The integrative approach of this study has shed light on the intricate genetic landscape of erectile dysfunction (ED) and cervical cancer. The treatment of cervical cancer, including surgery, radiation therapy, and chemotherapy, may have a significant impact on the sexual function of patients. Surgery may lead to vaginal shortening and narrowing, and radiation therapy is the main factor causing sexual pain. These physiological changes may lead to decreased sexual desire, difficulty in vaginal lubrication, reduced frequency of sexual activity, as well as increased pain and difficulty during intercourse. Research shows that 50% of gynecological cancer patients may experience temporary or persistent sexual problems. The overall prevalence of sexual dysfunction (SD) in cervical cancer patients is as high as 76%, and there are differences in the prevalence of SD among patients of different ages, educational backgrounds, and tumor stages.By harnessing the power of genome-wide association studies (GWAS) [19,20,21], single-cell RNA sequencing (scRNA-seq), and Mendelian randomization, we have uncovered a plethora of genetic variants and expressed genes that could serve as potential targets for therapeutic intervention. Incorporating these findings into genetics and molecular biology courses can enhance students’ understanding of the real-world applications of genomic research in complex diseases. Encouraging students to engage in research projects based on these findings can foster critical thinking and innovation. This can include exploring the role of identified genes in disease mechanisms or potential therapies.

The identification of the WISP1 gene as a key player in cancer, with its elevated expression in T cells, suggests a possible role in the immune response to tumor development [22,23,24,25]. The WISP1 gene, part of the CCN family, plays a role in cell signaling related to proliferation, differentiation, and survival. Its expression in T cells and potential involvement in cervical cancer. WISP1 may influence T cell activity, impacting immune responses. Its expression could affect T cell proliferation and differentiation, which are crucial for effective immune function. WISP1 might modulate inflammatory pathways, potentially affecting how T cells respond to cancerous cells.

This observation is of special interest as a fuller understanding has emerged for the contribution of the immune system to tumor progression and potential application in immunotherapies. These differences in expression profiles between reproductive and cervical cells demonstrate the tissue specificity of gene regulation that is critical for this disease state.

In the risk of ED and cervical cancer, Mendelian randomization studies have greatly contributed to etiology as well as causality. By the same randomised experimentation, this method functions as a sort of clinical trial which is less troubled by confounding effects when controlling for all observable factors—the results thus offer an evidence structure that provides robustity to our causal inferences.

ScRNA-seq analysis has revealed cellular heterogeneity within the tumor microenvironment as well as the nature of complex intercellular communication networkst [26, 27]. Sex-specific functional roles of immune cells in cancer and sexual dysfunction are indicated by differences in expression levels of secretory genes (FCN1, CD14, TCF7L2). For example, the abundant LYN expression in cDC2 cells may point to its potential contribution to dendritic cell maturation and antigen presentation—key mechanisms that serve as launchpads for successful adaptive immune responses.

Based on GO/KEGG analysis of the two genes, a number of related pathways might be disrupted in ED and cervical cancer, such as cAMP signaling pathway and MAPK signaling pathway. These pathways regulate a multitude of cellular functions—growth, differentiation, apoptosis, and immune response to name a few. Disregulation of these pathways may be implicated in distinct molecular mechanisms leading to the genesis and progression for both types of disorders.

The violin plots and PCA scatter plot derived from our single-cell preprocessing offer a perspective to the tumor microenvironment with respect to the heterogeneity of gene expression across samples. Tools such as Cellxgene, and the Leiden clustering algorithm that enables us to examine the clustering of cells into types, followed by annotation of these groups have allowed us to interrogate cellular heterogeneity and putative cell-type specific biomarkers.