ArticleBMC cancer2019
MUC16 impacts tumor proliferation and migration through cytoplasmic translocation of P120-catenin in epithelial ovarian cancer cells: an original research.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 52 citations in OpenAlex.
- Prime Editing, CRISPR-Cas9, and NanoCas Genome Editing for Cancer Treatment.Molecular biotechnology · 2026Review
- Integrating multi-omics and clinical features to model survival in epithelial ovarian cancer subtypes.Scientific reports · 2025Article
- Hormonally upregulated neu tumor-associated kinase (HUNK) modulates gastric cancer progression through the regulation of cell homeostasis.Cell communication and signaling : CCS · 2025Article
- Article
- Relationship Between Loss of Y Chromosome and Urologic Cancers: New Future Perspectives.Cancers · 2024Review
- MUC16: clinical targets with great potential.Clinical and experimental medicine · 2024Review
- Mesothelin-based CAR-T cells exhibit potent antitumor activity against ovarian cancer.Journal of translational medicine · 2024Article
- Structural basis for antibody recognition of the proximal MUC16 ectodomain.Journal of ovarian research · 2024Article
- Comprehensive review of CRISPR-based gene editing: mechanisms, challenges, and applications in cancer therapy.Molecular cancer · 2024Review
- Chimeric antibody targeting unique epitope on onco-mucin16 reduces tumor burden in pancreatic and lung malignancies.NPJ precision oncology · 2023Article
- Why loss of Y? A pan-cancer genome analysis of tumors with loss of Y chromosome.Computational and structural biotechnology journal · 2023Article
- Evaluation of serum CA125-Tn glycoform in peritoneal dissemination and surgical completeness of high-grade serous ovarian cancer.Journal of ovarian research · 2022Article
- Mucin 16 Promotes Colorectal Cancer Development and Progression Through Activation of Janus Kinase 2.Digestive diseases and sciences · 2022Article
- Proteomic analysis distinguishes extracellular vesicles produced by cancerous versus healthy pancreatic organoids.Scientific reports · 2022Article
- Transcriptomic Analysis of Laser Capture Microdissected Tumors Reveals Cancer- and Stromal-Specific Molecular Subtypes of Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- MUC16 promotes EOC proliferation by regulating GLUT1 expression.Journal of cellular and molecular medicine · 2021Article
- Article
- Review
- The Ovarian Cancer Tumor Immune Microenvironment (TIME) as Target for Therapy: A Focus on Innate Immunity Cells as Therapeutic Effectors.International journal of molecular sciences · 2020Review
- Prevalence of K-RAS mutations and CA125 tumor marker in patients with ovarian carcinoma.Caspian journal of internal medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial ovarian cancer (EOC) remains one of the most lethal gynecologic cancers, and its pathogenetic mechanism remains unclear. Here we show that MUC16 promotes the translocation of p120-catenin (p120ctn) to the cytoplasm and consequently activates ras homolog (Rho) GTPases RhoA/Cdc42 activation to modulate the proliferation and migration abilities of EOC cells.
methodsWe collect 94 ovarian cancer (OC) patients' tissue samples to constitute tissue microarray (TMA) and analyze the MUC16 and p120ctn expression levels. Lentivirus transfection is used to overexpress cytoplasmic tail domain (CTD) of MUC16 and CRISPR/Cas9 genome-editing system is firstly used to knock out MUC16 in EOC cells. The proliferation or migration ability of cells is analyzed by MTS or migration assay.
resultsWe find that MUC16 and p120ctn are aberrantly overexpressed in 94 clinical OC samples compared with benign ovarian tumors (BOT). MUC16 is a critical inducer of the proliferation and migration of EOC cells and the CTD of MUC16 plays an important role during this process. In addition, we reveal the relationship between MUC16 and p120ctn, which has not previously been studied. We show that MUC16 promotes the translocation of p120ctn to the cytoplasm and consequently activates Rho GTPases to modulate the proliferation and migration abilities of EOC cells. The cell proliferation and migration abilities induced by MUC16 are mediated by p120ctn through RhoA/Cdc42 activation.
conclusionsThe highly expressed MUC16 promotes the translocation of p120ctn to the cytoplasm, where it activates RhoA/Cdc42 to modulate the proliferation and migration abilities of EOC cells. These findings may provide new targets for the treatment of EOC.
Indexed as
Identifiers
What 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.