Involvement of activation of PI3K/Akt pathway in the protective effects of puerarin against MPP+-induced human neuroblastoma SH-SY5Y cell death

Zhu, Guoqi; Wang, Xuncui; Wu, Sheng-Bing; Li, Qinglin

doi:10.1016/j.neuint.2012.01.003

Cited by 99 publications

(74 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…15 Cells were seeded at 4 Â 10 5 cells per well in a 6-well plate and incubated overnight. Twenty-four hours after shRNA Gal-3 inhibition, cell lysates were assayed for Caspase-3 activity.…”

Section: Quantification Of Caspase-3 Activitymentioning

confidence: 99%

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

Sun

et al. 2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Galectins are thought to be prognosticators for survival in renal cell cancer. However, the biological activity of galectin-3 (Gal-3) in renal carcinoma cells is still debated. In this study, immunohistochemical staining confirmed a high expression of Gal-3 in tumor tissue from renal cell carcinoma. Critically, Gal-3 expression was related to tumor cell differentiation. Consistent with Gal-3 expression in renal cell cancer, strong expression of Gal-3 was also observed in several renal tumor cell lines but not in normal renal cells. A Gal-3 high-expression cell line Caki-1 was chosen to study the biological activity of Gal-3. Using short hairpin RNA method, Gal-3 expression in Caki-1 cells was knocked down. We evidenced that Gal-3 knockdown inhibited cell proliferation and invasion, induced Caspase-3-dependent apoptosis and arrested cell cycle at G1 phase. Mechanically, Cyclin D1 expression decreased, but p27 increased after Gal-3 knockdown. Taken together, these results suggest that Gal-3 is related to the development of renal cell cancer and could serve as a target to therapy renal cell cancer.

show abstract

Section: Quantification Of Caspase-3 Activitymentioning

confidence: 99%

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

Sun

et al. 2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

show abstract

“…Furthermore, we showed that puerarin could block CoCl 2 -induced hypoxic damage on b-cell function and survival, because CoCl 2 is also commonly used as a hypoxia-like inducer and the puerarin protection was mediated through upregulating the anti-oxidant Sod2 and Gpx1, and the anti-apoptotic Bcl-2, while decreasing the pro-apoptotic Bax. Puerarin has beneficial effects in various tissues, including hepatocyte, neural cells, kidney, endothelial cells, and osteoblastic cells, protecting the cell survival from a variety of damage, such as b-amyloid, lead, 1-methyl-4-phenylpyridinium iodide, cisplatin, especially oxidative stress, in which PI3K/Akt played a pivotal role (Hwang & Jeong 2008, Hwang et al 2011, Xing et al 2011, Zhang et al 2012, Zhu et al 2012. Here, in clonial MIN6 b-cells, we observed a rapid activation of Akt phosphorylation by puerarin.…”

Section: Discussionmentioning

confidence: 56%

Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

Li¹,

Shangguan²,

Liu³

et al. 2014

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Pancreatic b-cell loss because of apoptosis is the major cause of type 1 diabetes (T1D) and late stage T2D. Puerarin possesses anti-diabetic properties; whether it acts directly on pancreatic b-cell is not clear. This study was designed to investigate the effects of puerarin on pancreatic b-cell survival and function. Diabetes was induced in male C57BL/6 mice by a single peritoneal injection of streptozotocin (STZ). Pancreatic b-cell survival and function were assessed in diabetic mice by measuring b-cell apoptosis, b-cell mass, pancreatic insulin content, and glucose tolerance, and in cultured islets and clonial MIN6 b-cells by measuring b-cell viability and apoptosis and glucose-stimulated insulin secretion. We found that pre-treatment with puerarin decreased the incidence of STZ-induced diabetes. Puerarin increased pancreatic b-cell mass via b-cell apoptosis inhibition in diabetic mice, and increased serum insulin, whereas it decreased blood glucose levels and improved glucose tolerance. In cultured islets and MIN6 cells, puerarin protected b-cell from cobalt chloride (CoCl 2 )-induced apoptosis and restored the impaired capacity of glucose-stimulated insulin secretion. Puerarin protection of b-cell survival involved the phosphoinositide 3-kinase (PI3K) /Akt signaling pathway. In conclusion, puerarin protects pancreatic b-cell function and survival via direct effects on b-cells, and its protection of b-cell survival is mediated by the PI3K/Akt pathway. As a safe natural plant extraction, puerarin might serve as a preventive and/or therapeutic approach for diabetes.

show abstract

“…At 6 h later, the medium was changed into DMEM. The cells were then cultured in DMEM containing 10% FBS for another 24, 48 and 72 h. An MTT assay was utilized to detect cell proliferation, as previously described (15). In total, 150 µl DMSO (Sigma-Aldrich; Merck KGaA) was added to each well in order to dissolve formazan.…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

Anticancer effect of miR-96 inhibitor in bladder cancer cell lines

et al. 2018

Oncol Lett

View full text Add to dashboard Cite

Abstract. The present study aimed to investigate the role of microRNA-96 (miR-96) in the proliferation, invasion and apoptosis of bladder cancer cell lines, and the associated mechanisms. The expression of miR-96 and human ether-à-go-go-related (HERG1) potassium channel in the normal uroepithelium SV-HUC-1 cell line, and bladder cancer T24 and 5637 cell lines were examined using reverse transcription-polymerase chain reaction or/and western blotting. Transfection with miR-96 inhibitor or scrambled control (SC) was used to study the biological activities of miR-96 in bladder cancer cell lines. MTT, flow cytometric and Transwell assays were applied to detect cell viability, apoptosis and invasion, respectively. A dual-luciferase reporter assay was applied to determine the association between miR-96 and HERG1 expression. As demonstrated, miR-96 was highly expressed in the two bladder cancer cell lines, particularly in T24 cells. Following transfection with miR-96 inhibitor, miR-96 expression was significantly reduced in the T24 cell line, compared with SC. The miR-96 inhibitor suppressed cell proliferation and invasion, promoted apoptosis and arrested the cell cycle at the G 1 phase. Consistently, HERG1 was also highly expressed in the two bladder cancer cell lines at the mRNA and protein level, but not in the normal uroepithelium cell line. The miR-96 inhibitor also significantly decreased HERG1 expression compared with SC. The results of the dual-luciferase reporter assay indicated that miR-96 directly targeted wild-type HERG1. In conclusion, miR-96 inhibitor exhibited anticancer effects on bladder cancer cells by inhibiting proliferation and invasion of cells, and promoting their apoptosis. HERG1 was an important target of miR-96. These results provided experimental evidence supporting miR-96 as a therapeutic target for patients with bladder cancer.

show abstract

Involvement of activation of PI3K/Akt pathway in the protective effects of puerarin against MPP+-induced human neuroblastoma SH-SY5Y cell death

Cited by 99 publications

References 51 publications

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

Anticancer effect of miR-96 inhibitor in bladder cancer cell lines

Contact Info

Product

Resources

About