Roles of PTEN inactivation and PD-1/PD-L1 activation in esophageal squamous cell carcinoma
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Updated: Sep 29, 2025

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
Rong Qiu1, Wenxi Wang2, Juan Li1
1Department of Radiation Oncology, Fourth Hospital of Hebei Medical University, No. 12 Jian Kang Road, Shijiazhuang, Hebei Province, P. R. China.
Abstract:
Esophageal squamous cell carcinoma (ESCC) is the most common type of esophageal cancer in China and developing countries. The purpose of this review is to summarize the roles of inactivation of the tumor suppressor gene, phosphatase and tensin homolog (PTEN), and activation of the programmed cell death protein 1 (PD-1) upon binding to its ligand (PD-L1) in the promotion of ESCC. Studies of ESCC performed in vitro and in vivo indicated that PTEN and PD-L1 function in the regulation of cell proliferation, invasion, and migration; the epithelial-mesenchymal transition; resistance to chemotherapy and radiotherapy; and the PI3K/AKT signaling pathway. Certain genetic variants of PTEN are related to susceptibility to ESCC, and PTEN and PD-L1 also function in ESCC progression and affect the prognosis of patients with ESCC. There is also evidence that the expression of PD-L1 and PTEN are associated with the progression of certain other cancers. Future studies should further examine the relationship of PD-L1 and PTEN and their possible interactions in ESCC.
Insights
The tumor suppressor gene phosphatase and tensin homolog (PTEN) and programmed cell death protein 1 (PD-1) play key roles in esophageal squamous cell carcinoma (ESCC) promotion. Their inactivation and activation, respectively, influence ESCC progression and patient prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Esophageal squamous cell carcinoma (ESCC) is a prevalent cancer in China and developing nations.
- Tumor suppressor gene PTEN inactivation and PD-1/PD-L1 pathway activation are implicated in cancer development.
- Understanding these molecular mechanisms is crucial for ESCC treatment strategies.
Purpose of the Study:
- To review the roles of PTEN inactivation and PD-1/PD-L1 pathway activation in ESCC.
- To summarize their impact on cellular processes and signaling pathways.
- To explore their association with ESCC susceptibility, progression, and patient prognosis.
Main Methods:
- In vitro and in vivo studies of ESCC were analyzed.
- Literature review focusing on PTEN and PD-L1 in ESCC and other cancers.
- Examination of genetic variants and expression patterns.
Main Results:
- PTEN and PD-L1 regulate cell proliferation, invasion, migration, and epithelial-mesenchymal transition in ESCC.
- These factors influence resistance to chemotherapy and radiotherapy.
- PTEN and PD-L1 impact the PI3K/AKT signaling pathway and patient prognosis.
Conclusions:
- PTEN inactivation and PD-1/PD-L1 activation are significant drivers of ESCC.
- Genetic variants of PTEN are linked to ESCC susceptibility.
- Further research into the interaction between PTEN and PD-L1 in ESCC is warranted.
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