Retinoic acid is a highly active derivative of vitamin A. It can induce tumor cell terminal differentiation, and becomes normal or near normal cells. Then it achieves its therapeutic purposes.
Experiment shows the pathway of tretinoin on human cervical carcinoma cells by observing the impact of all-trans retinoic acid on cervical cancer cell growth, differentiation and oncogene.
ATRA is an effective differentiation inducer in the regulation of a variety of tissue and cell morphology, proliferation, growth and development, metabolism, and maintain stable internal environment has a wide range of biological roles. Observed before and after ATRA treatment cell proliferation, cell morphology, cell cycle, colony formation ability and oncogene expression changes that can be used to elaborate multi-way impact of ATRA on the biological behavior of cervical cancer cells.
With appropriate concentration of ATRA, HeLa cell proliferation is inhibited and has normal cell differentiation. Cell differentiation is manifested in two aspects of the morphology and function. Morphological differentiation of the phenotypic characteristics of cell differentiation, but also the basic characteristics of an objective response differentiation inducing agent to induce differentiation of cells. Observed by transmission electron microscopy of ATRA effect in HeLa cells to mature differentiation characteristics of mature cells. Such as the nucleus cytoplasm ratio decreases to reduce the nuclear small and the nucleolus, heterochromatin increase in the nucleus, mitochondria, Golgi complex and other well-differentiated organelles in the cytoplasm. Cell infinitely rapid proliferation is one of the basic characteristics of malignant cells, differentiation and proliferation was antagonistic state, cell proliferation slowed down is often the result of cell differentiation.
Oncogene overexpression in tumor cells is widespread. C myc in a classic oncogenes, and its encoded product is a cell proliferation-related nuclear protein, plays an important role in cell proliferation, differentiation and regulation. The experimental observation that the level of c myc transcription to ATRA down. Cells with ATRA for prolonged c-myc in the m RNA level decreased gradually, HeLa cells showed the characteristics of mature cells. C myc gene intron binding protein MIBP1 (p160) and RFX1 (of p130) isolated from HeLa cells, MIBP1/RFX1DNA the same binding site to the repetitive sequences can inhibit the c myc gene upstream promoter activity. ATRA for the cell MIBP1, the RFX1 protein expression, and enhanced inhibitory activity of DNA-binding region. It can be considered, The ATRA MIBP1/RFX1 down cmyc expression is the molecular mechanism of ATRA induced differentiation of cervical cancer cells.
Cell proliferation, differentiation of DNA metabolism is achieved through the cell cycle. The G1 / S checkpoint is important regulatory cells can enter the division cycle and the successful completion of the cell proliferation. In this study, flow cytometry results showed that, of ATRA concentrated block in DNA synthesis in quiescent-G1 phase HeLa cells, DNA synthesis of the active phase-S phase cells were decreased. Prompted ATRA tumor cells arrest in G1 phase, inhibition of cell proliferation and induce tumor cell differentiation and maturation.
The incidence of cervical cancer ranks first in gynecological tumors according to study from cosmetic raw material suppliers . It has showed an upward trend in recent years. Surgery and radiotherapy chemotherapy may control tumor development, but there are a considerable number of patients that can not tolerate surgery, radiotherapy and chemotherapy adverse reactions. So they give up the treatment, and ultimately died of tumor complications. Clinical trials show that ATRA can significantly reduce the degree of malignancy of HeLa cells. It is also induced to normal or near normal cells. The inhibitory effect of ATRA on the behavior of cervical cancer cells is a multi-link. This shows that ATRA is a promising drug for treatment of cancers.
Source:http://www.cosprm.com
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