Skin cancer is a complex and serious health condition with high metastatic abilities and comprises two types including melanoma, the most dangerous type, and non-melanoma skin cancer, such as basal cell carcinoma and squamous cell carcinoma. Skin cancer has a high prevalence ratio and millions of mortalities worldwide. Multiple risk factors account for the initiation, development, progression, and metastasis of skin cancer such as ultraviolet radiations, X-rays, immunocompromised situations, skin lesions, and alteration in genetic makeup. CEP55, FOXM1b, and HELLS genes play critical roles in the progression of the cell cycle, cell proliferation, cell division, DNA replication, and repair system. The overexpression of these genes involves complex molecular mechanisms and is linked with the development and progression of multiple cancers including skin cancer. This review article summarized the history and recent advancement of risk factors for skin tumorigenesis development and progression.

TP53 is a tumor suppressor gene that is mutated in most cancer types and has been extensively studied in cancer research. p53 plays a critical role in regulating the expression of target genes and is involved in key processes such as apoptosis, cell cycle regulation, and genomic stability, earning it the title “guardian of the genome.” Numerous studies have demonstrated p53’s influence on and regulation of autophagy, ferroptosis, the tumor microenvironment, and cell metabolism, all of which contribute to tumor suppression. Alterations in p53, specifically mutant p53 (mutp53), not only impair its tumor-suppressing functions but also enhance oncogenic characteristics. Recent data indicate that mutp53 is strongly associated with poor prognosis and advanced cancers, making it an ideal target for the development of novel cancer therapies. This review summarizes the post-translational modifications of p53, the mechanisms of mutp53 accumulation, and its gain-of-function, based on previous findings. Additionally, this review discusses its impact on metabolic homeostasis, ferroptosis, genomic instability, the tumor microenvironment, and cancer stem cells, and highlights recent advancements in mutp53 research.

Cancer stem cells (CSCs), or tumor-initiating cells (TICs), are cancerous cell subpopulations that remain while tumor cells propagate as a unique subset and exhibit multiple applications in several diseases. They are responsible for cancer cell initiation, development, metastasis, proliferation, and recurrence due to their self-renewal and differentiation abilities in many kinds of cells. Artificial intelligence (AI) has gained significant attention because of its vast applications in various fields including agriculture, healthcare, transportation, and robotics, particularly in detecting human diseases such as cancer. The division and metastasis of cancerous cells are not easy to identify at early stages due to their uncontrolled situations. It has provided some real-time pictures of cancer progression and relapse. The purpose of this review paper is to explore new investigations into the role of AI in cancer stem cell progression and metastasis and in regenerative medicines. It describes the association of machine learning and AI with CSCs along with its numerous applications from cancer diagnosis to therapy. This review has also provided key challenges and future directions of AI in cancer stem cell research diagnosis and therapeutic approach.

Skin cancer (SC) is the one of the widespread kind of cancers worldwide. Among other risk factors, Human Papillomavirus (HPV) is the potential causative agents for skin tumorigenesis. In previously scientific published research, the underlying role of HPV remained controversial about which kind of HPVs are involved on the onset initiation and progression of non-melanoma skin cancer (NMSC) such as squamous cell carcinoma (SCC), basal cell carcinoma (BCC) and malignant melanoma (MM). Apha and beta HPV have been found with the course and development of keratinocytes mutation and skin tumor malignancies. The pathogenicity of HPV lies in its oncogenic proteins such as E6 and E7 belong to Beta HPV kind along with various other transcriptional factors. E6 and E7 are found to deregulation in the tumor suppressor genes p53 and pRb to disturb normal activity of cell cycle and to help metastasize skin cancer. There are also increasing evidences of weakened immune system in melanoma and non-melanoma skin cancer patients associated with human papillomavirus. The combined influence of ultraviolet radiations (UVA and UVB) has detected with human papillomavirus to trigger and promote melanoma and non-melanoma skin cancer development. These results in altered chromosome structure, uncontrolled S-phase, and inhibit apoptosis to advance skin carcinoma. This review article summarizes not only previous arguments for the involvement of oncogenicity of HPVs strains with skin cancer types but also demonstrates an extensive review of the significant previously published data that were not covered yet.

MicroRNAs (miRNAs) are small non-coding RNAs, 19–25 nucleotides in length, that regulate gene expression. miRNAs are involved in various cellular, biological, and pathological activities, including the development and progression of malignant tumors. Numerous studies have highlighted the significant roles of miRNA deregulation in various cancer types, involving critical pathways such as gene deletions and amplifications, abnormal epigenetic changes, and dysfunctional miRNA regulatory systems. miRNAs can function both as oncogenes and tumor suppressor genes in different contexts. Several cancer hallmarks are associated with deregulated miRNAs, including resistance to cell death, metastasis, sustained proliferative signaling, promotion of angiogenesis, and the suppression of growth factors. Recent research has demonstrated that miRNAs contribute to drug resistance in tumor cells by targeting genes linked to drug resistance or by influencing genes that regulate the cell cycle, apoptosis, and proliferation. A single miRNA often has tissue-specific regulatory functions and can affect multiple genes. Various miRNA types have been identified as potential biomarkers for tumor diagnosis and critical targets for novel therapeutic approaches. This review aims to explore the role of miRNAs in cancer progression, metastasis, and potential therapeutic interventions.