ArticleFrontiers in oncology2016
Overexpression of Specific CD44 Isoforms Is Associated with Aggressive Cell Features in Acquired Endocrine Resistance.
Article in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Alternative splicing rewires breast cancer and opens therapeutic avenues.Cell communication and signaling : CCS · 2026Review
- CD44v6 is associated with tumor aggressiveness and chemoresistance in bladder cancer.Scientific reports · 2026Article
- Peptide-based inhibition of CD44v6 renders liver carcinomas more susceptible to therapeutic intervention.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Chimeric Antigen Receptor (CAR)-NK92 cells effective against glioblastoma, breast- and pancreatic cancer in vitro and in a murine xenograft model of ovarian cancer.Cancer cell international · 2025Article
- Review
- Mutant Allele of CD44 (rs8193C>T) and Pum2 Regulatory Element as A Prognosis Factor of Prostate Neoplasms: A Case-Control and In Silico Studies.Cell journal · 2022Article
- ERα-LBD, an isoform of estrogen receptor alpha, promotes breast cancer proliferation and endocrine resistance.NPJ breast cancer · 2022Article
- Role of CD44 isoforms in epithelial-mesenchymal plasticity and metastasis.Clinical & experimental metastasis · 2022Review
- The molecular underpinning of geminin-overexpressing triple-negative breast cancer cells homing specifically to lungs.Cancer gene therapy · 2022Article
- Understanding Hyaluronan Receptor (CD44) Interaction, HA-CD44 Activated Potential Targets in Cancer Therapeutics.Advanced pharmaceutical bulletin · 2021Review
- CD44 activation state regulated by the CD44v10 isoform determines breast cancer proliferation.Oncology reports · 2021Article
- Article
- Targeting the Extra-Cellular Matrix-Tumor Cell Crosstalk for Anti-Cancer Therapy: Emerging Alternatives to Integrin Inhibitors.Frontiers in oncology · 2020Review
- CD44v6 Targeted by miR-193b-5p in the Coding Region Modulates the Migration and Invasion of Breast Cancer Cells.Journal of Cancer · 2020Article
- The COOH-Terminal Proline-Rich Region of GRP78 Is a Key Regulator of Its Cell Surface Expression and Viability of Tamoxifen-Resistant Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2019Article
- GRP78 regulates CD44v membrane homeostasis and cell spreading in tamoxifen-resistant breast cancer.Life science alliance · 2019Article
- Effect of CD44st and HER2 expression on the postoperative prognosis of breast cancer patients.OncoTargets and therapy · 2019Article
- Preclinical evaluation of a novel engineered recombinant human anti-CD44v6 antibody for potential use in radio-immunotherapy.International journal of oncology · 2018Article
- The biology and role of CD44 in cancer progression: therapeutic implications.Journal of hematology & oncology · 2018Review
- A correlation study of the expression of HA-CD44st and HER-2 in breast cancer.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While endocrine therapy is the mainstay of ER+ breast cancer, the clinical effectiveness of these agents is limited by the phenomenon of acquired resistance that is associated with disease relapse and poor prognosis. Our previous studies revealed that acquired resistance is accompanied by a gain in cellular invasion and migration and also that CD44 family proteins are overexpressed in the resistant phenotype. Given the association of CD44 with tumor progression, we hypothesized that its overexpression may act to promote the aggressive behavior of endocrine-resistant breast cancers. Here, we have investigated further the role of two specific CD44 isoforms, CD44v3 and CD44v6, in the endocrine-resistant phenotype. Our data revealed that overexpression of CD44v6, but not CD44v3, in endocrine-sensitive MCF-7 cells resulted in a gain in EGFR signaling, enhanced their endogenous invasive capacity, and attenuated their response to endocrine treatment. Suppression of CD44v6 in endocrine-resistant cell models was associated with a reduction in their invasive capacity. Our data suggest that upregulation of CD44v6 in acquired resistant breast cancer may contribute to a gain in the aggressive phenotype of these cells and loss of endocrine response through transactivation of the EGFR pathway. Future therapeutic targeting of CD44v6 may prove to be an effective strategy alongside EGFR-targeted agents in delaying/preventing acquired resistance in breast cancer.
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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.