Overexpression of Capns1 Predicts Poor Prognosis and Correlates with Tumor Progression in Renal Cell Carcinoma

2021 ◽  
pp. 1-8
Author(s):  
Qianfeng Zhuang ◽  
Min Fan ◽  
Jie Shen ◽  
Zhen Chen ◽  
Dong Xue ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Prognostic Marker ◽  
Renal Cell ◽  
Poor Prognosis ◽  
Cox Regression ◽  
Migration And Invasion ◽  
Human Renal Cell Carcinoma ◽  
Tumor Tissues

<b><i>Introduction:</i></b> Calpain small subunit 1 (Capns1) has shown its correlation with the metastasis and invasion of hepatocellular carcinoma and intrahepatic cholangiocarcinoma. However, the expression and function of Capns1 in human renal cell carcinoma (RCC) have not been clarified. This study aimed to examine the expression of Capns1 in RCC tissues and cell lines and to assess its role performed in RCC. <b><i>Methods:</i></b> Capns1 expression was evaluated in 75 pairs of RCC and matched adjacent non-tumor tissues by immunohistochemistry. The prognostic value of Capns1 in RCC was assessed by Kaplan-Meier and Cox regression analyses. The action of Capns1 in the proliferation, adhesion, migration, and invasion of RCC cells and the effects on matrix metalloproteinase (MMP) 2 and 9 expression were evaluated after Capns1 silence. <b><i>Results:</i></b> Capns1 expression was significantly higher in RCC tissues compared with the adjacent non-tumor tissues. Multivariate analysis showed that Capns1 overexpression was an independent poor prognostic marker in RCC. The silencing of Capns1 prohibited cell adhesion and impaired the migration and invasion ability of 786-O cells in vitro. Furthermore, Capns1 silence reduced MMP2 and MMP9 expression. <b><i>Conclusion:</i></b> Capns1 overexpression predicts poor prognosis and correlates with tumor progression in RCC. Capns1 expression might serve a prognostic marker and therapeutic target for RCC.

scholarly journals Role of PDL1 as a prognostic marker in renal cell carcinoma: a prospective observational study in eastern India

2019 ◽  
Vol 11 ◽  
pp. 175628721986885
Author(s):  
Barun Kumar ◽  
Amlan Ghosh ◽  
Chhanda Datta ◽  
Dilip Kumar Pal
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Prognostic Marker ◽  
Renal Cell ◽  
Poor Prognosis ◽  
Disease Recurrence ◽  
Programmed Death ◽  
Specific Mortality ◽  
Cancer Specific Mortality

Background: Renal cell carcinoma (RCC) is one of the most common genitourinary malignancies. Programmed death ligand-1 (PDL1) is an immune checkpoint inhibitor, instrumental in ‘T cell escape’ of malignant cells. PDL1 has been shown to be associated with poor prognosis in multiple small studies. In this study, we want to study the role of PDL1 as a prognostic marker in RCC in an Indian population. Methods: A total of 30 patients who underwent radical or partial nephrectomy, with histopathological findings of RCC, were included in the study. PDL1 expression was studied in tumour tissue with immunohistochemistry. Patients were followed up for a period of 2 years for disease recurrence and cancer-specific mortality. Results: Expression of PDL1 was seen to be associated with higher grade and stage at presentation. PDL1 expression was also associated with statistically significant increased incidence of disease recurrence. Although cancer-specific mortality was higher in patients with positive PDL1 expression, it was seen to be statistically insignificant. Conclusions: PDL1 is a novel prognostic marker for RCC and is associated with poor prognosis. More studies with larger patient pool and multicentric studies will establish the role of PDL1 with certainty. This can be the torchbearer for the future management of RCC.

Altered glutathione anti-oxidant metabolism during tumor progression in human renal-cell carcinoma

2000 ◽  
Vol 91 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Lorenzo Lusini ◽  
Sergio Antonio Tripodi ◽  
Ranieri Rossi ◽  
Fabiola Giannerini ◽  
Daniela Giustarini ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Human Renal Cell Carcinoma ◽  
Anti Oxidant

scholarly journals HCRP-1 regulates cell migration and invasion via EGFR-ERK mediated up-regulation of MMP-2 with prognostic significance in human renal cell carcinoma

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Feifei Chen ◽  
Junpeng Deng ◽  
Xin Liu ◽  
Wang Li ◽  
Junnian Zheng
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Renal Cell ◽  
Prognostic Significance ◽  
Migration And Invasion ◽  
Human Renal Cell Carcinoma ◽  
Cell Migration And Invasion ◽  
Erk Phosphorylation

