scholarly journals Corrigendum: Myeloid-Derived Suppressor Cells Recruited by Chemokine (C-C Motif) Ligand 3 Promote the Progression of Breast Cancer via Phosphoinositide 3-Kinase-Protein Kinase B-Mammalian Target of Rapamycin Signaling

2020 ◽  
Vol 23 (5) ◽  
pp. 577
Author(s):  
Anqi Luo ◽  
Min Meng ◽  
Guanying Wang ◽  
Rui Han ◽  
Yujiao Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Suppressor Cells ◽  
Target Of Rapamycin ◽  
Myeloid Derived Suppressor Cells ◽  
Phosphoinositide 3 Kinase

Lupeol Inhibits Proliferation and Promotes Apoptosis of Ovarian Cancer Cells by Inactivating Phosphoinositide-3-Kinase/Protein Kinase B/ Mammalian Target of Rapamycin Pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 206-210
Author(s):  
Feng Chen ◽  
Bei Zhang
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Protein Kinase ◽  
Cell Viability ◽  
Cancer Cells ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Ovarian Cancer Cells ◽  
Phosphoinositide 3 Kinase

Lupeol exhibits multiple pharmacological activities including, anticancerous, anti-inflammatory, and antioxidant. The aim of this study was to explore the anticancerous activity of lupeol on ovarian cancer cells and examine its mechanism of action. To this end, increasing concentrations of lupeol on cell viability, cell cycle, and apoptosis in Caov-3 cells were evaluated. Lupeol inhibited cell viability, induced G1 phase arrest in cell cycle, increased cell apoptosis, and inhibited the ratio of phospho-Akt/protein kinase B and phospho-mammalian target of rapamycin/mammalian target of rapamycin. In conclusion, these data suggest that lupeol may play a therapeutic role in ovarian cancer.

Lupeol induces autophagy and apoptosis with reduced cancer stem-like properties in retinoblastoma via phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin inhibition

2021 ◽  
Author(s):  
Songtian Che ◽  
Shuai Wu ◽  
Peng Yu
Keyword(s):  
Protein Kinase ◽  
Cell Lines ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Inhibitory Effect ◽  
Target Of Rapamycin ◽  
Anticancer Effects ◽  
Retinoblastoma Cells ◽  
Phosphoinositide 3 Kinase

Abstract Objectives To evaluate the anticancer effects of lupeol in retinoblastoma cells. Methods WERI-Rb-1 and Y-79 cell lines were used to evaluate the anticancer effect of lupeol. After lupeol treatment, the viability, proliferation, apoptosis, cancer stem-like properties, autophagy and in vivo tumour xenograft formation were detected. Key findings In this study, lupeol decreased cell viability in both WERI-Rb-1 and Y-79 cell lines. Lupeol could also inhibit proliferation and induce apoptosis of RB cells, with increased Bax level and decreased Ki67, survivin and Bcl-2 levels. Furthermore, lupeol could suppress the spheroid formation and stem-like properties of RB cells. Moreover, LC3 II/LC3 I ratio and the levels of Beclin1 and ATG7 were increased after lupeol treatment, indicating that lupeol could induce autophagy in RB cells. Next, the inhibitory effect of lupeol on the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway was observed. In tumour-bearing mice, lupeol suppressed tumour growth, and this might relate to its role in cell apoptosis, autophagy and stem-like properties. Conclusions Lupeol suppressed proliferation and cancer stem-like properties, and promoted autophagy and apoptosis of RB cells by restraining the PI3K/AKT/mTOR pathway.

