ArticleNeoplasia (New York, N.Y.)2017
PLCE1 Promotes Esophageal Cancer Cell Progression by Maintaining the Transcriptional Activity of Snail.
Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study.Archives of toxicology · 2025Article
- Overarching roles of diacylglycerol signaling in cancer development and antitumor immunity.Science signaling · 2022Review
- HuR Affects the Radiosensitivity of Esophageal Cancer by Regulating the EMT-Related Protein Snail.Frontiers in oncology · 2022Article
- CircPLCE1 facilitates the malignant progression of colorectal cancer by repressing the SRSF2-dependent PLCE1 pre-RNA splicing.Journal of cellular and molecular medicine · 2021Article
- YAP-TEAD up-regulates IRS2 expression to induce and deteriorate oesophageal cancer.Journal of cellular and molecular medicine · 2021Article
- Identification of a PLCE1‑regulated competing endogenous RNA regulatory network for esophageal squamous cell carcinoma.Oncology reports · 2021Article
- CRISPR/Cas9 in Gastrointestinal Malignancies.Frontiers in cell and developmental biology · 2021Review
- SHARPIN Inhibits Esophageal Squamous Cell Carcinoma Progression by Modulating Hippo Signaling.Neoplasia (New York, N.Y.) · 2020Article
- Regulation of Hippo/YAP signaling and Esophageal Squamous Carcinoma progression by an E3 ubiquitin ligase PARK2.Theranostics · 2020Article
- Genetic Variants in EGFR/PLCE1 Pathway Are Associated with Prognosis of Esophageal Squamous Cell Carcinoma after Radical Resection.Current medical science · 2019Article
- RNF168 facilitates proliferation and invasion of esophageal carcinoma, possibly via stabilizing STAT1.Journal of cellular and molecular medicine · 2019Article
- Epigenetically upregulated oncoprotein PLCE1 drives esophageal carcinoma angiogenesis and proliferation via activating the PI-PLCε-NF-κB signaling pathway and VEGF-C/ Bcl-2 expression.Molecular cancer · 2019Article
- Article
- Evaluation of GWAS-Identified Genetic Variants for Gastric Cancer Survival.EBioMedicine · 2018Article
- The plasma peptides of ovarian cancer.Clinical proteomics · 2018Article
- Ablation of MCM10 using CRISPR/Cas9 restrains the growth and migration of esophageal squamous cell carcinoma cells through inhibition of Akt signaling.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal cancer is among the most deadly malignant diseases. However, the genetic factors contributing to its occurrence are poorly understood. Multiple studies with large clinic-based cohorts revealed that variations of the phospholipase C epsilon (PLCE1) gene were associated with esophageal cancer susceptibility. However, the causative role of PLCE1 in esophageal cancer is not clear. We inactivated the functional alleles of PLCE1 by CRISPR/Cas9 genome editing technology. The resultant PLCE1 inactivated cells were analyzed both in vitro and in vivo. Our results showed that loss of PLCE1 dramatically decreased the invasion and proliferation capacity of esophageal carcinoma cells in vitro. Moreover, such PLCE1 inactivated tumor grafts exhibited significantly decreased tumor size in mice. We found that PLCE1 was required to maintain protein level of snail a key transcription factor responsible for invasion. Our further transcriptomic data revealed that deficient cells were significantly decreased in expression of genes enriched as targets of Snail. Strikingly, recovery of Snail protein at least partially rescued the invasion and proliferation capacity in PLCE1 inactivated cells. In ESCC clinical specimens, PLCE1 was correlated with tumor stage (P<.0001). Interestingly, PLCE1 expression was positively correlated Snail by immunohistochemistry in such specimens (P<.0001). Therefore, our functional experiments showed the essential roles of PLCE1 in esophageal carcinoma cells and provided evidences that targeting PLCE1 and its downstream molecules could be effective therapies for esophageal cancer.
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