Background
Renal cell carcinoma (RCC) is a frequent and aggressive type of kidney cancer with limited therapeutic options. Although phosphatase and tensin homolog (PTEN) have been recognized as a potential tumor suppressor in all kinds of cancers, its function in RCC remains to be thoroughly elucidated.
Conclusion
Our findings demonstrate that PTEN overexpression in RCC cells leads to decreased PI3K/AKT signaling, decreasing cell viability and migration. This study highlights the critical role of PTEN in RCC progression and suggests potential therapeutic targets for intervention.
Methods
This study collected renal cancer and adjacent non-cancerous tissue samples from our hospital. HK-2 and 786-O cells were used, with 786-O cells divided into control, vector, and oe-PTEN groups. PTEN and related protein levels were detected using RT-qPCR and Western blot. Statistical analyses were performed using the Mann-Whitney U test and Kruskal-Wallis H test. Cell viability and migration were assessed using the CCK-8 assay and wound healing assay. All analyses were conducted with SPSS 22.0 software, with statistical significance defined as p < 0.05.
Objective
This article was recruited to examine the PTEN's role in managing the PI3K/AKT pathway and its impact on the RCC cell proliferation and migration.
Results
RT-qPCR results showed that PTEN expression was significantly increased in RCC tumor tissues compared to normal tissues (p < 0.01). However, PTEN mRNA levels were significantly reduced in 786-O cells compared to HK-2 cells (p < 0.01). In 786-O cells with low PTEN expression, further induction of PTEN overexpression significantly inhibited PI3K/AKT signaling activity (p < 0.01), accompanied by decreased cell viability and migration ability. These results indicate that the expression pattern of PTEN in RCC is complex, but its overexpression can exert tumor-suppressive effects by inhibiting the PI3K/AKT signaling pathway.