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. 2025 Feb 5;23(1):42.
doi: 10.1186/s12957-025-03658-9.

PTEN suppresses renal cell carcinoma proliferation and migration via inhibition of the PI3K/AKT pathway

Xu Xu #  1 , Yuan-Yue Tang #  1 , Xiaohong Liang #  2 , Wen Luo  1 , Dong-Mei Jiang  3 , Jie Chen  4
Affiliations

PTEN suppresses renal cell carcinoma proliferation and migration via inhibition of the PI3K/AKT pathway

Xu Xu et al. World J Surg Oncol. .

Abstract

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.

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.

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.

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.

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.

Keywords: Cell migration; Cell proliferation; PI3K/AKT pathway; PTEN; Renal cell carcinoma.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: The study protocol was approved by the Institutional Review Board of The First Affiliated Hospital of Naval Medical University. Informed consent was obtained from all patients participating in the study. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
PTEN mRNA and Protein Expression in RCC Tissues and Cell Lines. (A) PTEN mRNA levels in Normal and Tumor tissues; (B) PTEN mRNA levels in HK-2 and 786-O cell lines; (C) PTEN protein levels in HK-2 and 786-O cell lines. Compared to the Normal and HK-2 group, **p < 0.01
Fig. 2
Fig. 2
Effects of PTEN overexpression on RCC cells. (A) PTEN mRNA levels in Control, Vector, and oe-PTEN groups; (B) PTEN protein levels in Control, Vector, and oe-PTEN groups; (C) Cell viability assessed by CCK-8 assay in Control, Vector, and oe-PTEN groups; (D) Cell migration assessed by wound healing assay in Control, Vector, and oe-PTEN groups. Compared to the Vector group, *p < 0.05
Fig. 3
Fig. 3
Effects of PTEN overexpression on PI3K/AKT pathway proteins in RCC cells. (A) Western blot analysis of PTEN, p-AKT, AKT, p-PI3K, and PI3K protein levels in Control, Vector, and oe-PTEN groups; (B) Quantification of protein levels, showing significantly lower p-AKT/AKT and p-PI3K/PI3K ratios in the oe-PTEN group. Compared to the Vector group, *p < 0.05
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