impact factor: 15.828

Review 6.  TP53 Mutations and Outcomes in Breast Cancer: Reading beyond the Headlines.

Authors:  Ashkan Shahbandi; Hoang D Nguyen; James G Jackson
Journal:  Trends Cancer       Date:  2020-02-05

Review 7.  DNA damage and mitochondria in cancer and aging.

Authors:  Jaimin Patel; Beverly A Baptiste; Edward Kim; Mansoor Hussain; Deborah L Croteau; Vilhelm A Bohr
Journal:  Carcinogenesis       Date:  2020-12-31       Impact factor: 4.944

Review 8.  The DNA-damage response and nuclear events as regulators of nonapoptotic forms of cell death.

Authors:  Evgeniia A Prokhorova; Aleksandra Yu Egorshina; Boris Zhivotovsky; Gelina S Kopeina
Journal:  Oncogene       Date:  2019-08-28       Impact factor: 9.867

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

Authors:  Haitao Luo; Chuming Tao; Xiaoyan Long; Kai Huang; Xingen Zhu
Journal:  Aging (Albany NY)       Date:  2021-06-10       Impact factor: 5.682

Review 10.  Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma.

Authors:  Wei Jia; Cynthia Rajani; Hongxi Xu; Xiaojiao Zheng
Journal:  Protein Cell       Date:  2020-08-14       Impact factor: 14.870

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