Baicalin Induces Apoptotic Death of Human Chondrosarcoma Cells through Mitochondrial Dysfunction and Downregulation of the PI3K/Akt/mTOR Pathway

Planta Medica ◽  
2018 ◽  
Vol 85 (05) ◽  
pp. 360-369 ◽  
Author(s):  
Minyu Zhu ◽  
Jinwei Ying ◽  
Chaowei Lin ◽  
Yu Wang ◽  
Kelun Huang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase B ◽  
Tumour Size ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Human Chondrosarcoma ◽  
Apoptotic Death ◽  
Phosphoinositide 3 Kinase

AbstractThe aim of the present study was to investigate the cytotoxic and antitumour effects of baicalin in human chondrosarcoma both in vivo and in vitro. We examined the effects of baicalin on the growth and apoptosis of human chondrosarcoma cells. Baicalin inhibited the growth of SW1353 and CH2879 cells in a dose- and time-dependent manner, but did not inhibit the growth of normal chondrocytes. Baicalin reduced tumour growth and induced apoptotic death in SW1353-transplanted nude mice without reducing their body weight. Further studies showed that baicalin reduced the mitochondrial membrane potential, upregulated the expression of Bax and cytoplasmic cytochrome c, downregulated the expression of Bcl-2 and mitochondrial cytochromes, and activated caspase-3 and caspase-9. Baicalin inhibited the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway by decreasing the expression of phosphorylated phosphoinositide 3-kinase, phosphorylated protein kinase B, and phosphorylated mammalian target of rapamycin both in vivo and in vitro. Moreover, the mice that received SC79 and baicalin exhibited a greater tumour size compared with the mice that received baicalin. The mice that received LY294002 and baicalin showed a smaller tumour size compared with the mice that received baicalin. In the in vitro study, SC79 and LY294002 affected the baicalin-induced cytotoxic effects on chondrosarcoma cells in the same manner. Our data suggest baicalin has therapeutic efficacy in human chondrosarcoma through the induction of apoptosis and inhibition of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway. Baicalin can be considered a potential therapeutic agent for treating chondrosarcomas.

scholarly journals Proteomic Profile of Carbonylated Proteins Screen Regulation of Apoptosis via CaMK Signaling in Response to Regular Aerobic Exercise

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Wenfeng Liu ◽  
Li Li ◽  
Heyu Kuang ◽  
Yan Xia ◽  
Zhiyuan Wang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Aerobic Exercise ◽  
Protein Kinase B ◽  
Mammalian Target Of Rapamycin ◽  
Rat Striatum ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
Phosphoinositide 3 Kinase

To research carbonylated proteins and screen molecular targets in the rat striatum on regular aerobic exercise, male Sprague-Dawley rats (13 months old, n = 24) were randomly divided into middle-aged sedentary control (M-SED) and aerobic exercise (M-EX) groups (n = 12 each). Maximum oxygen consumption (VO2max) gradually increased from 50%–55% to 65%–70% for a total of 10 weeks. A total of 36 carbonylated proteins with modified oxidative sites were identified by Electrospray Ionization-Quadrupole-Time of Flight-Mass Spectrometer (ESI-Q-TOF-MS), including 17 carbonylated proteins unique to the M-SED group, calcium/calmodulin-dependent protein kinase type II subunit beta (CaMKIIβ), and heterogeneous nuclear ribonucleoprotein A2/B1 (Hnrnpa2b1), among others, and 19 specific to the M-EX group, ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCH-L1), and malic enzyme, among others. Regular aerobic exercise improved behavioral and stereological indicators, promoted normal apoptosis (P < 0.01), alleviated carbonylation of the CaMKIIβ and Hnrnpa2b1, but induced carbonylation of the UCH-L1, and significantly upregulated the expression levels of CaMKIIβ, CaMKIIα, and Vdac1 (p < 0.01) and Hnrnpa2b1 and UCH-L1 (p < 0.01), as well as the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways (PI3K/Akt/mTOR) pathway-related genes Akt and mTOR. Regular aerobic exercise for 10 weeks (incremental for the first 6 weeks followed by constant loading for 4 weeks) enhanced carbonylation of CaMKIIβ, Hnrnpa2b1, and modulated apoptosis via activation of CaMK and phosphoinositide 3-kinase/protein kinase B/mTOR signaling. It also promoted normal apoptosis in the rat striatum, which may have protective effects in neurons.

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