ArticleTranslational cancer research2020
ET-1 promotes the growth and metastasis of esophageal squamous cell carcinoma via activating PI3K/Akt pathway.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Yimusake ameliorates corporal endothelial dysfunction by down-regulating the NLRP3 inflammasome-mediated NF-κB signaling pathway and inhibiting oxidative stress.Sexual medicine · 2025Article
- Retraction: ET-1 promotes the growth and metastasis of esophageal squamous cell carcinoma via activating PI3K/Akt pathway.Translational cancer research · 2023Article
- Analysis of genetic biomarkers, polymorphisms in ADME-related genes and their impact on pharmacotherapy for prostate cancer.Cancer cell international · 2023Review
Corrections and comments
- Retraction · 2023-11-30Concerns/Issues about Results and/or Conclusions ·
- Retracted
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide. Previous studies confirmed that endothelin-1 (ET-1) serves as an oncogene and therapeutic target in various tumors. However, the role and mechanism of ET-1 in the progression of ESCC remains largely unclear.
methodsReverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the mRNA level of ET-1 in ESCC tissues and cell lines. Cell counting kit-8 (CCK-8), flow cytometry and Transwell assay were performed to examine the proliferation, cell cycle arrest, invasion and migration capacity of ESCC cells. Western blot was applied to measure the expression of ET-1 and PI3K/Akt pathway-related proteins. Furthermore, we also assessed the effect of ET-1 on tumor growth
resultsET-1 was highly expressed in ESCC tissues and associated with poor outcomes. Knockdown of ET-1 significantly inhibited the proliferation, migration and invasion capacity of ESCC cells and promoted cell cycle arrest. Mechanistically, silencing of ET-1 exerts anti-proliferation and anti-metastasis activities via inactivation of the PI3K/Akt signaling pathway in ESCC
conclusionsThese findings uncover the effective suppression of cell proliferation and metastasis through silencing of ET-1 and blocking the PI3K/Akt signaling pathway, which is an attractive therapeutic regimen for the treatment of ESCC.
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Registered trials
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.