Mechanism of OTUD5 in non‐small cell lung cancer cell proliferation, invasion, and migration

Authors

  • Xuebing Li Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China
  • Baohua Lu Department of Oncology, Beijing Chest Hospital, Capital Medical University, Beijing, China
  • Lina Zhang Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, China
  • Jing Yang Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China
  • Yurong Cheng Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China
  • Dong Yan Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China https://orcid.org/0000-0002-7053-3078

DOI:

https://doi.org/10.17305/bjbms.2022.7206

Keywords:

OTUD5, PTEN, miR-652-3p, non-small cell lung cancer, proliferation, migration, invasion, ubiquitination

Abstract

Ovarian tumor protease deubiquitinase 5 (OTUD5) has been discussed as a regulator of cancer development. Herein, the current study set out to explore the molecular mechanism of OTUD5 in non‐small cell lung cancer (NSCLC) cell proliferation, invasion, and migration. Firstly, the expression patterns of OTUD5, phosphatase and tensin homolog (PTEN), as well as microRNA (miR)-652-3p in cells were detected by qRT-PCR and Western blot. Cell viability, migration, and invasion were assessed with the help of cell-counting kit-8 and Transwell assays, in addition to the measurement of the ubiquitination and protein levels of PTEN. The binding relations between OTUD5 and PTEN, and miR-652-3p and OTUD5 were testified by co-immunoprecipitation or dual-luciferase assays. Cells were further treated with GSK2643943A (inhibitor of deubiquitinase) or miR-652-3p-inhibitor to explore the role of PTEN ubiquitination and miR-652-3p in NSCLC cells. OTUD5 and PTEN were both poorly-expressed, and miR-652-3p was highly-expressed in NSCLC cells. On the other hand, over-expression of OTUD5 suppressed NSCLC cell proliferation, invasion, and migration. OTUD5 deubiquitinated and stabilized PTEN, and miR-652-3p targeted and inhibited OTUD5 expression. Augmenting the ubiquitination levels of PTEN promoted NSCLC cell growth, whereas miR-652-3p inhibition promoted the tumor-suppressing effects of the OTUD5/ PTEN axis in NSCLC. Altogether, our findings highlighted that miR-652-3p restrained the role of OTUD5 in deubiquitinating PTEN to improve PTEN protein level, thereby promoting NSCLC cell proliferation, invasion, and migration.

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Author Biographies

  • Xuebing Li, Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China

    Department of Oncology

  • Baohua Lu, Department of Oncology, Beijing Chest Hospital, Capital Medical University, Beijing, China

    Department of Oncology

  • Lina Zhang, Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, China

    Department of Cellular and Molecular Biology

  • Jing Yang, Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China

    Department of Oncology

  • Yurong Cheng, Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China

    Department of Oncology

  • Dong Yan, Department of Oncology, Beijing Luhe Hospital Affiliated to Capital Medical University, Beijing, China

    Department of Oncology

Mechanism of OTUD5 in non‐small cell lung cancer

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Published

23-10-2022

Issue

Section

Molecular Biology

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How to Cite

1.
Mechanism of OTUD5 in non‐small cell lung cancer cell proliferation, invasion, and migration. Biomol Biomed [Internet]. 2022 Oct. 23 [cited 2024 May 19];22(6):901-1. Available from: https://www.bjbms.org/ojs/index.php/bjbms/article/view/7206