New pharmacotherapy options for cervical cancer

Dueñas‐González, Alfonso; Cetina, Lucely; Coronel, Jaime; Cano, C.; Dolores, Rigoberto

doi:10.1517/14656566.2014.855198

Cited by 4 publications

(4 citation statements)

References 40 publications

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“…However, many anti-tumor drugs improve patient survival but are harmful to their vital organs or fertility. 3,4 Therefore, the identification of novel, tumor-specific drugs with no adverse effects is an ultimate goal for anti-cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling

Xiao

et al. 2019

J Int Med Res

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Objective The present study explored how the inhibition of protease-activated receptor-2 (PAR-2) induced proliferation and apoptosis in cervical cancer in vitro and in vivo. Methods mRNA and protein expression of PAR2 and signal transducer and activator of transcription-3 (STAT-3) was determined by quantitative real-time PCR and western blotting. The proliferation and apoptosis of cervical cancer cells were assayed by the cell counting kit-8 kit, flow cytometry, and western blotting. The effects of PAR2 inhibition on cervical cancer were also examined in BALB/c nude mice in vivo. Results SLIGRL-NH2 (SL), a selective PAR-2 agonist, promoted proliferation and inhibited apoptosis of healthy cervical cancer cells and HeLa cells, while the PAR-2 antagonist FSLLRY-NH2 (FS) inhibited proliferation and led to apoptosis. SL also promoted the activation of STAT-3, while FS inhibited it and inhibited cancer growth in vivo. Conclusion FS inhibited cervical cancer by reducing proliferation and inducing apoptosis by interfering with STAT-3 signaling.

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Section: Introductionmentioning

confidence: 99%

Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling

Xiao

et al. 2019

J Int Med Res

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“…Cervical cancer ranked as the fourth most prevalent cause of cancer deaths worldwide among women in 2012, with 265,000 deaths and another 527,000 new cases 11 . The 5-year survival rate has not changed for 20 years, so current treatment strategies have plateaued in efficacy 12 . Vaccines cannot treat already-established cancer nor do they provide protection against all types of human papillomavirus (HPV) infection 11, 13, 14.…”

Section: Main Textmentioning

confidence: 99%

“…Vaccines cannot treat already-established cancer nor do they provide protection against all types of human papillomavirus (HPV) infection 11, 13, 14. Moreover, current strategies (radiotherapy, chemotherapy, and surgery) suffer from serious drawbacks, are harsh on normal cells, and have not shown adequate selectivity in targeting the malignant tissue of the cervix 12, 15, 16, 17, 18…”

Section: Main Textmentioning

confidence: 99%

The Therapeutic Potential of CRISPR/Cas9 Systems in Oncogene-Addicted Cancer Types: Virally Driven Cancers as a Model System

Jubair

McMillan

2017

Molecular Therapy - Nucleic Acids

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The field of gene editing is undergoing unprecedented growth. The first ex vivo human clinical trial in China started in 2016, more than 1000 US patents have been filed, and there is exponential growth in publications. The ability to edit genes with high fidelity is promising for the development of new treatments for a range of diseases, particularly inherited conditions, infectious diseases, and cancers. For cancer, a major issue is the identification of driver mutations and oncogenes to target for therapeutic effect, and this requires the development of robust models with which to prove their efficacy. The challenge is that there is rarely a single critical gene. However, virally driven cancers, in which cells are addicted to the expression of a single viral oncogene in some cases, may serve as model systems for CRISPR/Cas therapies, as they did for RNAi. These models and systems offer an excellent opportunity to test both preclinical models and clinical conditions to examine the effectiveness of gene editing, and here we review the options and offer a way forward.

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“…Cervical cancer, one of common gynaecological cancers, ranks the fourth place of female cancers and is the fourth death cause of malignancy worldwide . Almost 80% of cases are found in developing countries, and most patients have an advanced stage of cervical cancer .…”

mentioning

confidence: 99%

Combination of RIZ1 Overexpression and Radiotherapy Contributes to Apoptosis and DNA Damage of HeLa and SiHa Cervical Cancer Cells

Yang

Xing

et al. 2018

Basic Clin Pharma Tox

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Although radiotherapy has been widely applied to treating cervical cancer in the clinic, its therapeutic efficacy is often restricted to the radioresistance of cancer cells. Retinoblastoma protein-interacting zinc finger gene 1 (RIZ1) has been suggested as a tumour suppressor gene, whereas its role in cervical cancer with or without radiotherapy has been unclear. In this study, two cervical cancer cell lines, HeLa and SiHa cells, stably transfected with RIZ1 overexpression plasmid were subjected to ionizing radiation, and their survival fractions were calculated by assessing their clonogenic abilities. Our results showed that the forced overexpression of RIZ1 significantly reduced the clonogenic survival rates of both HeLa and SiHa cells exposed to ionizing radiation. By analysing the cell apoptotic status, we found that the RIZ1-overexpressed cervical cancer cells under ionizing radiation were more vulnerable to damage, and more γ-H2AX foci were found in these cells. Furthermore, the volumes of tumour xenografts formed by the RIZ1-overexpressed cells in nude mice under ionizing radiation were smaller than those generated by the control cells. There were more morphological changes, apoptosis cells and lower expression of PCNA in RIZ1-overexpressed tumour tissues of mice after exposure to ionizing radiation. Taken together, our study demonstrates that the overexpression of RIZ1 combined with radiotherapy facilitates apoptosis and DNA damage of cervical cancer cells.

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New pharmacotherapy options for cervical cancer

Cited by 4 publications

References 40 publications

Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling

Inhibition of protease-activated receptor-2 induces apoptosis in cervical cancer by inhibiting signal transducer and activator of transcription-3 signaling

The Therapeutic Potential of CRISPR/Cas9 Systems in Oncogene-Addicted Cancer Types: Virally Driven Cancers as a Model System

Combination of RIZ1 Overexpression and Radiotherapy Contributes to Apoptosis and DNA Damage of HeLa and SiHa Cervical Cancer Cells

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