Background <p>Recent advancements in the study of SPOCD1 have highlighted its potential role in carcinogenesis. Nevertheless, the specific correlation between SPOCD1 expression level, survival outcomes, and immune cell infiltration in clear cell renal cell carcinoma (ccRCC) has not been fully elucidated.</p> Methods <p>To determine the possible connection between SPOCD1 expression levels, clinical pathological information, and overall survival (OS) in individuals with ccRCC, multiple databases encompassing TCGA, Gene Expression Profiling Interaction Analysis (GEPIA), and UALCAN were employed. Additionally, a comprehensive examination of the connection between tumor-infiltrating immune cells (TIIC) and SPOCD1 was executed through TIMER, GEPIA, and TISIDB databases. Western blot (WB) and Quantitative Real-Time PCR (qRT-PCR) were implemented to measure the SPOCD1 expression level in ccRCC cell lines. Immunohistochemistry (IHC) staning was utilized to identify the SPOCD1 expression in ccRCC tissues.</p> Results <p>SPOCD1 expression was discovered to have a notable correlation with the TNM stage, pathologic stage, and histologic grade. Elevated SPOCD1 expression exhibited associations with poor Disease-Specific Survival (DSS) and OS outcomes (<i>p</i> &lt; 0.01). Subsequent evaluation identified a notable connection between SPOCD1 overexpression and the expression of immunomodulators and chemokines. Additionally, SPOCD1 overexpression was linked to increased infiltration of macrophages, regulatory T cells (Treg), Th1 cells, dendritic cells (DC), and Th2 cells in ccRCC tissues. Validation through qRT-PCR, WB, and IHC confirmed that SPOCD1 acts as an oncogene in ccRCC.</p> Conclusions <p>SPOCD1 represents a potential prognostic indicator for patients with ccRCC. Elevated SPOCD1 expression is strongly associated with unfavorable clinicopathological features, poorer survival outcomes, and increased immune cell infiltration in ccRCC.</p>

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SPOCD1 expression in clear cell renal cell carcinoma: its implications for the prognosis and immunotherapy

  • Wu Xu,
  • Lingfei Yan,
  • Yufeng Liu,
  • Dawei Liu,
  • Dali Wu,
  • Yang Luo,
  • Cuilian Li,
  • Qing Li,
  • Tao Wang

摘要

Background

Recent advancements in the study of SPOCD1 have highlighted its potential role in carcinogenesis. Nevertheless, the specific correlation between SPOCD1 expression level, survival outcomes, and immune cell infiltration in clear cell renal cell carcinoma (ccRCC) has not been fully elucidated.

Methods

To determine the possible connection between SPOCD1 expression levels, clinical pathological information, and overall survival (OS) in individuals with ccRCC, multiple databases encompassing TCGA, Gene Expression Profiling Interaction Analysis (GEPIA), and UALCAN were employed. Additionally, a comprehensive examination of the connection between tumor-infiltrating immune cells (TIIC) and SPOCD1 was executed through TIMER, GEPIA, and TISIDB databases. Western blot (WB) and Quantitative Real-Time PCR (qRT-PCR) were implemented to measure the SPOCD1 expression level in ccRCC cell lines. Immunohistochemistry (IHC) staning was utilized to identify the SPOCD1 expression in ccRCC tissues.

Results

SPOCD1 expression was discovered to have a notable correlation with the TNM stage, pathologic stage, and histologic grade. Elevated SPOCD1 expression exhibited associations with poor Disease-Specific Survival (DSS) and OS outcomes (p < 0.01). Subsequent evaluation identified a notable connection between SPOCD1 overexpression and the expression of immunomodulators and chemokines. Additionally, SPOCD1 overexpression was linked to increased infiltration of macrophages, regulatory T cells (Treg), Th1 cells, dendritic cells (DC), and Th2 cells in ccRCC tissues. Validation through qRT-PCR, WB, and IHC confirmed that SPOCD1 acts as an oncogene in ccRCC.

Conclusions

SPOCD1 represents a potential prognostic indicator for patients with ccRCC. Elevated SPOCD1 expression is strongly associated with unfavorable clinicopathological features, poorer survival outcomes, and increased immune cell infiltration in ccRCC.