ArticleCell death & disease2019
The Kindlin2-p53-SerpinB2 signaling axis is required for cellular senescence in breast cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Corneal biomechanical cues mediated by PAI-2: the origin of PM2.5-induced corneal disease.EMBO molecular medicine · 2026Article
- Article
- Kindlin-2-Mediated Hematopoiesis Remodeling Regulates Triple-Negative Breast Cancer Immune Evasion.Molecular cancer research : MCR · 2025Article
- Kindlin-2 regulates the oncogenic activities of integrins and TGF-β in triple-negative breast cancer progression and metastasis.Oncogene · 2024Article
- Role of Kindlin 2 in prostate cancer.Scientific reports · 2024Article
- Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells.Cell reports. Medicine · 2024Article
- KPNA2 promotes the progression of gastric cancer by regulating the alternative splicing of related genes.Scientific reports · 2024Article
- Review
- Key variants via the Alzheimer's Disease Sequencing Project whole genome sequence data.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Kindlin-2 inhibits TNF/NF-κB-Caspase 8 pathway in hepatocytes to maintain liver development and function.eLife · 2023Article
- Identification of a novel GR-ARID1a-P53BP1 protein complex involved in DNA damage repair and cell cycle regulation.Oncogene · 2022Article
- Article
- The NOGO receptor NgR2, a novel αVβ3 integrin effector, induces neuroendocrine differentiation in prostate cancer.Scientific reports · 2022Article
- CircRNA expression profiles of breast cancer and construction of a circRNA-miRNA-mRNA network.Scientific reports · 2022Article
- Article
- Genome-wide CRISPR-Cas9 screens identify mechanisms of BET bromodomain inhibitor sensitivity.iScience · 2021Article
- Alzheimer's genetic risk factor FERMT2 (Kindlin-2) controls axonal growth and synaptic plasticity in an APP-dependent manner.Molecular psychiatry · 2021Article
- The Multifaceted Role of Plasminogen in Cancer.International journal of molecular sciences · 2021Review
- SERPINB2-its regulation and interplay with aryl hydrocarbon receptor.Journal of applied genetics · 2021Review
- The roles of integrins in cancer.Faculty reviews · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In cancer, cellular senescence is a complex process that leads to inhibition of proliferation of cells that may develop a neoplastic phenotype. A plethora of signaling pathways, when dysregulated, have been shown to elicit a senescence response. Two well-known tumor suppressor pathways, controlled by the p53 and retinoblastoma proteins, have been implicated in maintaining the cellular senescence phenotype. Kindlin-2, a member of an actin cytoskeleton organizing and integrin activator proteins, has been shown to play a key role in the regulation of several hallmarks of several cancers, including breast cancer (BC). The molecular mechanisms whereby Kindlin-2 regulates cellular senescence in BC tumors remains largely unknown. Here we show that Kindlin-2 regulates cellular senescence in part through its interaction with p53, whereby it regulates the expression of the p53-responsive genes; i.e., SerpinB2 and p21, during the induction of senescence. Our data show that knockout of Kindlin-2 via CRISPR/Cas9 in several BC cell lines significantly increases expression levels of both SerpinB2 and p21 resulting in the activation of hallmarks of cellular senescence. Mechanistically, interaction between Kindlin-2 and p53 at the promotor level is critical for the regulated expression of SerpinB2 and p21. These findings identify a previously unknown Kindlin-2/p53/SerpinB2 signaling axis that regulates cellular senescence and intervention in this axis may serve as a new therapeutic window for BCs treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.