Observational studyMolecular medicine reports2022
Knockdown of CCL28 inhibits endometriosis stromal cell proliferation and invasion via ERK signaling pathway inactivation.
Observational study in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Knockdown of Long Non-coding RNA-MALAT1 Ameliorates Diabetic Lower Limb Atherosclerotic Disease Through MiR-17-5p-Mediated Endothelial Cell Pyroptosis.Biochemical genetics · 2026Article
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- Sirtuins as mediators and targets of arsenic toxicity: unraveling signaling pathway crosstalk.Archives of toxicology · 2025Review
- Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025Review
- ONC206, an imipridone derivative, demonstrates anti-colorectal cancer activity against stem/progenitor cells in 3D cell cultures and in patient-derived organoids.Pharmacological reports : PR · 2025Article
- Extracellular vesicles derived from bone marrow mesenchymal stem cells ameliorate chronic liver damage via microRNA-136-5p.Molecular and cellular biochemistry · 2025Article
- LncRNA GAS5 modulates Schwann cell function and enhances facial nerve injury repair via the miR-138-5p/CXCL12 axis.Journal of molecular histology · 2024Article
- The role of PFKFB3 in maintaining colorectal cancer cell proliferation and stemness.Molecular biology reports · 2022Review
- Regulation of ferroptosis by noncoding RNAs: a novel promise treatment in esophageal squamous cell carcinoma.Molecular and cellular biochemistry · 2022Review
- Article
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
Endometriosis (EM), the presence of functional endometrial glands and stroma outside the uterine cavity, is a common gynecological disorder. At present, the pathogenesis of EM has not been fully elucidated, so there is still a lack of effective therapy. The present study aimed to explore the role of C‑C motif chemokine ligand 28 (CCL28) and its underlying mechanism in endometrial stromal cells to propose a novel therapy for EM treatment. The expression of CCL28 and CC chemokine receptor 10 (CCR10) were examined. After CCL28 knockdown or overexpression by lentivirus infection, cell proliferation and invasion were measured. It was revealed that compared with normal, the expression levels of CCL28 and CCR10 were significantly elevated in endometrial tissues of patients with EM. Knockdown of CCL28 in endometrial stromal cells significantly suppressed cell proliferation and invasion, and this was accompanied by significantly reduced expression levels of CCR10, MMP2, MMP9, integrin β1 (ITGB1) and phosphorylated (p)‑ERK/ERK ratio. The addition of the CCL28 recombinant protein had an opposite effect to CCL28 downregulation. Furthermore, the ERK inhibitor, PD98059, reduced CCL28‑induced cell proliferation and invasion, as well as the expression levels of MMP2, MMP9, ITGB1 and p‑ERK. Therefore, the present study indicated that CCL28 may contribute to the progression of EM by regulating MMP2, MMP9 and ITGB1 expression and function via the activation of the ERK signaling pathway.
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