LUCAT1 Activates the Malignant Phenotypes of Lung Cancer Cells via Regulating P53 Ubiquitination

Junfeng Zhang; Weiyi Gong; Xinle Wang; Longbo Yang

doi:10.18502/ijph.v53i9.16458

Junfeng Zhang Department of Thoracic Surgery, Zhongkegengjiu Hospital of Anhui/Gengjiu Clinical Medical College, Anhui Medical University, Hefei, 230001, China
Weiyi Gong Department of Thoracic Surgery, Zhongkegengjiu Hospital of Anhui/Gengjiu Clinical Medical College, Anhui Medical University, Hefei, 230001, China
Xinle Wang Department of Thoracic Surgery, Zhongkegengjiu Hospital of Anhui/Gengjiu Clinical Medical College, Anhui Medical University, Hefei, 230001, China
Longbo Yang Department of Thoracic Surgery, Zhongkegengjiu Hospital of Anhui/Gengjiu Clinical Medical College, Anhui Medical University, Hefei, 230001, China

DOI: https://doi.org/10.18502/ijph.v53i9.16458

Keywords: Lung cancer associated transcript 1; P53; Ubiquitination; Non-small-cell lung cancer

Abstract

Background: Long non-coding RN (lncRNAs) have been implicated in lung cancer, but the mechanisms stay unclear. We investigated the theatrical role and mechanism of lncRNA Lung cancer associated transcript 1 LUCAT1 in the malignant progress of lung cancer.

Methods: From May 2022 to March 2023, a total of thirty normal and cancerous tissues were collected from patients diagnosed with non-small cell lung cancer at Zhongke Gengjiu Hospital in Anhui Province, China. The human SPC-A1 and A549 cell lines were chosen as the subjects for the relevant cellular experiments in this study. LncRNAs were expressed in a different manner identified by bioinformatics methods, and the expression levels in lung cancer tissues as well as cells were verified by the qRT-PCR assay. The biological role of LUCAT1 in NSCLC was determined by CCK-8, EdU, and transwell assay.

Results: The regulation of ubiquitin of P53 by LUCAT1 was studied, which showed that LUCAT1 was significantly elevated in NSCLC cell lines and patients’ tissues (P<0.05). High levels of LUCAT1 promoted the proliferation, invasion, and migration of NSCLC cells. Mechanism studies showed that LUCAT1 was mainly located in the nucleus, which bound to P53 and mediated the ubiquitinated degradation of P53. Meanwhile, LUCAT1 knockdown attenuated the ubiquitination process of P53. In addition, rescue experiments illustrated that LUCAT1 induced the proliferation and invasion of NSCLC cells, and played a key role in the survival and tumorigenicity of NSCLC cells by mediating the ubiquitination of P53.

Conclusion: Collectively, LUCAT1 activated the malignant phenotypes of NSCLC cells via regulating P53 ubiquitination, which provided a new idea for the diagnosis and treatment of NSCLC.