scholarly journals Hexokinase 2 Promotes Cell Growth and Tumor Formation Through the Raf/MEK/ERK Signaling Pathway in Cervical Cancer

2020 ◽  
Vol 10 ◽  
Author(s):  
Nan Cui ◽  
Lu Li ◽  
Qian Feng ◽  
Hong-mei Ma ◽  
Dan Lei ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Tumor Formation ◽  
Erk Signaling ◽  
Cyclin A1 ◽  
Hexokinase 2 ◽  
Cervical Cancer Cells

Hexokinase 2 (HK2) is a member of the hexokinases (HK) that has been reported to be a key regulator during glucose metabolism linked to malignant growth in many types of cancers. In this study, stimulation of HK2 expression was observed in squamous cervical cancer (SCC) tissues, and HK2 expression promoted the proliferation of cervical cancer cells in vitro and tumor formation in vivo by accelerating cell cycle progression, upregulating cyclin A1, and downregulating p27 expression. Moreover, transcriptome sequencing analysis revealed that MAPK3 (ERK1) was upregulated in HK2-overexpressing HeLa cells. Further experiments found that the protein levels of p-Raf, p-MEK1/2, ERK1/2, and p-ERK1/2 were increased in HK2 over-expressing SiHa and HeLa cells. When ERK1/2 and p-ERK1/2 expression was blocked by an inhibitor (FR180204), reduced cyclin A1 expression was observed in HK2 over-expressing cells, with induced p27 expression and inhibited cell growth. Therefore, our data demonstrated that HK2 promoted the proliferation of cervical cancer cells by upregulating cyclin A1 and down-regulating p27 expression through the Raf/MEK/ERK signaling pathway.

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.

scholarly journals LGR5 promotes the proliferation and tumor formation of cervical cancer cells through the Wnt/β-catenin signaling pathway

Oncotarget ◽  
2014 ◽  
Vol 5 (19) ◽  
pp. 9092-9105 ◽  
Author(s):  
Qing Chen ◽  
Hao-Zhe Cao ◽  
Peng-Sheng Zheng
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Tumor Formation ◽  
Cervical Cancer Cells

scholarly journals Baicalein inhibits the invasion of human cervical cancer cells by inhibiting the hedgehog/Gli signaling pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 115-120
Author(s):  
Hai Yang ◽  
Jiyi Xia ◽  
Yan Li ◽  
Yong Cao ◽  
Li Tang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Colony Formation ◽  
Diphenyltetrazolium Bromide ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Purpose: To identify the role of baicalein in human cervical cancer and to determine whether baicalein treatment affects hedgehog/Gli signaling pathway. Methods: Cell proliferation was evaluated by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and colony formation assays. Cell death rate was assessed by PI-staining and FACS assay. Furthermore, cell invasion was assessed by Transwell assay while the levels of the key proteins were measured by western blotting analysis. Results: Baicalein suppressed the viability and proliferation of HeLa cells. The colony formation ability and relative migration rate were significantly decreased in the HeLa cells treated with 50 μM baicalein. Furthermore, the levels of Shh, Gli1, MMP-9, and VEGF declined significantly in baicalein-treated cells. Conclusion: The results demonstrate that baicalein inhibits the growth and invasiveness of cervical cancer cells partly by suppressing the activation of hedgehog/Gli signaling pathway in a concentrationdependent manner. Keywords: Cervical cancer, baicalein, hedgehog/Gli pathway, MMP-9

Eriodictyol Suppresses Survival of Cervical Cancer Cells Through Mediation of PTEN/Akt Signaling Pathway

2019 ◽  
Vol 18 (2) ◽  
pp. 196-200
Author(s):  
Yu Lixiao ◽  
Liu Xiaoyun
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Akt Signaling ◽  
Dependent Manner ◽  
Akt Signaling Pathway ◽  
Cervical Cancer Cells

Cervical cancer is one of the most malignant cancers of the female reproductive system with high morbidity and mortality. In the current study, we have examined the effect of eriodictyol on cell survival including cell growth, cell cycle and apoptosis of cervical cancer cells and also explored the underlying mechanism(s). To this end, CCK-8 assay, flow cytometry and western blotting assays were performed in cervical cancer HeLa cells. Eriodictyol significantly inhibited cell survival including impeding the cell viability, arresting the cell cycle at the G1 phase and potentiating cell apoptosis in a concentration-dependent manner. Also, ERI activated PTEN, P21, cleaved caspase-3/-9 expression and downregulated P-Akt and cyclin D1 expression in a dose-dependent manner. In conclusion, ERI can inhibit cervical cancer HeLa cells viability via impeding cell cycle and inducing apoptosis by regulating PTEN/Akt signaling pathway.

