Only in Titles

Search results for: p27

paperclip

#33984593   2021/04/18 To Up

Fuzheng Jiedu Xiaoji formulation inhibits hepatocellular carcinoma progression in patients by targeting the AKT/CyclinD1/p21/p27 pathway.

Hepatocellular carcinoma (HCC) is a common malignant tumor with limited treatment options. Conventional antitumor therapy combined with traditional Chinese medicine (TCM) to limit tumor progression has gradually become the focus of complementary and alternative therapies for HCC treatment. The Fuzheng Jiedu Xiaoji formulation (FZJDXJ) alleviates the clinical symptoms of patients and inhibits tumor progression, but its curative effect still requires extensive clinical research and mechanistic analysis.
Xue Yang, Ying Feng, Yao Liu, Xieqiong Ye, Xiaomin Ji, Le Sun, Fangyuan Gao, Qun Zhang, Yuxin Li, Bingbing Zhu, XianBo Wang

1247 related Products with: Fuzheng Jiedu Xiaoji formulation inhibits hepatocellular carcinoma progression in patients by targeting the AKT/CyclinD1/p21/p27 pathway.

2 Pieces/Box

Related Pathways

    No related Items
paperclip

#33981016   2021/05/12 To Up

Targeting the actin/tropomyosin cytoskeleton in epithelial ovarian cancer reveals multiple mechanisms of synergy with anti-microtubule agents.

Anti-microtubule agents are widely used to treat ovarian cancers, but the efficacy is often compromised by drug resistance. We investigated co-targeting the actin/tropomyosin cytoskeleton and microtubules to increase treatment efficacy in ovarian cancers and potentially overcome resistance.
Xing Xu, Yao Wang, Nicole S Bryce, Katrina Tang, Nicola S Meagher, Eun Young Kang, Linda E Kelemen, Martin Köbel, Susan J Ramus, Michael Friedlander, Caroline E Ford, Edna C Hardeman, Peter W Gunning

1416 related Products with: Targeting the actin/tropomyosin cytoskeleton in epithelial ovarian cancer reveals multiple mechanisms of synergy with anti-microtubule agents.



Related Pathways

paperclip

#33980961   2021/05/12 To Up

Sex-dependent effects of forced exercise in the body composition of adolescent rats.

Determining the body composition during adolescence can predict diseases such as obesity, diabetes, and metabolic syndromes later in life; and physical activity became an effective way to restore changes in body composition. However, current available literature assessing the body composition before, during and after adolescence in female and male rodents by in vivo techniques is scarce. Thus, by using computerized tomography, we aimed to define the baseline of the weight and body composition during the adolescence and young adulthood of female and male Sprague-Dawley rats (on P30, P60 and P90) under standard diet. Then, we determined the effect of 18 days of forced exercise on the body weight and composition during the early adolescence (P27-45). The highest percentual increments in weight, body volume and relative adipose contents occurred during the female and male adolescence. Forced running during the early adolescence decreased weight, body volume and relative adipose delta and increment values in males only. The adolescence of rats is a period of drastic body composition changes, where exercise interventions have sex-dependent effects. These results support a model that could open new research windows in the field of adolescent obesity.
Y Kutsenko, A Barreda, A Toval, D Garrigos, M Martínez-Morga, B Ribeiro Do Couto, J L Ferran

1983 related Products with: Sex-dependent effects of forced exercise in the body composition of adolescent rats.

0.1mg96 tests1 5 G

Related Pathways

paperclip

#33979259   2021/05/12 To Up

Romidepsin (FK228) fails in counteracting the transformed phenotype of rhabdomyosarcoma cells but efficiently radiosensitizes, and , the alveolar phenotype subtype.

