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TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer

Tiewa Zhang1, Cheng Liu2, Yan Yu3

  • 1Department of Thoracic Surgery, The First Affiliated Hospital of Harbin Medical University, 150001, Harbin, China.

Cancer Gene Therapy
|June 28, 2019
PubMed

Insights

Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) is upregulated in nonsmall cell lung carcinoma (NSCLC), promoting cancer cell survival, proliferation, and metastasis. Targeting TBL1XR1 may improve NSCLC treatment and overcome chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Nonsmall cell lung carcinoma (NSCLC) is a leading cause of cancer mortality worldwide.
  • Metastasis and chemoresistance significantly impede NSCLC treatment outcomes.
  • The role of Transducin (β)-like 1 X-linked receptor 1 (TBL1XR1) in lung cancer is largely unknown, despite its association with metastasis in other cancers.

Purpose of the Study:

  • To investigate the role of TBL1XR1 in nonsmall cell lung carcinoma (NSCLC).
  • To determine if TBL1XR1 can serve as a prognostic biomarker and therapeutic target for NSCLC.

Main Methods:

  • Analysis of TBL1XR1 expression in matched NSCLC and adjacent normal lung tissues and patient sera.
  • In vitro assessment of TBL1XR1's influence on cancer phenotypes using CRISPR-Cas9 knockout (A549 cells) and overexpression (H460 cells) models.
  • Investigation of TBL1XR1's regulatory role in MEK, Akt, and c-Met signaling pathways.

Main Results:

  • TBL1XR1 is significantly overexpressed in NSCLC tissues and sera compared to normal controls.
  • TBL1XR1 overexpression enhances NSCLC cell survival, proliferation, invasion, and metastasis.
  • TBL1XR1 regulates the MEK and Akt pathways via the master regulator c-Met, with c-Met activation decreasing in the absence of TBL1XR1.

Conclusions:

  • TBL1XR1 is a potential prognostic biomarker for NSCLC.
  • TBL1XR1 may serve as a therapeutic target to improve treatment efficacy and overcome cisplatin resistance in NSCLC.

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