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Knockdown of ALPK2 blocks development and progression of renal cell carcinoma
Jie Jiang1, Peng Han1, Jian Qian1
1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract:
Renal cell carcinoma (RCC) is one of the most common malignant tumors in the urinary system, whose molecular mechanism is still not clear. ALPK2 is a member of alpha protein kinase family, and its relationship with RCC is never reported. In this study, expression of ALPK2 in tumor tissues or cells of RCC was detected by qPCR, western blotting and immunohistochemical analysis. The effects of ALPK2 knockdown on cell proliferation, colony formation, cell migration and apoptosis were assessed by MTT, colony formation assay, wound-healing assay, Transwell assay and flow cytometry, respectively. The influence of ALPK2 knockdown on tumor growth in vivo was evaluated by mice xenograft models. The results demonstrated that ALPK2 was upregulated in tumor tissues of RCC and its high expression was significantly associated with advanced stage and poor prognosis. Knockdown of ALPK2 could inhibited cell proliferation, colony formation and cell migration of RCC cells, while promoting cell apoptosis. The suppression of tumor growth in vivo by ALPK2 knockdown was also showed by using mice xenograft models. Moreover, the regulation of RCC by ALPK2 may involve Akt, CDK6, Cyclin D1 and PIK3CA signaling. Therefore, our studies suggested that ALPK2 may act as a tumor promotor in the development and progression of RCC, and could be considered as a novel therapeutic target for RCC treatment.
Insights
Alpha-protein kinase 2 (ALPK2) is upregulated in renal cell carcinoma (RCC) and promotes tumor growth. Inhibiting ALPK2 suppressed RCC progression and may offer a new therapeutic target for this common urinary system cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Renal cell carcinoma (RCC) is a prevalent urinary system malignancy with unclear molecular underpinnings.
- The role of alpha-protein kinase 2 (ALPK2) in RCC pathogenesis has not been previously investigated.
Purpose of the Study:
- To investigate the expression and functional role of ALPK2 in renal cell carcinoma (RCC).
- To evaluate ALPK2 as a potential therapeutic target for RCC treatment.
Main Methods:
- Quantitative PCR, Western blotting, and immunohistochemistry were used to assess ALPK2 expression in RCC tissues and cells.
- In vitro assays (MTT, colony formation, wound-healing, Transwell, flow cytometry) evaluated the impact of ALPK2 knockdown on RCC cell behavior.
- In vivo studies utilized mice xenograft models to assess the effect of ALPK2 knockdown on tumor growth.
Main Results:
- ALPK2 expression was significantly upregulated in RCC tumor tissues, correlating with advanced stage and poorer prognosis.
- ALPK2 knockdown inhibited RCC cell proliferation, colony formation, and migration, while inducing apoptosis.
- In vivo, ALPK2 knockdown suppressed tumor growth in mice xenograft models.
- ALPK2's regulatory role in RCC may involve the Akt, CDK6, Cyclin D1, and PIK3CA signaling pathways.
Conclusions:
- ALPK2 functions as a tumor promoter in the development and progression of renal cell carcinoma.
- ALPK2 represents a potential novel therapeutic target for the treatment of RCC.
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