Knockdown of CCL28 inhibits endometriosis stromal cell proliferation and invasion via ERK signaling pathway inactivation

Yingting Wu, Feilong Zhu, Wenqin Sun, Weiwei Shen, Qin Zhang, Huifen Chen
Molecular medicine reports · 2021 · vol. 25(2) · doi:10.3892/mmr.2021.12573 · PMID:34913072 · PMC8711019 · W4200457092
article OA: gold CC0 ⤵ 3 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that knocking down CCL28 in endometriosis stromal cells inhibited proliferation and invasion by inactivating the ERK signaling pathway and reducing MMP2, MMP9, and ITGB1 expression.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated whether CCL28 and its receptor CCR10 regulate behaviors of endometrial stromal cells, using endometriosis (EM) and control endometrial tissues from 15 EM patients and 15 non-EM patients plus serum from additional participants. The authors found that CCL28 and CCR10 were significantly elevated in EM tissues, and that lentiviral knockdown of CCL28 in primary EM stromal cells suppressed cell proliferation and invasion while decreasing CCR10, MMP2, MMP9, ITGB1, and the p-ERK/ERK ratio; recombinant CCL28 had opposite effects, and the ERK inhibitor PD98059 reduced CCL28-induced proliferation/invasion and associated marker expression. A key limitation is that the work is largely mechanistic and cell/tissue-based, with no in vivo validation or broader clinical correlation reported beyond expression and serum measurements. This paper is centrally about endometriosis — it links CCL28-driven ERK signaling to stromal cell proliferation and invasion in EM.

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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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Condition tags

endometriosis

MeSH descriptors

Chemokines, CC Endometriosis Endometrium Stromal Cells Adult Cell Movement Cell Proliferation Cells, Cultured Chemokines, CC Chemokines, CC Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Gene Knockdown Techniques Humans Laparoscopy MAP Kinase Signaling System

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