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Updated: Mar 2, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
Downregulation of ATP1A1 promotes cancer development in renal cell carcinoma
Dan Zhang1, Peng Zhang2, Pengbo Yang1
1State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, No.17 Section 3, People's South Road, Chengdu, 610041 People's Republic of China.
Background:
Aberrant expression of Na+/K+-ATPase α1 subunit (ATP1A1) is widely observed in multiple types of tumors, and its tissue-specific expression relates to cancer development. However, the functions and molecular mechanisms in renal cell carcinoma (RCC) are not fully understood.
Methods:
We investigated the ATP1A1 expression changes and possible roles in RCC through a quantitative proteomic approach and an integrative biochemical assessment. We detected ATP1A1 in RCC with LC-MS/MS, and further validated its expression with immunohistochemical analyses of 80 pairs of the RCC tumor and non-tumor tissues samples. The association of ATP1A1 expression with RCC pathology was statistically analyzed. Cell proliferation, migration and apoptosis were measured by CCK-8, boyden chamber assay and flow cytometry, respectively. The production of reactive oxygen species (ROS) was labeled with a single staining using a commercial kit, and was further detected with flow cytometry.
Results:
The ATP1A1 shows a significantly decreased expression in human RCC tissues than in the adjacent non-tumor tissues. The RCC patients with ATP1A1-positive expression exhibit longer overall survival time than the ATP1A1-negative patients. The exogenous overexpression of ATP1A1 inhibits RCC cell proliferation and cell migration by increasing the production of ROS. In addition, ATP1A1-mediated Raf/MEK/ERK signaling pathway is suppressed in RCC cells, indicating the possible occurrence of induced cell apoptosis.
Conclusions:
Our in vitro and in vivo data of ATP1A1 inhibitory roles in RCC progression suggest that ATP1A1 is a potential novel suppressor protein for renal cancer.
Insights
The Na+/K+-ATPase α1 subunit (ATP1A1) is decreased in renal cell carcinoma (RCC) and acts as a tumor suppressor. Higher ATP1A1 expression correlates with better patient survival, inhibiting RCC progression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Aberrant Na+/K+-ATPase α1 subunit (ATP1A1) expression is linked to various cancers.
- The specific role of ATP1A1 in renal cell carcinoma (RCC) progression remains unclear.
Purpose of the Study:
- To investigate ATP1A1 expression and its functional significance in RCC.
- To elucidate the molecular mechanisms underlying ATP1A1's role in renal cancer.
Main Methods:
- Quantitative proteomics (LC-MS/MS) and immunohistochemistry were used to assess ATP1A1 expression in 80 RCC and adjacent non-tumor tissues.
- Cellular assays (CCK-8, Boyden chamber, flow cytometry) measured proliferation, migration, and apoptosis.
- Reactive oxygen species (ROS) production and the Raf/MEK/ERK pathway were analyzed.
Main Results:
- ATP1A1 expression was significantly decreased in RCC tissues compared to non-tumor tissues.
- Positive ATP1A1 expression in RCC patients correlated with longer overall survival.
- Overexpression of ATP1A1 inhibited RCC cell proliferation and migration, increased ROS production, and suppressed the Raf/MEK/ERK pathway, promoting apoptosis.
Conclusions:
- ATP1A1 acts as a suppressor protein in renal cell carcinoma.
- Decreased ATP1A1 expression is associated with RCC progression and poorer prognosis.
- ATP1A1 represents a potential therapeutic target for renal cancer.
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