scholarly journals Overexpression of TROP2 Predicts Poor Prognosis of Patients with Cervical Cancer and Promotes the Proliferation and Invasion of Cervical Cancer Cells by Regulating ERK Signaling Pathway

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e75864 ◽  
Author(s):  
Ting Liu ◽  
Yueyang Liu ◽  
Xiangxiang Bao ◽  
Jiguang Tian ◽  
Yang Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Erk Signaling ◽  
Cervical Cancer Cells ◽  
Proliferation And Invasion

scholarly journals Ginsenoside Rg3 Inhibit The Proliferation And Metastasis of Cervical Cancer Cells in Vitro By Regulating NF-κB Signaling Pathway

2021 ◽  
Vol 5 (2) ◽  
Keyword(s):  
Cervical Cancer ◽  
Survival Rate ◽  
Protein Expression ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Ginsenoside Rg3 ◽  
Cervical Cancer Cells ◽  
Proliferation And Metastasis

Objective: To investigate the effect and mechanism of ginsenoside Rg3 on the proliferation and metastasis of cervical. Methods: Cervical cancer cells HeLa were treated with different concentrations (0, 0.12, 0.24, 0.48 mmol/L) of ginsenoside Rg3, and then the survival rate of HeLa cells was detected by CCK-8 method, and the migration and invasion of HeLa cells were assessed using Transwell test, and expression of E-cadherin, N-cadherin, vimentin, Toll receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), phosphorylated nuclear transcription factor κB p65 (P-NF-κB p65) proteins were calculated by Western blot. Results: After ginsenoside Rg3 (0.12, 0.24, 0.48 mmol/L) treatment, the survival rate, migration number, invasion number, and N-cadherer number, and N-cadherin, Vimentin, TLR4, MyD88, p-NF-κB p65 protein expression of HeLa cells were significantly reduced (P<0.05) Ginsenoside protein expression was significantly increased (P<0.05), and showed a concentration-dependent relationship. Conclusion: Ginsenoside Rg3 could inhibit the proliferation and metastasis of cervical cancer cells in vitro, and its mechanism might be related to the inhibition of NF-κB signaling pathway.

scholarly journals Fra-1 Inhibits Cell Growth and the Warburg Effect in Cervical Cancer Cells via STAT1 Regulation of the p53 Signaling Pathway

2020 ◽  
Vol 8 ◽  
Author(s):  
Manying Zhang ◽  
Lin Liang ◽  
Junyu He ◽  
Zhengxi He ◽  
Chunxue Yue ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Warburg Effect ◽  
P53 Signaling ◽  
Cervical Cancer Cells ◽  
P53 Signaling Pathway ◽  
The Warburg Effect

Effect of daidzein on cell growth, cell cycle, and telomerase activity of human cervical cancer in vitro

2004 ◽  
Vol 14 (5) ◽  
pp. 882-888 ◽  
Author(s):  
J. M. Guo ◽  
G. Z. Kang ◽  
B. X. Xiao ◽  
D. H. Liu ◽  
S. Zhang
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Hela Cells ◽  
Flow Cytometric Analysis ◽  
Telomerase Activity ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Phytoestrogens are some plant compounds exhibiting estrogen-like activities. However, some studies have shown that they also affect the growth of some nonhormone-dependent diseases. In this study, daidzein – one of the most common phytoestrogens – was used to investigate its effects on human cervical cancer cells HeLa in vitro. First, the cell growth was measured by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Then, the distributions of cell cycle and apoptosis were analyzed with the help of flow cytometry. Finally, the telomerase activity was detected by using real-time quantitative reverse transcription-polymerase chain reaction. The results showed that at the concentrations from 6.25 to 100 μmol/l, daidzein inhibited the growth of HeLa cells. Flow cytometric analysis showed that cancer cells were arrested at G0 / G1 or G2 / M phase with daidzein. The inductive effects of apoptosis were more obviously observed in low-concentration groups. After HeLa cells were treated with daidzein, the expression of human telomerase catalytic subunit mRNA decreased. These meant that daidzein affected human nonhormone-dependent cervical cancer cells in several ways, including cell growth, cell cycle, and telomerase activity in vitro.

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