. Radiation therapy is often the main curative treatment.
However, some patients are resistant to radiation therapy. Research has suggested that a phenomenon called DNA methylation has a major influence on radioresistance.
Radioresistance can be reduced by the use of ‘radiosensitizers,’ chemical compounds that make cells more vulnerable to radiation.
“DNA methylation is an epigenetic change, which means that it is caused by a change in how the genes are expressed rather than a mutation in the genetic code. As a result, epigenetic changes are reversible and can often be modulated by phytochemicals. Taking a cue from earlier studies, we investigated if SMY can alter DNA methylation status in NPC cells and whether such changes influenced the radiosensitivity of the cells,” explains Dr. Qin Fan of Southern Medical University and Dr. Ying Lv of NanFang Hospital, China.
For their study, researchers first compared the DNA methylation levels in two different cell lines of NPC, radiosensitive NPC cells CNE-2 and radioresistant NPC cells CNE-2R.
The CNE-2R cells initially had lower levels of methylated genes than the CNE-2 cells. However, after treating the CNE-2R cells with SMY, the researchers found that the methylation of some of these genes was restored.
One of these genes was one that encodes Tenascin-C (TNC), a glycoprotein that is involved in various cellular processes, including the invasion, invasiveness, and migration of tumor cells.
Previous studies have shown that reducing the methylation of the ‘promoter’ region of this gene increases the expression of TNC.
Then compared the expression of TNC in both cell lines and found that it was overexpressed in CNE-2R cells. They then found that SMY reduced the production of TNC in cancer cells. This occurs due to the restoration of the methylation status of TNC by SMY.
This new study suggests that SMY contributes to the methylation of certain promoter regions of the TNC gene called CpG sites. When a protein called specificity protein 1 (SP1) binds to methylated CpG sites, it inhibits the expression of TNC.
The findings of the study shed light on three very important aspects of SMY as a therapeutic supplement during radiotherapy. Besides reducing the side effects of radiation, it can increase the efficacy of radiotherapy and reduce the side effects of radiotherapy in NPC.
SMY because of its anti-tumorigenic effect, can serve as a preventive supplement for a community that always relied on the healing power of traditional medicine. It also proves to be an alternative for developing a cost-effective ‘radiosensitizer’ for the pharmaceutical industry.