scholarly journals The synergistic therapeutic effect of cisplatin with Human papillomavirus E6/E7 short interfering RNA on cervical cancer cell lines in vitro and in vivo

2011 ◽  
Vol 130 (8) ◽  
pp. 1925-1936 ◽  
Author(s):  
Hun Soon Jung ◽  
Ozgur Cem Erkin ◽  
Mi Jeong Kwon ◽  
Seok Hyung Kim ◽  
Jae In Jung ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Therapeutic Effect ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Short Interfering Rna ◽  
Interfering Rna

Doxycycline inhibits proliferation and induces apoptosis of both human papillomavirus positive and negative cervical cancer cell lines

2016 ◽  
Vol 94 (5) ◽  
pp. 526-533 ◽  
Author(s):  
Yan Zhao ◽  
Xinyu Wang ◽  
Lei Li ◽  
Changzhong Li
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cervical Cancer Cell ◽  
Cervical Cancer Cells

The clinical management of cervical cancer remains a challenge and the development of new treatment strategies merits attention. However, the discovery and development of novel compounds can be a long and labourious process. Drug repositioning may circumvent this process and facilitate the rapid translation of hypothesis-driven science into the clinics. In this work, we show that a FDA-approved antibiotic, doxycycline, effectively targets human papillomavirus (HPV) positive and negative cervical cancer cells in vitro and in vivo. Doxycycline significantly inhibits proliferation of a panel of cervical cancer cell lines. It also induces apoptosis of cervical cancer cells in a time- and dose-dependent manner. In addition, the apoptosis induced by doxycycline is through caspase-dependent pathway. Mechanism studies demonstrate that doxycycline affects oxygen consumption rate, glycolysis, and reduces ATP levels in cervical cancer cells. In HeLa xenograft mouse model, doxycycline significantly inhibits growth of tumour. Our in vitro and in vivo data clearly demonstrate the inhibitory effects of doxycycline on the growth and survival of cervical cancer cells. Our work provides the evidence that doxycycline can be repurposed for the treatment of cervical cancer and targeting energy metabolism may represent a potential therapeutic strategy for cervical cancer.

scholarly journals In Vitro and In Vivo Synergistic Therapeutic Effect of Cisplatin with Human Papillomavirus16 E6/E7 CRISPR/Cas9 on Cervical Cancer Cell Line

2016 ◽  
Vol 9 (6) ◽  
pp. 498-504 ◽  
Author(s):  
Shuai Zhen ◽  
Jiao-Jiao Lu ◽  
Li-Jie Wang ◽  
Xiao-Min Sun ◽  
Jia-Qi Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Line ◽  
Therapeutic Effect ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Cervical Cancer Cell ◽  
Cervical Cancer Cell Line

scholarly journals Targeting HMGB3/hTERT axis for radioresistance in cervical cancer

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Zongjuan Li ◽  
Yang Zhang ◽  
Silei Sui ◽  
Yijun Hua ◽  
Anshi Zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cervical Cancer Cell ◽  
Htert Expression ◽  
Signaling Axis

Abstract Background Radiotherapy is regarded as a milestone for the cure of cervical cancer. However, clinical outcome heavily be hindered by radioresistance. So, exploring the underlying mechanism of radioresistance, and find potential target, well deserve fully emphasis. Methods In this study, we developed two novel radiation resistance cervical cancer cell lines, which could mimic clinical radioresistance. In order to find new potential targets, RNA-Seq, database analysis, streptavidin-agarose and LC/MS were used. Pull-down, luciferase and rescue assays were conducted to explore the regulatory mechanisms. To further evaluate the correlation between therapeutic responses and HMGB3/hTERT expression, 172 cervical cancer patients were recruited. Results Knockdown of HMGB3 significantly inhibit the DNA damage repair and induced more γH2AX foci, leading to enhanced chemo- and radio-sensitivity in vitro and in vivo, whereas HMGB3 overexpression has the opposite effects. HMGB3 promotes cell growth and radioresistance by transcriptionally up-regulating hTERT via the specifical binding of HMGB3 at the hTERT promoter region from − 902 to − 321. HMGB3 knockdown-mediated radiosensitization could be reversed by the overexpressed hTERT in both cervical cancer cell lines and xenograft tumor mouse model. Furthermore, clinical data from 172 cervical cancer patients proved that there was a positive correlation between HMGB3 and hTERT expression, and high expression of HMGB3/hTERT predicted poor response to radiotherapy, worse TNM stages and shorter survival time. Conclusion Here, we have identified HMGB3/hTERT signaling axis as a new target for cervical cancer radioresistance. Our results provide new insights into the mechanism of cervical cancer radioresistance and indicate that targeting the HMGB3/hTERT signaling axis may benefit cervical cancer patients.

