NUPR1 CONTRIBUTION TO AUTOPHAGY IN PRIMARY BONE TUMOR CELLS BY REGULATING THE AKT/MTOR SIGNALING PATHWAY

Weiwei Liu^{1, *}, Zhengzhong Feng², Nana Qu¹, Rui Li¹, Yangfang Niu¹ 

¹Department of Spinal Surgery, Suizhou Central Hospital, Affiliated Hospital of Hubei Medical College, Suizhou, Hubei441300, China - ²Emergency Department, Taihe Hospital, Affiliated Hospital of Hubei Medical College, Shiyan, Hubei430050, China

Objective: The study aimed to explore nuclear protein 1 (nupr1) involvement in cell autophagy in primary bone tumors through regulation of protein kinase B (Akt)/mammalian target of rapamycin (TOR) signaling pathway. 

Methods: Primary bone tumor cells were selected; after culture, they were divided into model blank and silenced nupr1 groups to detect nupr1 mRNA and Akt mRNA, and mTOR mRNA expression, respectively. Further, Akt, mTOR, Bax, Bcl-2, PCNA, and PTEN protein expression was determined using Western blot to detect cell invasion and migration. Finally, cell proliferation, apoptosis, and autophagy were analyzed. 

Results: Compared with the model blank group, the mRNA of nupr1 decreased in the group with silenced nupr1, accompanied by decreased mRNA expression of Akt and mTOR. Compared with the model blank group, the protein expression of Akt and mTOR was lower in the group with silenced nupr1. Also, the silenced nupr1 group showed higher Bax protein expression and lower Bcl-2 protein expression compared to the model blank group. PCNA protein expression was lower, and PTEN protein expression was higher in the group with silenced nupr1 than the model group. Compared with the blank group, the number of invasive cells and the number of migrated cells in the group with upregulated nupr1 were lower. Finally, compared with the blank group, the upregulated nupr1 group showed a lower cell proliferation rate and a higher apoptosis rate. 

Conclusion: In primary bone tumor cells, nupr1 is targeted to regulate Akt/mTOR signaling pathway; simultaneously, it has a certain link with cell autophagy, and through nupr1 silencing expression, it decreases bone tumor cell invasion and migration, inhibits cell proliferation, elevates the rate of apoptosis, and promotes cell autophagy.