Cervical cancer Continues to be a significant public health challenge, especially in poor industrializing countries. It ranks as the fourth most common cancer among females worldwide, Cervical cancer led to approximately 528000 new cases and approximately 266000 deaths in the year 2012. In Mexico for instance the figure regarding the rates of cervical cancer mortality is quite worrisome: 11.9% of all the cancer registered deaths (Ferlay et al, 2015).
Epidemiological studies have indicated that some geographical areas that have been distributions of iodine may have high incidences of some types of cancer such as stomach and breast cancer. These factors may also be responsible for the incidence of cervical cancer.
Infections with the oncogenic strains of the Human Papilloma Virus (HPV) are a foremost risk factor for cervical cancer. The E6 E7 High risk HPV virus takes over the genetic material causing the synthesis of oncogenic proteins denominated as E6 and E7. These oncoproteins inhibit two of the central cell cycle regulator proteins, p53 and pRb, causing aberrant cellular senescence and division, hence facilitating the growth of tumor cells (Boulet et al 2007; Ueno et al 2006).
The Cancer Stem Cell Hypothesis
Different cells constitute a tumor. In fact, tumors are quite varied and, for instance, cancer stem cells (CSCs) have attracted great interest amongst the many different cells as they are the ones responsible for starting cancer, spilling from primary tumors, and are responsible for most cancer treatments failing: chemo and radiation. They are often defined due to their self-renewal capacity, treatment resistance, and the ability to lead to cancer relapse.
The cancer stem cell population within various tumors, including cervical cancer, plays a crucial role in influencing tumor growth, treatment resistance, and prognosis.
For cervical cancer, CD49fe and cytokeratin 17 (CK17) have been reported as cancer stem cell markers, for example in cervical cancer. These special cells are called cervical cancer stem cells (CCSCs) (Martens et al, 2004; Feng et al, 2009).
Definition of Cervical Cancer
Based on different reports, it is estimated that about 528 000 new cases of cervical cancer are diagnosed every year and 266 000 die of it. One of the challenges associated with this condition is the need to find efficiencies such as prevention, diagnosis, and treatment of the disease since both incidences and mortality are high.
This might explain why the human papillomavirus HPV, is found in most sexually active individuals. Most of these dermatologic infections resolve groups themselves , while some others might act like several years inducing cervical cancer in the horizon.
There is no doubt challenges like cervical cancer cancer have been posing a threat to many economically in all regions and cervical cancer, in particular, 500,000 new cases are recorded in a year. It occurs as the fourth largest number of incidences of different ribs to the lung cervical cancer among women.
Mostly cervical cancer incidence and mortality rates stand at 528 000 and 266 000 respectively. Quite high incidences of both ‘high cervical cancer proportions’ and treatment seekers parallelly exist hence expansion of diagnostic and therapeutic measures at the health system level is essential.
Molecular Iodine: A Promising Therapeutic Agent
Such circumstances call for a rescue and development of new therapeutic approaches. One of such potential therapies is molecular iodine (I2). It has shown antitumor effects across different cancer models. However, recently the effect of I2 on CSCs has started to be explored, especially considering the aspect of how to impede the growth of CSCs and the size of the tumor (Rosner et al., 2009).
That is why researchers have undertaken or continued research on the I2 effect especially in cervical cancer. The cervical cancer cells HeLa and SiHa were taken for the research. Both monolayers of these cells as well as CSC-enriched cultures, termed cervospheres, were treated with 200 μM of I2. I2 treatment has the potential to eliminate cancer stem cells effectively, suggesting further preclinical studies to evaluate its anti-cancer properties.
The results were promising: cell proliferation was significantly inhibited and tumor formation was reduced in vivo upon I2 supplementation. This effect was due to downregulation of important “stemness” factors CD49f, CK17, OCT-4, SOX2, KLF4 and NANOG. Also increased activation of PPARγ receptors that help control apoptosis and cell proliferation was observed (Bigoni-Ordóñez et al., 2018). Comparison between treated and untreated HeLa monolayer cells showed significant differences in tumorigenicity and stemness markers.
How Does Molecular Iodine Work? The Role of PPARγ and PTEN
One of the ways I2 exerts its action is via the PPARγ receptor activation. The function of these receptors is known to include the regulation of genes responsible for processes like cell differentiation and apoptosis (programmed cell death).
Understanding the signaling pathways involved in the antiproliferative effects of molecular iodine is crucial. Specific substances, like 6-iodolactone, mediate apoptotic effects, suggesting that these pathways play a significant role in elucidating iodine's role in cancer treatment.
PPARγ has been known to regulate a number of genes, one of which is the PTEN gene, which is a typifying tumor suppressor gene responsible for cell growth regulation (Teresi & Waite, 2008).
In the research concerning I2-treated HeLa cells, the expression of both PPARγ and PTEN was upregulated in cancer cells. From this we infer that I2 could potentially aid in harnessing endogenous tumor-suppressive pathways helping in the reduction of CSCs capability to promote cancer.
Methods: Cell Culture and I2
Cell culture is an essential laboratory procedure involving the growth of cells in controlled conditions which makes it easier to examine their function and the effect of different treatment types on them. In the present study, cervical cancer cell lines including HeLa and SiHa were employed to assess the effect of molecular iodine (I2) on cervical cancer stem cells.
The HeLa and SiHa cells were grown in a medium that approximates the body conditions. Though limited, this environment enables the cells to grow and multiply which is ostensible to be the aim of experiment. Molecular iodine (I2) was then applied into the culture media to study its actions on the cells.
In order to examine the effects of I2, a few analytical methods were used. Expression of stem cell markers was analyzed by flow cytometry in order to study whether cancer stem cells exist in the population and their characteristics. Furthermore, Western blot assay was also done to determine the level of protein expression of certain proteins involved in the processes of cell division and death.
