PTEN loss promotes oncogenic function of STMN1 via PI3K/AKT pathway in lung cancer

Guangsu Xun1, Wei Hu2, Bing Li2

  • 1Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1. Eastern Jianshe Road, Zhengzhou, 450052, Henan, China. xungsu@163.com.

Scientific Reports
|July 13, 2021
PubMed

Insights

This study reveals that Stathmin (STMN1) is overexpressed in lung cancer, driving tumor growth and metastasis. Loss of PTEN promotes STMN1, worsening patient outcomes and highlighting a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Lung cancer is a leading cause of cancer death globally, necessitating improved understanding of its molecular mechanisms.
  • Stathmin (STMN1), a protein regulating cell processes, is dysregulated in various tumors, but its role in lung cancer remains unclear.

Purpose of the Study:

  • To investigate the role of Stathmin (STMN1) in lung cancer progression and its relationship with PTEN.
  • To elucidate the molecular mechanisms by which STMN1 influences lung cancer cell behavior and drug sensitivity.

Main Methods:

  • Analysis of STMN1 expression in lung cancer tissues and correlation with patient survival.
  • Inhibition of STMN1 in lung cancer cells to assess effects on growth, migration, invasion, and drug sensitivity.
  • Investigation of the PTEN/PI3K/AKT pathway in regulating STMN1 expression.

Main Results:

  • STMN1 was found to be overexpressed in lung cancer tissues, correlating with poorer survival rates.
  • Inhibiting STMN1 suppressed lung cancer cell proliferation, migration, and invasion, while enhancing drug sensitivity.
  • Loss of PTEN was shown to promote STMN1 expression via the PI3K/AKT pathway, and this loss counteracted the effects of STMN1 knockdown.

Conclusions:

  • STMN1 is an oncogenic protein in lung cancer, promoting tumor progression and negatively impacting patient survival.
  • The PTEN/PI3K/AKT pathway plays a critical role in regulating STMN1 expression and its oncogenic functions in lung cancer.
  • Targeting STMN1 or restoring PTEN function may represent potential therapeutic strategies for lung cancer.

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