ArticleInternational journal of molecular medicine2018
A regulation loop between Nrf1α and MRTF-A controls migration and invasion in MDA-MB-231 breast cancer cells.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.Clinical and experimental medicine · 2026Review
- Understanding the Transcription Factor NFE2L1/NRF1 from the Perspective of Hallmarks of Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Pan-cancer and single-cell analysis of actin cytoskeleton genes related to disulfidptosis.Open medicine (Warsaw, Poland) · 2024Article
- Long non-coding RNA urothelial cancer associated 1 can regulate the migration and invasion of colorectal cancer cells (SW480) via myocardin-related transcription factor-A.Oncology letters · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a strong transactivator of promoters containing CarG boxes, myocardin‑related transcription factor A (MRTF‑A) is critical for the process of metastasis in tumor cells. Nuclear factor erythroid 2‑like 1 (Nrf1) is well known as an important regulator of oxidative stress, which exists in multiple splicing forms with many unknown functions. The present study demonstrated a novel regulation loop between Nrf1α (the longest splicing form of Nrf1) and MRTF‑A that regulated the migration and invasion of breast cancer MDA‑MB‑231 cells. The underlying mechanism of this regulation look was further investigated. In particular, Nrf1α inhibited migration and invasion of breast cancer cells through inhibiting the expression of MRTF‑A via miR‑219. The current results revealed that miR‑219 could bind to the MRTF‑A 3'‑UTR to directly regulate its expression. However, MRTF‑A could reverse activate the Nrf1α expression through binding to the CarG box in the Nrf1α promoter. It can be speculated that this regulation loop may be a homeostasis mechanism in cells against tumorigenesis.
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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.