Herein we describe the and activity of FK228 (Romidepsin), an inhibitor of class I HDACs, in counteracting and radiosensitizing embryonal (ERMS, fusion-negative) and alveolar (ARMS, fusion-positive) rhabdomyosarcoma (RMS). RH30 (ARMS, fusion-positive) and RD (ERMS, fusion-negative) cell lines and human multipotent mesenchymal stromal cells (HMSC) were used. Flow cytometry analysis, RT-qPCR, western blotting and enzymatic assays were performed. Irradiation was delivered by using an x-6 MV photon linear accelerator. FK228 (1.2 mg/kg) activity, combined or not with radiation therapy (2 Gy), was assessed in murine xenografts. Compared to HMSC, RMS expressed low levels of class I HDACs. , FK228, as single agents, reversibly downregulated class I HDACs expression and activity, and induced oxidative stress, DNA damage and a concomitant growth arrest associated to PARP-1-mediated transient non-apoptotic cell death. Surviving cells upregulated the expression of cyclin A, B, D1, p27, Myc and activated PI3K/Akt/mTOR and MAPK signaling, known to be differently involved in cancer chemoresistance. Interestingly, while no radiosensitizing effects were detected, or , on RD cells, FK228 markedly radiosensitized RH30 cells by impairing antioxidant and DSBs repair pathways . Further, FK228 when combined with RT significantly reduced tumor mass in mouse RH30 xenografts. FK228 did not show antitumor activity as single agent whilst its combination with RT resulted in radiosensitization of fusion-positive RMS cells, thus representing a possible strategy for the treatment of the most aggressive RMS subtype.
Alessandra Rossetti, Francesco Petragnano, Luisa Milazzo, Francesca Vulcano, Giampiero Macioce, Silvia Codenotti, Matteo Cassandri, Silvia Pomella, Francesca Cicchetti, Irene Fasciani, Cristina Antinozzi, Luigi Di Luigi, Claudio Festuccia, Francesca De Felice, Massimo Vergine, Alessandro Fanzani, Rossella Rota, Roberto Maggio, Antonella Polimeni, Vincenzo Tombolini, Giovanni Luca Gravina, Francesco Marampon

2800 related Products with: Romidepsin (FK228) fails in counteracting the transformed phenotype of rhabdomyosarcoma cells but efficiently radiosensitizes, and , the alveolar phenotype subtype.

125 mg 100 G200 units

Related Pathways

paperclip

#33976742   2021/04/07 To Up

The Yunnan national medicine Maytenus compound inhibits the proliferation of hepatocellular carcinoma (HCC) by suppressing the activation of the EGFR-PI3K-AKT signaling pathway.

To investigate the effects of Maytenus compound on the proliferation of hepatocellular carcinoma (HCC) cells and and to explore the underlying mechanism. The half maximal inhibitory concentration (IC50) values of Maytenus compound in HepG2 and BEL-7402 cells were determined by the MTS assay. HepG2 and BEL-7402 cells were treated with different concentrations of Maytenus compound. MTS assays, colony formation assays and cell cycle analyses were performed to clarify the inhibitory effect of Maytenus compound on the proliferation of HepG2 and BEL-7402 cells . After subcutaneous injection of HepG2 cells, nude mice were randomly divided into a vehicle control group and a drug intervention group, which were intragastrically administered ddHO or Maytenus compound, respectively. The inhibitory effect of Maytenus compound on the proliferation of HepG2 cells was analyzed using subcutaneous tumor growth curves, tumor weight, the tumor growth inhibition rate and the immunohistochemical detection of BrdU-labeled cells in S phase. The organ toxicity of Maytenus compound was initially evaluated by comparing the weight difference and organ index of the two groups of nude mice. The main proteins in the EGFR-PI3K-AKT signaling pathway were detected by Western blot after Maytenus compound intervention and . Maytenus compound showed favorable antiproliferation activity against HepG2 and BEL-7402 cells with IC50 values of 79.42±11.71 µg/mL and 78.48±8.87 µg/mL, respectively. MTS assays, colony formation assays and cell cycle analyses showed that Maytenus compound at different concentration gradients within the IC50 concentration range significantly suppressed the proliferation of HepG2 and BEL-7402 cells and inhibited cell cycle progression from G1 to S phase. Additionally, Maytenus compound, at an oral dose of 2.45 g/kg, dramatically inhibited, without obvious organ toxicity, the proliferation of subcutaneous tumors formed by HepG2 cells in nude mice. In addition, the tumor growth inhibition rate for Maytenus compound was 66.94%. Furthermore, Maytenus compound inhibited the proliferation of liver orthotopic transplantation tumors in nude mice. Western blot analysis showed that Maytenus compound significantly downregulated the expression of p-EGFR, p-PI3K, and p-AKT and upregulated the expression of p-FOXO3a, p27, and p21 and . Maytenus compound significantly inhibited the proliferation of HCC cells and . The downregulation of the EGFR-PI3K-AKT signaling pathway and subsequent inhibition of cell cycle progression from G1 to S phase is one of the possible mechanisms. Maytenus compound has a high tumor growth inhibition rate and has no obvious organ toxicity, which may make it a potential anti-HCC drug, but the results from this study need to be confirmed by further clinical trials in HCC patients.
Wen-Tao Zhao, Liu-Xin Han, Lin Liu, Bao-Zhen Zeng, Yi Zhang, Liu-Fang Zhao, Hong-Yan Hu, Jia-Wei Xia, Yi-Ze Li, Xu-Dong Xiang, Xiao-Lin Lin, Di Lu, Gao-Feng Li

