1. Academic Validation
  2. LZTS3/TAGLN Suppresses Cancer Progression in Human Colorectal Adenocarcinoma Through Regulating Cell Proliferation, Migration, and Actin Cytoskeleton

LZTS3/TAGLN Suppresses Cancer Progression in Human Colorectal Adenocarcinoma Through Regulating Cell Proliferation, Migration, and Actin Cytoskeleton

  • Arch Med Res. 2023 Oct 6;54(7):102894. doi: 10.1016/j.arcmed.2023.102894.
Xinpei Gu 1 Shuhui Chen 2 Zhaojin Wang 3 Qianwen Bu 4 Shuhong An 5
Affiliations

Affiliations

  • 1 Department of Human Anatomy, Shandong First Medical University and Shandong Academy of Medical Sciences, Tai'an, China; School of Pharmaceutical Sciences, Guangdong Provincial Key Laboratory of New Drug Screening, Southern Medical University, Guangzhou, China.
  • 2 Department of Gastrointestinal surgery, The Affiliated Tai'an City Central Hospital of Qingdao University, Tai'an, Shandong, China.
  • 3 Department of Human Anatomy, Shandong First Medical University and Shandong Academy of Medical Sciences, Tai'an, China.
  • 4 State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Eye Institute of Shandong First Medical University, Qingdao, China.
  • 5 Department of Human Anatomy, Shandong First Medical University and Shandong Academy of Medical Sciences, Tai'an, China. Electronic address: shha@sdfmu.edu.cn.
Abstract

Background: Numerous studies have confirmed that the leucine zipper tumor suppressor (LZTS) gene family plays a vital role in modulating transcription and cell cycle control, especially in colorectal Cancer. This study aimed to evaluate the potential of leucine zipper tumor suppressor family member 3 (LZTS3) as a marker for COAD.

Methods: Bioinformatics, immunohistochemistry, and Western blotting were applied to assess the expression of LZTS3 in tissues. Gene overexpression or silencing was used to examine the biological roles of LZTS3 and validated using an in vivo nude mouse-human tumor model.

Results: The results obtained in this study indicate that LZTS3 is highly expressed in COAD. RTCA, Transwell, actin stain, and in vitro transfection experiments confirmed that LZTS3 expression inhibits tumor cell proliferation and cell migration. The results obtained in the nude mouse-human tumor model are consistent with those obtained in vitro. In particular, LZTS3 may exert biological effects by targeting the Notch signaling pathway. Furthermore, TAGLN was demonstrated to be a downstream target of LZTS3.

Conclusion: This is the first study to demonstrate the important role of LZTS3 in the proliferation and migration of COAD and to shed LIGHT on the molecular mechanism underlying the tumor-suppressing role of LZTS3.

Keywords

LZTS3; NOTCH; TAGLN; Tumor growth.

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