Ang-(1-7) promotes the migration and invasion of human renal cell carcinoma cells via Mas-mediated AKT signaling pathway

2015 ◽  
Vol 460 (2) ◽  
pp. 333-340 ◽  
Author(s):  
Shuai Zheng ◽  
Ying Yang ◽  
Ran Song ◽  
Xiaomei Yang ◽  
Hua Liu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Akt Signaling ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Human Renal Cell Carcinoma

scholarly journals Ampelopsin Inhibits Cell Viability and Metastasis in Renal Cell Carcinoma by Negatively Regulating the PI3K/AKT Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Zhonghe Zhao ◽  
Yan Jiang ◽  
Zhongguo Liu ◽  
Qingyan Li ◽  
Tiantian Gao ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway

Background. Previous studies have shown that Ampelopsin has an inhibitory effect on human tumors. However, the effect of Ampelopsin on renal cell carcinoma (RCC) is rarely reported. Therefore, this study aims to explain the role of Ampelopsin in RCC. Methods. Different concentrations of Ampelopsin (0, 10, 25, 50, and 100 μM) were used to treat 786-O cells. Cell viability was detected by MTT assay, colony formation assay, and flow cytometry assay. Transwell assay and Wound healing assay were used to detect cell migration and invasion. Western blot analysis was applied to detect protein expression. Results. Ampelopsin inhibited cell proliferation and induced apoptosis in RCC. And Ampelopsin can inhibit cell migration and invasion in RCC. All these results changed in a dose-dependent manner. Ampelopsin (100 uM) had the strongest inhibitory effect on cell viability and metastasis. In addition, Ampelopsin negatively regulated the PI3K/AKT signaling pathway in RCC cells. Moreover, Ampelopsin was only cytotoxic to RCC cells. Conclusion. Ampelopsin inhibits cell viability and metastasis in RCC by negatively regulating the PI3K/AKT signaling pathway.

scholarly journals Tuftelin 1 (TUFT1) Promotes the Proliferation and Migration of Renal Cell Carcinoma via PI3K/AKT Signaling Pathway

2021 ◽  
Vol 27 ◽  
Author(s):  
Hua Lin ◽  
Weifeng Zeng ◽  
Yuhang Lei ◽  
Desheng Chen ◽  
Zhen Nie
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Growth ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Akt Signaling ◽  
Pi3k Inhibitor ◽  
Akt Signaling Pathway ◽  
And Migration ◽  
Proliferation And Migration

Tuftelin 1 (TUFT1), a protein functioning distinctively in different tissues, is reported to be elevated in several types of cancers and the elevation of TUFT1 is correlated with unfavorable clinicopathologic characteristics and poor survival. However, the involvement of TUFT1 in renal cell carcinoma (RCC) remains unknown. In the current study, we investigated the role of TUFT1 in RCC and potential underlying mechanisms. RT-PCR and Western blot analysis showed that both the mRNA and protein levels of TUFT1 were increased in primary RCC tissue and RCC cell lines. TUFT1 overexpression in RCC cells resulted in enhanced cell proliferation and migration while knockdown of TUFT1 by contrast decreased the growth and migration of the RCC cells, indicating TUFT1 expression is involved in RCC cell growth and migration. The involvement of TUFT1 in the epithelial-mesenchymal transition (EMT) of RCC cells was also determined by measuring the expression of EMT-related markers. Our data showed that TUFT1 overexpression promoted RCC cell EMT progression while knockdown of TUFT1 suppressed such process. Further signaling pathway inhibition assay revealed that TUFT1-induced RCC cell growth, migration and EMT was significantly suppressed by PI3K inhibitor, but not JNK or MEK inhibitors. In addition, TUFT1 overexpression enhanced the AKT phosphorylation, a key member of the PI3K signaling pathway, while PI3K inhibitor suppressed such process. Taken together, our study showed that TUFT1 expression was elevated in RCC and such elevation promoted the proliferation, migration and EMT of RCC cells in vitro, through PI3K/AKT signaling pathway. The findings of our current study imply that TUFT1 is involved in RCC tumorigenesis, and it may serve as a biomarker for RCC diagnosis and a potential target for RCC treatment.

KIR2DL4 promotes the proliferation of renal cell carcinoma cells by PI3K/AKT signaling pathway activation

2021 ◽  
Author(s):  
Xiao-Fei Ding ◽  
Huai-Lu Ma ◽  
Jie Chen ◽  
Yong Liang ◽  
Yun-Fei Wang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Expression Profiles ◽  
Soft Agar ◽  
Akt Signaling ◽  
Akt Signaling Pathway

Abstract Background: Killer cell immunoglobulin-like receptor 2DL4 (KIR2DL4) is a transmembrane glycoprotein that is expressed by natural killer (NK) cells and certain subsets of T cells. It has been reported to serve an important role in the immune response. However, its expression profiles and function in solid tumor progression remain poorly defined.Methods: In the present study, using bioinformatics analysis, immunohistochemistry, immunoblotting, MTT assay, soft agar colony formation assay and a renal cell carcinoma (RCC) cell xenograft model in nude mice, we examined whether KIR2DL4 is expressed by RCC and its possible roles in RCC progression. Results: We confirmed that KIR2DL4 is overexpressed by RCC cells. MTT and soft agar cloning assays showed that KIR2DL4 knockdown delayed cell proliferation in RCC cell lines, Caki-1 and 769-P, in vitro. By contrast, KIR2DL4 overexpression promoted Caki-1 cell proliferation both in vitro and in vivo, which was observed in a BALB/c-nu/nu xenograft mouse model. Moreover, RNA sequencing data demonstrated that the differentially expressed genes between vector controlled and KIR2DL4-overexpressed Caki-1 cells were highly associated with cancer development, of which those related to the phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (AKT) signaling pathway were particularly enriched. Immunoblotting data showed that the level of AKT phosphorylation was higher in KIR2DL4-overexpressing Caki-1 cells compared with that in the parallel-controlled cells. Conclusions: Our results indicate that KIR2DL4 is also expressed by RCC cells, which promotes RCC progression through the PI3K/AKT signaling pathway.

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