Roles of PTEN inactivation and PD-1/PD-L1 activation in esophageal squamous cell carcinoma

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.

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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