Abstract Previous studies indicated a role of hepatocellular carcinoma-related protein-1(HCRP-1) in human cancers, however, its expression pattern in renal cell carcinoma (RCC) and the molecular mechanism of HCRP-1 on cancer progression have not been characterized. In the present study, HCRP-1 expression was examined in a RCC tissue microarray. The negative expression of HCRP-1 was significantly correlated with tumor grade (P = 0.002), TNM stage (P = 0.001) and pT status (P = 0.003). Furthermore, we showed a strong correlation between negative HCRP-1 expression and worse overall and disease-specific survival (P = 0.0003 and P = 0.0012, respectively). Knockdown of HCRP-1 promoted cell migration and invasion in 786-O and OS-RC-2 cell lines. HCRP-1 depletion increased matrix metalloproteinase (MMP)-2 protein level, with increased extracellular signal-regulatedkinase (ERK) phosphorylation, which could be reversed by ERK siRNA or ERK inhibitor, PD98059. Further analysis showed that HCRP-1 knockdown induced epidermal growth factor receptor (EGFR) phosphorylation. Treatment with EGFR inhibitor or EGFR siRNA blocked HCRP-1-mediated up-regulation of EGFR, ERK phosphorylation and MMP-2 expression. In summary, our results showed that negative HCRP-1 expression is an independent prognostic factor for RCC patients and promotes migration and invasion by EGFR-ERK-mediated up-regulation of MMP-2. HCRP-1 may serve as a therapeutic target for RCC.

scholarly journals Expression of lactate dehydrogenase C correlates with poor prognosis in renal cell carcinoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769596 ◽  
Author(s):  
Yibo Hua ◽  
Chao Liang ◽  
Jundong Zhu ◽  
Chenkui Miao ◽  
Yajie Yu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Lactate Dehydrogenase ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Poor Prognosis ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Lactate Dehydrogenase C

Lactate dehydrogenase C is an isoenzyme of lactate dehydrogenase and a member of the cancer–testis antigens family. In this study, we aimed to investigate the expression and functional role of lactate dehydrogenase C and its basic mechanisms in renal cell carcinoma. First, a total of 133 cases of renal cell carcinoma samples were analysed in a tissue microarray, and Kaplan–Meier survival curve analyses were performed to investigate the correlation between lactate dehydrogenase C expression and renal cell carcinoma progression. Lactate dehydrogenase C protein levels and messenger RNA levels were significantly upregulated in renal cell carcinoma tissues, and the patients with positive lactate dehydrogenase C expression had a shorter progression-free survival, indicating the oncogenic role of lactate dehydrogenase C in renal cell carcinoma. In addition, further cytological experiments demonstrated that lactate dehydrogenase C could prompt renal cell carcinoma cells to produce lactate, and increase metastatic and invasive potential of renal cell carcinoma cells. Furthermore, lactate dehydrogenase C could induce the epithelial–mesenchymal transition process and matrix metalloproteinase-9 expression. In summary, these findings showed lactate dehydrogenase C was associated with poor prognosis in renal cell carcinoma and played a pivotal role in the migration and invasion of renal cell carcinoma cells. Lactate dehydrogenase C may act as a novel biomarker for renal cell carcinoma progression and a potential therapeutic target for the treatment of renal cell carcinoma.

scholarly journals LncRNA POU3F3 Promotes Cancer Cell Proliferation, Migration, and Invasion in Renal Cell Carcinoma by Downregulating LncRNA GAS5

2021 ◽  
pp. 1-7
Author(s):  
Lei Zhang ◽  
Cezheng Wang ◽  
Min Ma
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
In Situ Hybridization ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Tumor Tissues ◽  
Lncrna Gas5

<b><i>Background:</i></b> LncRNAs play regulatory roles in diverse nephrological disorders, including renal cancer. Overexpression of lncRNA POU3F3 (POU3F3) has only been reported in esophageal squamous-cell carcinomas, indicating POU3F3 may be an oncogene in this disease. LncRNA GAS5 (GAS5) was reported to be a suppressor in various tumors. However, the roles and underlying mechanism of POU3F3 and GAS5 involved in renal cell carcinoma (RCC) remain unknown. <b><i>Methods:</i></b> Real-time quantitative PCR and in situ hybridization were performed to determine the expression of POU3F3 and GAS5 in paired tumor and adjacent healthy tissues donated by 68 RCC patients. The prognostic values of POU3F3 and GAS5 for RCC were analyzed by performing a 5-year follow-up study. Overexpression of POU3F3 and GAS5 was achieved in RCC cells to explore the interactions between them. Transwell assay and cell proliferation assay were performed to evaluate the role of POU3F3 and GAS5 in regulating RCC cell proliferation, migration, and invasion. <b><i>Results:</i></b> In the present study, we found that POU3F3 was upregulated while GAS5 was downregulated in tumor tissues than that in adjacent healthy tissues of patients with RCC. In situ hybridization analysis showed that POU3F3 was mostly expressed in tumor tissues, while GAS5 was mostly expressed in adjacent healthy tissues. High level of POU3F3 and low level of GAS5 were closely correlated with poor prognosis of RCC patients. Expression levels of POU3F3 and GAS5 were significantly and inversely correlated in tumor tissues but not in adjacent healthy tissues of RCC patients. Overexpression of POU3F3 mediated the downregulation of GAS5 in RCC cells, while GAS5 overexpression failed to significantly affect POU3F3 expression. Overexpression of POU3F3 led to promoted, while GAS5 overexpression led to inhibited proliferation, migration, and invasion of RCC cells. In addition, GAS5 overexpression attenuated the enhancing effects of POU3F3 overexpression on cancer cell proliferation, migration, and invasion. <b><i>Conclusion:</i></b> POU3F3 promoted cell proliferation, migration, and invasion in RCC possibly by downregulating GAS5.

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