European journal of pharmacology · 2026
CCN5 overexpression suppresses trophoblast HTR-8/SVneo cell proliferation, migration, invasion, and epithelial-mesenchymal transition.
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Gong Yi, Li Jinjing, Wang Chenyang, Bai Jie, Huang Jianmei, Wang Zhe, Yin Qinlan, Liao Shixiu, Liu Mian
Аннотация
BACKGROUND: Preeclampsia (PE) is a highly prevalent, significant obstetric condition associated with aberrant placental trophoblast cell proliferation and infiltration. Cellular communication network factor 5 (CCN5), also referred to as WISP-2, is involved in essential cellular functions, including growth, adhesion, and migration. Nevertheless, the specific roles of CCN5 in trophoblast-related functions remain unexplored.
METHODS: CCN5 expression levels in placental samples from 30 individuals diagnosed with PE and healthy pregnant controls were initially assessed via quantitative reverse transcription PCR (qRT-PCR). Next, cultured human trophoblast cells (HTR-8/SVneo) were transfected with CCN5 short hairpin RNA (shRNA) or CCN5-overexpression plasmids. The efficacy of CCN5 transfection was validated by qRT-PCR and western blotting. Cell proliferation was assessed using colony formation and CCK-8 assays, whereas cell migration and invasion were measured using wound-healing and Transwell assays. Western blotting was performed to analyze the expression levels of extracellular signal-regulated kinase (ERK), phosphorylated-ERK (p-ERK), Twist1, E-cadherin, N-cadherin, and ZO-1 proteins.
RESULTS: Our study initially demonstrated that placental tissues from PE patients had significantly higher CCN5 levels than those from the control group. Functionally, silencing CCN5 in HTR-8/SVneo cells markedly enhanced proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), whereas overexpression significantly inhibited these processes. Notably, CCN5 has been identified as a regulator of EMT, thereby influencing the functional behavior of trophoblast cells. Mechanistically, CCN5 reduced p-ERK levels in HTR-8/SVneo cells, leading to a reduction in Twist1 expression, thereby suppressing EMT.
CONCLUSION: CCN5 overexpression may reduce proliferation and EMT in humans trophoblast cells via the ERK/Twist1 pathway. This finding suggests that CCN5 could serves as a viable target in PE treatment.
METHODS: CCN5 expression levels in placental samples from 30 individuals diagnosed with PE and healthy pregnant controls were initially assessed via quantitative reverse transcription PCR (qRT-PCR). Next, cultured human trophoblast cells (HTR-8/SVneo) were transfected with CCN5 short hairpin RNA (shRNA) or CCN5-overexpression plasmids. The efficacy of CCN5 transfection was validated by qRT-PCR and western blotting. Cell proliferation was assessed using colony formation and CCK-8 assays, whereas cell migration and invasion were measured using wound-healing and Transwell assays. Western blotting was performed to analyze the expression levels of extracellular signal-regulated kinase (ERK), phosphorylated-ERK (p-ERK), Twist1, E-cadherin, N-cadherin, and ZO-1 proteins.
RESULTS: Our study initially demonstrated that placental tissues from PE patients had significantly higher CCN5 levels than those from the control group. Functionally, silencing CCN5 in HTR-8/SVneo cells markedly enhanced proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), whereas overexpression significantly inhibited these processes. Notably, CCN5 has been identified as a regulator of EMT, thereby influencing the functional behavior of trophoblast cells. Mechanistically, CCN5 reduced p-ERK levels in HTR-8/SVneo cells, leading to a reduction in Twist1 expression, thereby suppressing EMT.
CONCLUSION: CCN5 overexpression may reduce proliferation and EMT in humans trophoblast cells via the ERK/Twist1 pathway. This finding suggests that CCN5 could serves as a viable target in PE treatment.