Activates the Malignant Phenotypes of Lung Cancer Cells via Regulating Ubiquitination.

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 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 in NSCLC was determined by CCK-8, EdU, and transwell assay.

RESULTS

The regulation of ubiquitin of by was studied, which showed that was significantly elevated in NSCLC cell lines and patients' tissues (<0.05). High levels of promoted the proliferation, invasion, and migration of NSCLC cells. Mechanism studies showed that was mainly located in the nucleus, which bound to and mediated the ubiquitinated degradation of . Meanwhile, knockdown attenuated the ubiquitination process of . In addition, rescue experiments illustrated that 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 .

CONCLUSION

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