ArticleMedical oncology (Northwood, London, England)2022
MORC2/β-catenin signaling axis promotes proliferation and migration of breast cancer cells.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Dual Biological Effects and Mechanisms of Gut Microbiota in Breast Cancer: A Review.Current pharmaceutical biotechnology · 2026Review
- Missense mutations of GPER1 in breast invasive carcinoma: Exploring gene expression, signal transduction and immune cell infiltration with insights from cellular pharmacology.Biomedical reports · 2025Article
- Oncogenic MORC2 in cancer development and beyond.Genes & diseases · 2024Review
- Novel Insights into the Role of Chromatin Remodeler MORC2 in Cancer.Biomolecules · 2023Review
- MORC2 and MAX contributes to the expression of glycolytic enzymes, breast cancer cell proliferation and migration.Medical oncology (Northwood, London, England) · 2023Article
- Inhibition of MORC2 Mediates HDAC4 to Promote Cellular Senescence through p53/p21 Signaling Axis.Molecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although Microrchidia 2 (MORC2) is overexpressed in many types of human cancer, its role in breast cancer progression remains unknown. Here, we report that the chromatin remodeler MORC2 expression positively correlates with β-catenin expression in breast cancer cell lines and patients. Overexpression of MORC2 augmented the expression of β-catenin and its target genes, cyclin D1 and c-Myc. Consistent with these results, we found MORC2 knockdown resulted in decreased expression of β-catenin and its target genes. Surprisingly, we observed that c-Myc, the target gene of β-catenin, regulated the MORC2-β-catenin signaling axis through a feedback mechanism. We demonstrated that MORC2 regulates β-catenin expression and function by modulating the phosphorylation of AKT. In addition, we observed reduced proliferation and migration of MORC2 overexpressing breast cancer cells upon β-catenin inhibition. Overall, our results demonstrate that MORC2 promotes breast cancer cell proliferation and migration by regulating β-catenin signaling.
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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.