ArticleEuropean journal of histochemistry : EJH2022
Inhibition of APLN suppresses cell proliferation and migration and promotes cell apoptosis in esophageal cancer cells <em>in vitro</em>, through activating PI3K/mTOR signaling pathway.
Article in European journal of histochemistry : EJH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Integrative bioinformatics and experiments identify RIBC2 as a key regulator in the esophageal cancer.PloS one · 2026Article
- CREB5 promotes nodal metastasis of cervical cancer by regulation of APLN-induced lymphangiogenesis.Cell death discovery · 2025Article
- Selection of tumor invasion-related genes to build a prognostic model and predict immune response and potential drugs for esophageal cancer patients based on WGCNA.Discover oncology · 2025Article
- [Apelin promotes proliferation, migration, and angiogenesis in bladder cancer by activating the FGF2/FGFR1 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025Review
- Potential 'anti-cancer' effects of esketamine on proliferation, apoptosis, migration and invasion in esophageal squamous carcinoma cells.European journal of medical research · 2023Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal cancer is the sixth leading cause of cancer mortalities globally with a high incidence rate. Apelin (APLN) plays regulatory roles in different organs. However, its role in esophageal cancer remains unknown. Therefore, our study aims to explore the effect of APLN on esophageal cancer. One hundred and eighty-four (184) esophageal tumor tissues samples from patients with esophageal cancer, and 11 esophageal tissues samples from healthy volunteers were analyzed for the expression of APLN. APLN was highly expressed in the tumor of patients with esophageal cancer and esophageal cancer cells. Patients with high expressions of APLN had a lower survival rate than the ones with low to medium expressions of APLN. Human esophageal carcinoma cell lines, TE-1 and ECA-109 cells were transfected with APLN siRNA to knockdown APLN, or transfected with pcDNA-APLN to overexpress APLN. Inhibition of APLN by siRNA-APLN reduced proliferative, migrative, and invasive abilities of esophageal cancer cells and promoted cell apoptosis, which could be all restored by pcDNA-APLN. Moreover, knocking down APLN by siRNA-APLN suppressed the PI3K/mTOR signaling pathway. These findings identify that APLN inhibition might ameliorate esophageal cancer through activating the PI3K/mTOR signaling pathway, thus APLN could be a potential target for esophageal cancer.
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