Crvical Carcinogenesis

Introduction

The underlying purpose of the experiments performed in the study, Promoter Hypermethylation of KLF4 Inactivates its Tumor Suppressor Function in Cervical Carcinogenesis, is to investigate the mechanism by which the KLF4 gene is silenced in cervical carcinomas. Cervical cancer accounts for 250,000 female deaths every year. Developing therapies for cervical cancer has been limited due to the lack of genetic and epigenetic data of the mechanism causing the cancer. The KLF4 gene is a transcriptional regulator of cell growth and differentiation. It functions as a tumor suppressor in cervical cancer, but is found to be inactivated in cervical cancer. The overexpression of KLF4 protein is known to inhibit cervical cancer cell growth and tumor formation by activating a cell cycle suppressor. Promoter CpG island hypermethylation can result in transcriptional silencing of many tumor suppressing genes. Two CpG regions, BSQ1 and BSQ3, were examined in this experiment.

Experimental Methods and Results

Cervical cancer tissues and normal cervical tissues were collected from 24 newly diagnosed patients with primary cervical cancer, in order to perform the experiments outlined in the paper. Experiments were also performed on the following human cervical carcinoma cell lines: HeLa, SiHa, C33A, and CaSki, which were purchased from a company. The researchers extracted the genomic DNA from the samples collected. The DNA was then bisulfite modified and amplified using PCR. The PCR product was then examined through gel electrophoresis to insure a single band was obtained, and then sequenced by Invitrogen. Methylation-specific PCR was then carried out of the bisulfate-treated DNA. This was done to check the consistency of the ...

... middle of paper ...

...rs had tested more cancer cell lines, they may have come to drastically different conclusions. In addition, the experiment drew some drastic conclusions about the mechanism of silencing of KFL4 and how the treatment with 5-Aza affects the cancer cell lines. Maybe other treatments would have the same or even better effects on the cancer cell lines. In order to improve the conclusions of the paper, the researches should have repeated these experiments on a much larger sample. Testing people with different forms and stages of cervical cancer would have been beneficial. Testing people of different heritages could also have an effect on the conclusions drawn from the experiments. Overall, I believe the study did a decent job in researching the mechanism of how the KLF4 gene is silenced in cervical cancer, but a few changes could have been made to improve the study.