Benzobijuglone, a novel cytotoxic compound from Juglans mandshurica, induced apoptosis in HeLa cervical cancer cells

Phytomedicine ◽  
2007 ◽  
Vol 14 (12) ◽  
pp. 846-852 ◽  
Author(s):  
Zhi-Bo Li ◽  
Jing-Yun Wang ◽  
Bo Jiang ◽  
Xiu-Li Zhang ◽  
Li-Jia An ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Juglans Mandshurica ◽  
Cytotoxic Compound ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis

scholarly journals Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-26
Author(s):  
Liubing Hu ◽  
Yan Wang ◽  
Zui Chen ◽  
Liangshun Fu ◽  
Sheng Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Cell Apoptosis ◽  
Hsp90 Inhibitor ◽  
Cervical Cancer Cells ◽  
Ros Scavenger ◽  
Induced Apoptosis ◽  
Human Cervical Cancer

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent cancer cell apoptosis-inducing factor that can induce apoptosis in a variety of cancer cells. However, resistance to TRAIL in cancer cells is a huge obstacle in creating effective TRAIL-targeted clinical therapies. Thus, agents that can either enhance the effect of TRAIL or overcome its resistance are needed. In this study, we combined TRAIL with SNX-2112, an Hsp90 inhibitor we previously developed, to explore the effect and mechanism that SNX-2112 enhanced TRAIL-induced apoptosis in cervical cancer cells. Our results showed that SNX-2112 markedly enhanced TRAIL-induced cytotoxicity in HeLa cells, and this combination was found to be synergistic. Additionally, we found that SNX-2112 sensitized TRAIL-mediated apoptosis caspase-dependently in TRAIL-resistant HeLa cells. Mechanismly, SNX-2112 downregulated antiapoptosis proteins, including Bcl-2, Bcl-XL, and FLIP, promoted the accumulation of reactive oxygen species (ROS), and increased the expression levels of p-JNK and p53. ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53. Moreover, SNX-2112 induced the upregulation of death-receptor DR5 in HeLa cells. The silencing of DR5 by siRNA significantly decreased cell apoptosis by the combined effect of SNX-2112 and TRAIL. In addition, SNX-2112 inhibited the Akt/mTOR signaling pathway and induced autophagy in HeLa cells. The blockage of autophagy by bafilomycin A1 or Atg7 siRNA abolished SNX-2112-induced upregulation of DR5. Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTα were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway. Thus, the combination of SNX-2112 and TRAIL may provide a novel strategy for the treatment of human cervical cancer by overcoming cellular mechanisms of apoptosis resistance.

Suppression of human 8-oxoguanine DNA glycosylase (OGG1) augments ultrasound-induced apoptosis in cervical cancer cells

Ultrasonics ◽  
2016 ◽  
Vol 72 ◽  
pp. 1-14
Author(s):  
Tao Xu ◽  
Yongli Nie ◽  
Jiao Bai ◽  
Linjun Li ◽  
Bo Yang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Dna Glycosylase ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis

Mechanism of ricin-induced apoptosis in human cervical cancer cells

2005 ◽  
Vol 69 (5) ◽  
pp. 855-865 ◽  
Author(s):  
P.V. Lakshmana Rao ◽  
R. Jayaraj ◽  
A.S.B. Bhaskar ◽  
Om Kumar ◽  
R. Bhattacharya ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Sevoflurane Inhibits Growth and Metastasis of Cervical Cancer Through Up-Regulating miR-203 by Targeting Tumor Protein Translationally Controlled 1

2020 ◽  
Vol 10 (6) ◽  
pp. 874-883
Author(s):  
Li Zhang ◽  
Shiyou Wei ◽  
Zhenkai Xu ◽  
Wen Sun ◽  
Lihua Hang
Keyword(s):  
Cervical Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter System ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis ◽  
Cancer Tissues

Background: Cervical cancer is a type of malignancy with high incidence and high mortality in women all over the world. Recent findings revealed the role of sevoflurane in the inhibition of development of various cancer types. This study aimed to explore whether sevoflurane could suppress cells proliferation and metastasis through adjusting miR-203 expression in cervical cancer. Methods: The effects of sevoflurane on HeLa cell viability was assessed using CCK-8 assay. miR-203 level in Hela cells was determined by qRT-PCR. In addition, cells apoptosis, migration and invasion were evaluated using flow cytometry and transwell analysis respectively after sevoflurane treatment or miR-203 expression changes. Bioinformatics software (TargetScan) was used to predict the potential target genes for miR-203 and the prediction was validated using dual-luciferase reporter system. Results: Sevoflurane effectively inhibited cell viability, metastasis and stimulated apoptosis in cervical cancer. miR-203 demonstrated a low expression in cervical cancer tissues and cells and sevoflurane significantly up-regulated miR-203 expression in cervical cancer cells. Upregulation of miR-203 significantly suppressed cell growth and metastasis and induced apoptosis, while down-regulation of miR-203 presented the opposite effects in cervical cancer cells. In addition, the inhibitory effects of sevoflurane were eliminated by down-regulating miR-203 in cervical cancer cells. In addition, TPT1 was confirmed as a target gene for miR-203. Conclusion: Sevoflurane inhibited cervical cancer cells viability and metastasis through up-regulation of miR-203 expression by targeting TPT1.

scholarly journals Protein kinase C β inhibits autophagy and sensitizes cervical cancer Hela cells to cisplatin

2017 ◽  
Vol 37 (2) ◽  
Author(s):  
Na Li ◽  
Wei Zhang
Keyword(s):  
Cervical Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Hela Cells ◽  
B Cell Lymphoma ◽  
Kinase C ◽  
Cervical Cancer Cells ◽  
Pkc Β ◽  
Induced Apoptosis

Recently, autophagy has been indicated to play an essential role in various biological events, such as the response of cervical cancer cells to chemotherapy. However, the exact signalling mechanism that regulates autophagy during chemotherapy remains unclear. In the present study, we investigated the regulation by cisplatin on protein kinase C β (PKC β), on B-cell lymphoma 2 (Bcl-2) and on apoptosis in cervical cancer Hela cells. And then we examined the regulation by cisplatin on autophagy and the role of autophagy on the chemotherapy in Hela cells. In addition, the regulation of the PKC β on the autophagy was also investigated. Our results indicated that cisplatin promoted PKC β in Hela cells. The PKC β inhibitor reduced the cisplatin-induced apoptosis, whereas increased the cisplatin-induced autophagy in Hela cells. On the other side, the PKC β overexpression aggravated the cisplatin-induced apoptosis, whereas down-regulated the cisplatin-induced autophagy. Taken together, our study firstly recognized the involvement of PKC β in the cytotoxicity of cisplatin via inhibiting autophagy in cervical cancer cells. We propose that PKC β would sensitize cervical cancer cells to chemotherapy via reducing the chemotherapy induced autophagy in cancer cells.

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