The aim of this study was therefore to assess the effect of I2 on the activities of cervical cancer stem cells, given that it may help them exploit this knowledge to target hard-to-eradicate cancer stem cells with potential reproductive factors.
In Vivo Results: Molecular Iodine Reduces Tumor Size in Mice
Researchers carried out in vivo experiments in NOD/SCID mice to check the in vivo efficacy of I2. The tumors formed by the I2 treated cervical cancer cells were comparatively smaller than the non-treated counterparts.
Iodide excess induces apoptosis through mechanisms involving oxidative stress and tumor growth inhibition, highlighting its potential in targeting cancer stem cells and combating tumor resistance.
This is important since it indicates that I2 may be efficient in eliminating CSCs hence decreasing the overall size of the tumor and even enhancing the chances of successful treatment.
Conclusion: A Promising Future for Molecular Iodine in Cancer Treatment?
The research depicts that molecular iodine has reasonable potential as an anti cervico-uterine cancer agent. Transforming a number of CSC markers and eliciting mechanisms that hinder tumor progression may make I2 an oncomodulatory agent by itself or in conjunction with standard cancer therapies.
Studies have shown that iodine exhibits antiproliferative and cytotoxic activities against various human carcinoma cell lines, indicating its potential role in cancer treatment and the underlying mechanisms of how iodine can induce apoptosis in these cell lines.
Because of the favorable side effects of I2 in the treatment of other diseases for example, mammary fibrocystic disease, there is need to go deeper into why I2 works in the treatment of cancers.
Frequently Asked Questions (FAQs)
What is molecular iodine?
Iodine molecule, or molecular iodine (I2), is defined by the presence of two iodine atoms and is hypothesized to have anticancer capabilities. Its mechanism is studied as the ability to suppress the growth of cancers, especially in cancer stem cells.
How does molecular iodine help in treating cervical cancer?
Molecular iodine appears to reduce key expressions necessary for cancer stem cell growth and metastasis by suppressing the growth of such CSCs. It also changes the pathways to promote cell death resulting in reduction of tumor size.
Is molecular iodine safe to use?
Molecular iodine has shown to be within safe limits even for unapproved conditions like fibrocystic breast disease treatment. Additionally, research indicates that molecular iodine may have potential therapeutic effects on breast cancer cells, reducing tumor proliferation and inducing apoptosis. Further clinical studies are warranted to ensure its safety and efficacy in cancer management.
Can molecular iodine replace conventional cancer treatments?
Though I2 shows potential, it is more likely that I2 would still not replace standard medical therapies like chemotherapy or radiotherapy. The therapeutic implications of iodine in both benign conditions and cancer prevention in breast tissue, particularly focusing on breast cancer cells, are significant. It may however come as an adjunct to such therapies which already exist especially in the area of targeting CSCs.
What are cancer stem cells, and why are they important?
Cancer stem cells are a distinct subset of cells in the tumor with self-renewable capabilities and resistance to therapy. They are mostly implicated in tumor growth, spread and once again reappearance after treatment and are thus an important focus in cancer research.
Manage Your Skincare with Iodine Pure
At Iodine Pure, we get it. Skincare and nail care can be a problem, which is why we have created products that tackle both. We have packed them with Iodine to handle the stuff that really bothers you like acne and toenail fungus.
For your skin, our acne treatment is all about clearing up those breakouts. It fights off the bacteria that causes acne and helps keep your skin looking clear. Plus, it helps prevent new pimples from showing up. Who doesn’t want that? Right
As for your nails, we have got you covered. Our nail care goes straight to the source of toenail fungus. The iodine fights off the fungus, strengthens your nails, and keeps infections from coming back. Simple as that.
Bottom line? With EZ Clear Skin Iodine Spray, you’re giving your skin and nails the care they actually deserve with an ingredient that works.
References
- Arroyo-Helguera, O., Rojas, E., Delgado, G., & Aceves, C. (2008). Signaling pathways involved in the antiproliferative effect of molecular iodine in normal and tumoral breast cells: Evidence that 6-iodolactone mediates apoptotic effects. Endocrine-Related Cancer, 15(4), 1003-1011.
- Bigoni-Ordóñez, G. D., Ortiz-Sánchez, E., Rosendo-Chalma, P., Valencia-González, H. A., Aceves, C., & García-Carrancá, A. (2018). Molecular iodine inhibits the expression of stemness markers on cancer stem-like cells of established cell lines derived from cervical cancer. BMC Cancer, 18, 928.
- Boulet, G., Horvath, C., Broeck, V. D., Sahebali, S., & Bogers, J. (2007). Human papillomavirus: E6 and E7 oncogenes. International Journal of Biochemistry & Cell Biology, 39(11), 2006-2011.
- Ferlay, J., Soerjomataram, I., Dikshit, R., Eser, S., Mathers, C., Rebelo, M., ... & Bray, F. (2015). Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012. International Journal of Cancer, 136(5), E359-E386.
- Martens, J. E., Arends, J., Van der Linden, P. J., De Boer, B. A., & Helmerhorst, T. J. (2004). Cytokeratin 17 and p63 are markers of the HPV target cell, the cervical stem cell. Anticancer Research, 24(2B), 771-775.
- Teresi, R. E., & Waite, K. A. (2008). PPARgamma, PTEN, and the fight against cancer. PPAR Research, 2008, 932632.
- Ueno, T., Sasaki, K., Yoshida, S., Kajitani, N., Satsuka, A., Nakamura, H., & Sakai, H. (2006). Molecular mechanisms of hyperplasia induction by human papillomavirus E7. Oncogene, 25(30), 4155-4164.
