ReviewCancer research2016
Kruppel-like Pluripotency Factors as Modulators of Cancer Cell Therapeutic Responses.
Review in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 63 citations in OpenAlex.
- Tissue-Specific Chromatin Accessibility Regions and Transcription Factor Binding Sites in Pig Brain and Endocrine Tissues.Molecular neurobiology · 2025Article
- Role of KLF5 in enhancing ovarian cancer stemness and PARPi resistance: mechanisms and therapeutic targeting.Journal of translational medicine · 2025Article
- Hypoxia LUAD H1975 cell-derived exosomal miR-671-3p promotes angiogenesis via regulating KLF2-VEGFR2 axis.Scientific reports · 2025Article
- The miR-1305/KLF5 negative regulatory loop affects pancreatic cancer cell proliferation and apoptosis.Human cell · 2025Article
- Gastric Adenocarcinomas with CDX2 Induction Show Higher Frequency ofJournal of clinical medicine · 2024Article
- Effect of Kruppel-like factor 4 on PTZ-induced acute seizure mice.Journal of cellular and molecular medicine · 2024Article
- Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer.Heliyon · 2024Review
- [Overexpression of tuftelin and KLF-5 and its clinicopathological features in hepatitis B virus-related hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Article
- The Effect ofJournal of experimental pharmacology · 2024Article
- Exploring the promising potential of induced pluripotent stem cells in cancer research and therapy.Molecular cancer · 2023Review
- KLF5 and p53 comprise an incoherent feed-forward loop directing cell-fate decisions following stress.Cell death & disease · 2023Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Butterfly eyespots exhibit unique patterns of open chromatin.F1000Research · 2023Article
- KLF4 is a therapeutically tractable brake on fibroblast activation that promotes resolution of pulmonary fibrosis.JCI insight · 2022Article
- KLF5 inhibition overcomes oxaliplatin resistance in patient-derived colorectal cancer organoids by restoring apoptotic response.Cell death & disease · 2022Article
- MiR-135b-5p is an oncogene in pancreatic cancer to regulate GPRC5A expression by targeting transcription factor KLF4.Cell death discovery · 2022Article
- α-Catulin promotes cancer stemness by antagonizing WWP1-mediated KLF5 degradation in lung cancer.Theranostics · 2022Article
- Roles and Mechanisms of Deubiquitinases (DUBs) in Breast Cancer Progression and Targeted Drug Discovery.Life (Basel, Switzerland) · 2021Review
- Depletion of Kruppel-like factor 15 sensitized gliomas to temozolomide cytotoxicity throughBiochemistry and biophysics reports · 2021Article
- miR-9 modulates and predicts the response to radiotherapy and EGFR inhibition in HNSCC.EMBO molecular medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tumor cells inherit from their normal precursors an extensive stress response machinery that is critical for survival in response to challenges including oxidative stress, wounding, and shear stress. Kruppel-like transcription factors, including KLF4 and KLF5, are rarely affected by genetic alteration during tumorigenesis, but compose key components of the stress response machinery in normal and tumor cells and interact with critical survival pathways, including RAS, p53, survivin, and the BCL2 family of cell death regulators. Within tumor cells, KLF4 and KLF5 play key roles in tumor cell fate, regulating cell proliferation, cell survival, and the tumor-initiating properties of cancer stem-like cells. These factors can be preferentially expressed in embryonic stem cells or cancer stem-like cells. Indeed, specific KLFs represent key components of a cross-regulating pluripotency network in embryonic stem cells and induce pluripotency when coexpressed in adult cells with other Yamanaka factors. Suggesting analogies between this pluripotency network and the cancer cell adaptive reprogramming that occurs in response to targeted therapy, recent studies link KLF4 and KLF5 to adaptive prosurvival signaling responses induced by HER2-targeted therapy. We review literature supporting KLFs as shared mechanisms in stress adaptation and cellular reprogramming and address the therapeutic implications. Cancer Res; 76(7); 1677-82. ©2016 AACR.
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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.