scholarly journals Human Papillomavirus 58 E7 T20I/G63S Variant Confers More Aggressive Phenotypes to Cervical Cancer Cell with In vitro and In vivo

2021 ◽  
Vol 83 ◽  
Author(s):  
T. Ding ◽  
Min Wang ◽  
Yang Li ◽  
Sha Sha Zhang ◽  
Fenfen Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cell ◽  
Cervical Cancer Cell

scholarly journals Expression of the H19 Oncofetal Gene in Premalignant Lesions of Cervical Cancer: A Potential Targeting Approach for Development of Nonsurgical Treatment of High-Risk Lesions

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Tomer Feigenberg ◽  
Ofer N. Gofrit ◽  
Galina Pizov ◽  
Avraham Hochberg ◽  
Abraham Benshushan
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
Premalignant Lesions ◽  
Cervical Cancer Cell ◽  
Two Samples ◽  
H19 Gene

Background. Recent data suggest a role for H19 gene in promoting cancer transformation and progression. Cervical cancer, progresses from high-grade lesions (CIN3). At present, it is unclear if CIN lesions express H19. Objectives. To determine H19 expression in patient samples of CIN3 as well as the ability of a construct in which the promoter from the H19 gene drives expression of the diphtheria toxin A chain (DTA) to inhibit cervical cancer cell growth in vitro. Methods. H19 transcript levels were evaluated on 10 biopsies of CIN3 using in situ hybridization. PCR was used to examine H19 expression in cervical cancer cell lines and in two samples from a patient with cervical carcinoma. Cell lines were transfected with H19-DTA to determine its impact on cell number. Results. H19 gene was expressed in the area of CIN3 in 9 out of 10 samples. RT-PCR indicated expression of H19 in cervical cancer samples and in one of the three cell lines examined. Transfection of all cell lines with H19-DTA vector resulted in inhibited cell growth. Conclusions. H19 is expressed in the majority of CIN3 samples. These results suggest that most CIN3 lesions could be targeted by H19-DTA. Further in vivo preclinical studies are thus warranted.

scholarly journals HOXB4 inhibits the proliferation and tumorigenesis of cervical cancer cells by downregulating the activity of Wnt/β-catenin signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Dan Lei ◽  
Wen-Ting Yang ◽  
Peng-Sheng Zheng
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Tumor Formation ◽  
Cervical Cancer Cell ◽  
Cancer Cell Growth ◽  
Bioinformatics Analyses

AbstractHomeobox B4 (HOXB4), which belongs to the homeobox (HOX) family, possesses transcription factor activity and has a crucial role in stem cell self-renewal and tumorigenesis. However, its biological function and exact mechanism in cervical cancer remain unknown. Here, we found that HOXB4 was markedly downregulated in cervical cancer. We demonstrated that HOXB4 obviously suppressed cervical cancer cell proliferation and tumorigenic potential in nude mice. Additionally, HOXB4-induced cell cycle arrest at the transition from the G0/G1 phase to the S phase. Conversely, loss of HOXB4 promoted cervical cancer cell growth both in vitro and in vivo. Bioinformatics analyses and mechanistic studies revealed that HOXB4 inhibited the activity of the Wnt/β-catenin signaling pathway by direct transcriptional repression of β-catenin. Furthermore, β-catenin re-expression rescued HOXB4-induced cervical cancer cell defects. Taken together, these findings suggested that HOXB4 directly transcriptional repressed β-catenin and subsequently inactivated the Wnt/β-catenin signaling pathway, leading to significant inhibition of cervical cancer cell growth and tumor formation.

scholarly journals Lactobacilli inhibit cervical cancer cell migration in vitro and reduce tumor burden in vivo through upregulation of E-cadherin

2017 ◽  
Vol 38 (3) ◽  
pp. 1561-1568 ◽  
Author(s):  
Xiaoxi Li ◽  
Hong Wang ◽  
Xingxing Du ◽  
Wenna Yu ◽  
Jingwen Jiang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Tumor Burden ◽  
Cervical Cancer Cell ◽  
Cancer Cell Migration ◽  
Reduce Tumor Burden ◽  
E Cadherin

scholarly journals Fibulin-3 knockdown inhibits cervical cancer cell growth and metastasis in vitro and in vivo

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Juan Li ◽  
Chen Qi ◽  
Xia Liu ◽  
Changzhong Li ◽  
Jie Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Cancer Cell Growth
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