1531 related Products with: The Yunnan national medicine Maytenus compound inhibits the proliferation of hepatocellular carcinoma (HCC) by suppressing the activation of the EGFR-PI3K-AKT signaling pathway.

100ul100.00 ul 100 G100 U200 units1100 500IU

Related Pathways

paperclip

#33973497   2021/05/11 To Up

Deregulation of cell cycle and related microRNA expression induced by vinyl chloride monomer in hepatocytes of rats.

Vinyl chloride (VC) is a confirmed human carcinogen associated with hepatocellular carcinoma and angiosarcoma. However, the role of microRNAs (miRNAs) in liver cell cycle changes under VC exposure remains unclear, which prevents research on the mechanism of VC-induced carcinogenesis. In this study, male rats were injected intraperitoneally with VC (0, 5, 25, and 125 mg/kg body weight) for 6, 8, and 12 weeks. Cell cycle analysis of liver cells, miRNA-222, miRNA-199a, miRNA-195, and miRNA-125b expression in the liver and serum, and target protein expression were performed at different time points. The results showed a higher percentage of hepatocytes in the G1/G0 and S phases at the end of 6 and 12 weeks of VC exposure, respectively. MiRNA-222 expression decreased initially and then increased, whereas miRNA-199a, miRNA-195, and miRNA-125b expression increased initially and then decreased, which corresponded with changes in cell cycle distribution and related target proteins expression (p27, cyclinA, cyclinD1, and CDK6). The corresponding expression levels of miRNAs in serum did not change. Dynamic changes in miR-222, miR-199a, miR-195, and miR-125b induced by VC can lead to cell cycle deregulation by affecting cell cycle-related proteins, and these miRNAs can serve as early biomarkers for malignant transformation caused by VC.
Weizhe Pan, Shengnan Yu, Jin Jia, Junyang Hu, Liang Jie, Panhong Zhang, Qian Wang, Xiaoyan Yan, Yulan Qiu

1149 related Products with: Deregulation of cell cycle and related microRNA expression induced by vinyl chloride monomer in hepatocytes of rats.

100 ul2 Pieces/Box1 mg96 assays2 Pieces/Box400 ug2 Pieces/Box400 ug50 ul100 ul1 mg50 ul

Related Pathways

paperclip

#33971912   2021/05/10 To Up

Effects of a robot-aided somatosensory training on proprioception and motor function in stroke survivors.

Proprioceptive deficits after stroke are associated with poor upper limb function, slower motor recovery, and decreased self-care ability. Improving proprioception should enhance motor control in stroke survivors, but current evidence is inconclusive. Thus, this study examined whether a robot-aided somatosensory-based training requiring increasingly accurate active wrist movements improves proprioceptive acuity as well as motor performance in chronic stroke.
I-Ling Yeh, Jessica Holst-Wolf, Naveen Elangovan, Anna Vera Cuppone, Kamakshi Lakshminarayan, Leonardo Capello, Lorenzo Masia, Jürgen Konczak

2184 related Products with: Effects of a robot-aided somatosensory training on proprioception and motor function in stroke survivors.

