Maslinic Acid Inhibits Proliferation of Renal Cell Carcinoma Cell Lines and Suppresses Angiogenesis of Endothelial Cells

Thakor, Parth; Song, Wenzhe; Subramanian, R. B.; Thakkar, Vasudev R.; Vesey, David A.; Gobé, Glenda C.

doi:10.15586/jkcvhl.2017.64

Cited by 37 publications

(24 citation statements)

References 49 publications

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“…Cells were seeded in 96-well plates (5 × 10 3 cells/well/100 μl) and MTT assay was performed as per previous reports ( 35 – 37 ). After pre-determined time periods (24 h–120 h), 5 μl of MTT (Sigma, MO, USA), from a 5 mg/ml stock in PBS, were added to each well of the culture plates and incubated for 90 min at 37 ° C in a humidified atmosphere of 95% air and 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Fully validated TaqMan Gene Expression Assay (Life Technologies) for Bax (Hs00180269_m1), Bcl2 (Hs00236808_m1), IL-6 (Hs00985639_m1), IL-8 (Hs00174103_m1) and VEGFA (Hs00900055_m1) was used with the SensiFAST™ Probe No-ROX Kit (Bioline, London, UK) in a LightCycler 480 (Roche Applied Science, Penzberg, Germany) to determine relative gene expression by the comparative Ct method. TBP (TATA box binding protein; Hs00427620_m1) was used as an internal control and for normalisation ( 35 – 37 ).…”

Section: Methodsmentioning

confidence: 99%

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Characterisation of the Morphological, Functional and Molecular Changes in Sunitinib-Resistant Renal Cell Carcinoma Cells

Kamli

Gobé

et al. 2018

jkcvhl

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Sunitinib resistance is a major clinical problem hampering the treatment of renal cell carcinoma (RCC). Studies on the comprehensive characterisation of morphological, functional and molecular changes in sunitinib-resistant RCC cells are lacking. The aim of the current study was to develop sunitinib resistance in four human RCC cell lines (786-0, Caki-1, Caki-2 and SN12K1), and to characterise the changed cell biology with sunitinib resistance. RCC cells were made resistant by continuous, chronic exposure to 10 μM of sunitinib over a period of 12 months. Cell proliferation, morphology, transmigration, and gene expression for interleukin-6 (IL-6), interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), Bcl-2 and Bax were studied. There was no significant difference in growth rate or transmigration between the parental and resistant cells. Sunitinib-resistant cells were significantly hypertrophic compared with parental cells as evidenced by increases in the surface areas of the whole cells and the nuclei. IL-6 was significantly increased in all resistant cells. IL-8 was increased in sunitinib-resistant Caki-2 and SN12K1 cells and decreased in 786-0 without any significant changes in Caki-1. VEGF was increased in resistant Caki-2 and SN12K1 cells but not in 786-0 and Caki-1. The Bcl2/Bax ratio was increased in Caki-1, Caki-2 and SN12K1 cells but decreased in 786-0 cells. The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Characterisation of the Morphological, Functional and Molecular Changes in Sunitinib-Resistant Renal Cell Carcinoma Cells

Kamli

Gobé

et al. 2018

jkcvhl

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“…Forty-eight hours later, total RNA was isolated using PureLink RNA Mini Kit (Life technologies, Carlsbad, CA) as per the manufacturer's protocol and quantified with Nano drop (Thermoscientific, Waltham, MA). cDNA was synthesized using a high capacity cDNA Reverse Transcription Kit (Life Technologies) as described before (Thakor et al 2017). In brief, 1 mg of RNA in an RT-PCR reaction mixture (2 mL 10Â buffer, 0.8 mL dNTP, 2 mL r-hex, 1 mL enzyme, water to 20 mL per reaction) was subjected to the following PCR conditions: 25 C 10 min, 37 C 60 min, 37 C 60 min, and 80 C for 5 min followed by holding at 4 C. The cDNA was diluted to 50 mL with 30 mL of RNAse-free water.…”

Section: Gene Expression Studiesmentioning

confidence: 99%

Indoxyl Sulfate Induces Apoptosis and Hypertrophy in Human Kidney Proximal Tubular Cells

