ArticleAmerican journal of cancer research2018
Imbalance of a KLF4-miR-7 auto-regulatory feedback loop promotes prostate cancer cell growth by impairing microRNA processing.
Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- Deletion in a regulatory region is associated with underexpression of miR-148b‑3p in patients with prostate cancer.Biomedical reports · 2024Article
- MiR-135b-5p is an oncogene in pancreatic cancer to regulate GPRC5A expression by targeting transcription factor KLF4.Cell death discovery · 2022Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- miR-152-3p Affects the Progression of Colon Cancer via the KLF4/IFITM3 Axis.Computational and mathematical methods in medicine · 2020Article
- Downregulation of circular RNA hsa_circ_0000735 boosts prostate cancer sensitivity to docetaxel via sponging miR-7.Cancer cell international · 2020Article
- Regulation of Krüppel-Like Factor 4 (KLF4) expression through the transcription factor Yin-Yang 1 (YY1) in non-Hodgkin B-cell lymphoma.Oncotarget · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microRNA-transcription factor auto-regulatory feedback loop is a pivotal mechanism for homeostatic regulation of gene expression, and dysregulation of the feedback loop is tightly associated with tumorigenesis and progression. However, the mechanism underlying such dysregulation is still not well-understood. Here we reported that Krüppel-like factor 4 (KLF4), a stemness-associated transcription factor, promotes the transcription of miR-7 to repress its own translation so that a KLF4-miR-7 auto-regulatory feedback loop is established for mutual regulation of their expression. Interestingly, this feedback loop is unbalanced in prostate cancer (PCa) cell lines and patient samples due to an impaired miR-7-processing, leading to decreased mature miR-7 production and attenuated inhibition of KLF4 translation. Mechanistically, enhanced oncogenic Yes associated protein (YAP) nuclear translocation mediates sequestration of p72, a co-factor of the Drosha/DGCR8 complex for pri-miR-7s processing, leading to attenuation of microprocessors' efficiency. Knockdown of YAP or transfection with a mature miR-7 mimic can significantly recover miR-7 expression to restore this feedback loop, and in turn to inhibit cancer cell growth by repressing KLF4 expression
Indexed as
Identifiers
29511594PMC5835691W3022983591What OpenQuestion holds
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.