18 kgs100ug200 10 mg100 μg100ug Lyophilized500 mg100 μg

Related Pathways

paperclip

#33971196   2021/05/07 To Up

LxCxD motif of the APC/C coactivator subunit FZR1 is critical for interaction with the retinoblastoma protein.

Retinoblastoma protein (pRB) regulates cell cycle by utilizing different regions of its pocket domain for interacting with E2F family of transcription factors and with cellular and viral proteins containing an LxCxE motif. The LxCxE motif is present on FZR1, an adaptor protein of the multi-subunit E3 ligase complex anaphase-promoting complex/cyclosome (APC/C). The APC/C complex regulates the timely degradation of multiple cell cycle proteins for mitotic exit and maintains G1 state. FZR1 has been reported to interact with pRB through LxCxE. By using point mutations, we found that the cysteine residue in the FZR1 LxCxE motif is critical for direct interaction with pRb. The direct binding of the LxCxE motif of FZR1 to the pRB LxCxE binding pocket is confirmed by using human papillomavirus protein E7 as a competitor, both in vitro and in vivo. While mutation of the cysteine residue significantly disrupts FZR1 interaction with pRB, this motif does not affect FZR1 and core APC/C association. Expression of the FZR1 point mutant results in accumulation of S-phase kinase-associated protein 2 (SKP2) and Polo-like kinase 1 (PLK1), while p27 and p21 proteins are downregulated, indicating a G1 cell cycle defect. Consistently, cells containing point mutant FZR1 enter the S phase prematurely. Together our results suggest that the LxCxE motif of FZR1 is a critical determinant for the interaction between FZR1 and pRB and is important for G1 restriction.
Ajeena Ramanujan, Shivangee Bansal, Manalee Guha, Nupur T Pande, Swati Tiwari

2671 related Products with: LxCxD motif of the APC/C coactivator subunit FZR1 is critical for interaction with the retinoblastoma protein.

0.1 mg0.1 mg100 U1 Set100ug Lyophilized100ug Lyophilized100μg1 Set100ug Lyophilized100ug Lyophilized100ug Lyophilized1 Set

Related Pathways

paperclip

#33969806   2020/12/01 To Up

Synergistic effects of BKM120 and panobinostat on pre-B acute lymphoblastic cells: an emerging perspective for the simultaneous inhibition of PI3K and HDACs.

The reputation of conventional treatment in acute lymphoblastic leukemia (ALL) has recently been questioned due to the considerable increment in the number of relapsed patients. The remarkable role of histone deacetylase (HDAC) enzymes in induction of chemo-resistance has provided an opportunity for HDAC inhibitors to be used as a treatment strategy in ALL; however, the compensatory activation of oncogenic pathways may negatively affect their promising effects. In the present study, we found an attenuating effect for PI3K axis on the anti-leukemic effects of panobinostat in pre-B ALL-derived Nalm-6 cells, as the harnessing of this pathway using BKM120 or CAL-101 resulted in a significant reduction in the number of viable cells as well as the metabolic activity. Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. The companionship of the PI3K inhibitor with HDAC inhibitor also potentiated panobinostat-induced apoptotic cell death and enhanced the mRNA of Foxo3a and Foxo4. Conclusively, this study sheds light on the adjuvantive effects of BKM120 on panobinostat efficacy and outlined that the simultaneous inhibition of PI3K and HDACs may be a promising therapeutic approach to improve the cure rates of ALL.
Mahdieh Mehrpouri, Majid Momeny, Davood Bashash

2634 related Products with: Synergistic effects of BKM120 and panobinostat on pre-B acute lymphoblastic cells: an emerging perspective for the simultaneous inhibition of PI3K and HDACs.

25 mg96T 5 G100 mg1000 TESTS/0.65ml10 mg 5 G2.5 mg2.5 mg100ul1 mg100ug

Related Pathways

paperclip

Error loading info... Pleas try again later.