Ellis

Small

et al. 2018

Toxicol Pathol

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Indoxyl sulfate (IS) is a protein-bound uremic toxin that accumulates in patients with declining kidney function. Although generally thought of as a consequence of declining kidney function, emerging evidence demonstrates direct cytotoxic role of IS on endothelial cells and cardiomyocytes, largely through the expression of pro-inflammatory and pro-fibrotic factors. The direct toxicity of IS on human kidney proximal tubular epithelial cells (PTECs) remains a matter of debate. The current study explored the effect of IS on primary cultures of human PTECs and HK-2, an immortalized human PTEC line. Pathologically relevant concentrations of IS induced apoptosis and increased the expression of the proapoptotic molecule Bax in both cell types. IS impaired mitochondrial metabolic activity and induced cellular hypertrophy. Furthermore, statistically significant upregulation of pro-fibrotic (transforming growth factor-β, fibronectin) and pro-inflammatory molecules (interleukin-6, interleukin-8, and tumor necrosis factor-α) in response to IS was observed. Albumin had no influence on the toxicity of IS. The results of this study suggest that IS directly induced a pro-inflammatory and pro-fibrotic phenotype in proximal tubular cells. In light of the associated apoptosis, hypertrophy, and metabolic dysfunction, this study demonstrates that IS may play a role in the progression of chronic kidney disease.

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“…In addition, it was reported that one-third of patients who underwent partial lesion resection experienced recurrence (4). The median survival rate of patients with metastatic cancer is ~13 months (5). Therefore, a more effective treatment for Rcc is urgently required.…”

Section: Introductionmentioning

confidence: 99%

“…Junctional adhesion molecule 3 (Jam3) is a vascular adhesion molecule, which regulates adhesion and interactions among or between cells and the extracellular matrix (5). It has been reported that Jam3 enhances the expression and activation of adhesion molecules in vascular endothelial cells (7,8).…”

Section: Introductionmentioning

confidence: 99%

Jam3 promotes migration and suppresses apoptosis of renal carcinoma cell lines

Yin

Zhang

et al. 2018

Int J Mol Med

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As a common type of renal cancer, renal cell carcinoma (RCC) has a high annual mortality rate. The incidence of RCC has been increasing in China and worldwide. A large number cases of RCC are diagnosed at late stages, often with local and/or systematic metastasis. Surgical resection of RCC is only suitable for a small number of patients with early stage tumors, and thus, novel therapeutic methods are required. Junctional adhesion molecule 3 (Jam3) is a member of the junctional adhesion molecule family, which has been linked to epithelial and cancer cell proliferation. The present study investigated whether the Jam3 gene affected RCC growth via proliferation and apoptosis. The expression and biological function of Jam3 in renal carcinoma cells was investigated. The mRNA and protein levels of Jam3 were examined by reverse transcription‑polymerase chain reaction and western blot analyses. The role of Jam3 in the migration and apoptosis of renal carcinoma cells was determined using small interfering RNA, wound‑healing assays, flow cytometry, and cell migration assays. In the cell migration assays, E‑cadherin, N‑cadherin, integrin β1, and matrix metalloproteinase (MMP)‑2 proteins were detected by western blot analysis. It was shown that the expression of Jam3 was significantly elevated in human renal carcinoma cells compared with that in renal tubular epithelial cells. The knockdown of Jam3 inhibited renal carcinoma cell migration and promoted renal carcinoma cell apoptosis. It also increased the protein levels of E‑cadherin and reduced the protein levels of N‑cadherin, integrin β1 and MMP‑2. The inhibition of Jam3 promoted migration and suppressed apoptosis of renal carcinoma cells via regulation of the expression of E‑cadherin, N‑cadherin, integrin β1 and MMP‑2. Therefore, Jam3 was suggested as a novel target gene for the diagnosis and treatment of RCC.

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Maslinic Acid Inhibits Proliferation of Renal Cell Carcinoma Cell Lines and Suppresses Angiogenesis of Endothelial Cells

Cited by 37 publications

References 49 publications

Characterisation of the Morphological, Functional and Molecular Changes in Sunitinib-Resistant Renal Cell Carcinoma Cells

Characterisation of the Morphological, Functional and Molecular Changes in Sunitinib-Resistant Renal Cell Carcinoma Cells

Indoxyl Sulfate Induces Apoptosis and Hypertrophy in Human Kidney Proximal Tubular Cells

Jam3 promotes migration and suppresses apoptosis of renal carcinoma cell lines

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