Results from a two-stage Mendelian randomization procedure regarding the relationship between triacylglycerol levels and cervical cancer. One common disease in female reproductive health that poses a significant global risk to women's health is cervical cancer. Cervical cancer is classified as one of the three most common cancer kinds affecting women under 45 years old, with an average age of 53 at diagnosis and an average age of 59 at death. The World Health Organization reports that more than 310,000 women die from cervical cancer annually, and that 85% of these deaths take place in lower- to middle-income countries[1]. This information emphasizes how cervical cancer has a significant global impact on women's health. In addition, the incidence of cervical cancer is rising, particularly in some developing nations where the disease's prevalence and death rates are rising as a result of inadequate access to healthcare, a dearth of cervical cancer screening programs, and poor vaccination rates[2]. Therefore, there is an urgent need to increase the speed at which cervical cancer is treated, establish precise goals for diagnosis and treatment, encourage widespread use of cervical cancer medical technologies, and improve training for healthcare professionals[3, 4].
Recent studies have demonstrated that, in addition to traditional viral infection sources, lipid molecules may play a critical role in the initiation and progression of cervical cancer. Lipid molecules play an essential role in the formation and function of cell membranes, and aberrant lipid metabolism can disrupt cellular signaling pathways, hence accelerating the growth of malignancies. Moreover, some studies suggest that lipid molecules may affect the way that HPV (human papillomavirus) infects cells, which may lead to the onset of cervical cancer [5]. For example, certain lipid components may interfere with HPV particles' ability to adhere to cervical epithelial cell membranes, affecting the virus's ability to invade and replicate. Lipid molecules play a number of roles in the development of cervical cancer. Lipid molecules have been found to have a high correlation with the initiation, progression, and prognosis of cancers. It's critical to realize that abnormalities in lipid metabolism may accelerate the growth and spread of tumors by encouraging cellular invasion and the formation of blood vessels [6, 7]. Lipids can also interact with specific cytokines and promote inflammation in the body, which can either enhance or prevent the spread of cancerous tumors and distant metastases. Lipid molecules may also influence the growth and death of cervical cancer cells by modifying their signaling pathways. Ultimately, it is plausible that lipid molecules regulate the course and prognosis of cervical cancer through modulating the immune system's reaction[8]. As such, further research into relevant lipid compounds and their mechanisms of action is required. Lipid molecules may play a significant role in regulating the progression of cervical cancer in general. Extensive investigation of this molecule will improve our understanding of the causes of cervical cancer and provide new knowledge and strategies for its future treatment and prevention[7, 9].
Immune cells play a critical role in the human body's defense mechanisms against infections. The processes behind immune system regulation are becoming more and more of a focus as advances in immunology and molecular biology technology progress. Lipid molecules, essential components of cell membranes, support the structure of cells and play a critical role in regulating the functions of immune cells10. It's critical to realize that lipid molecules play a crucial role in immune cell activation and signaling. As an immunomodulatory mediator in a variety of physiological and pathological responses, lipids are essential. Both lipid molecules, phosphatidylinositol (PI) and phosphatidylinositol-4-5-diphosphate (PIP2), are essential to the signaling pathway that regulates the activity and expression of immune cells11. These lipid molecules also help regulate immunological tolerance and aid in the immune system's specific recognition and removal of autoantigens. Additionally, it is well recognized that specific lipid signaling pathways, such as the Sphingomyelin Phosphoinositides pathway, are important for immune cell proliferation, differentiation, and apoptosis[10–12]. Immune cells are crucial in the treatment of cancer. On the one hand, immune cells may recognize and eliminate abnormal cells, which impedes the growth of tumors. This provides strong theoretical support for immunotherapy. From an alternative perspective, tumor cells can evade immune monitoring and eradication by releasing substances that weaken the immune system and limit the function of immune cells, which accelerates the growth and spread of tumors.Thus, a comprehensive study of the interactions between immune cells and tumor cells can help identify new targets for treatment and increase the efficacy of immunotherapy9. For example, inhibiting the PD-1/PD-L1 signaling pathway restored T cell activation and improved its ability to eradicate tumor cells. Moreover, immunotherapies such as tumor vaccines and CAR-T cell therapy have shown promising clinical results, reviving cancer treatments[13, 14].
Mendelian randomization (MR) is a research tool that is highly valued in the field of epidemiology since it helps to understand the genesis of diseases. When single nucleotide polymorphisms (SNPS) are used as instrumental variables (IVs) in multiple regression (MR), it becomes easier to investigate the relationships that may exist between exposure phenotypes and illness outcomes[15, 16]. Their ability to adjust to changes in the environment and the randomization of genetic differences throughout pregnancy considerably lessen the influence of external factors in MR. Genetic indicators are therefore occasionally utilized to forecast pregnancy outcomes or choose the best course of treatment. With an emphasis on lipid molecules, we chose effective instrumental variables (IVs) for our investigation from a variety of collected and published data in genome-wide association studies (GWAS). Every section of human tumor and cancer tissue was included in the samples[17].