ABSTRACT
Cancer stem cells (CSCs) play an essential role in tumour progression and metastasis. These cells have the unique ability to self-renew and differentiate into specific tissue cell types. Their capacity for self-renewal enables CSCs to persist over time, thereby contributing to cancer relapse and therapy resistance. Therefore, targeting CSCs has emerged as a promising cancer treatment strategy. CSCs exhibit differentiation, self-renewal, and plasticity, and they contribute to multiple aspects of malignant tumours, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. While conventional treatments predominantly target cancer cells that are not CSCs, CSCs frequently survive, resulting in tumour recurrence and relapse. This article concentrates on the development of novel therapeutic strategies that combine conventional treatments with CSC inhibitors to eradicate cancer cells and CSCs, thereby treating cancer and preventing its recurrence. However, the diversity of CSCs poses a significant obstacle to the development of CSC-targeted therapies, necessitating extensive research for a better understanding and exploration of therapeutic approaches. Future development of CSC-targeted therapies will rely heavily on overcoming this obstacle.
ABSTRACT
BACKGROUND: The gene interaction network is a set of genes interconnected by functional interactions among the genes. The gene interaction networks are studied to determine pathways and regulatory mechanisms in model organisms. In this research, the enrichment study of bone cancer-causing genes is undertaken to identify several hub genes associated to the development of bone cancer. MATERIALS AND METHODS: Data on bone cancer is obtained from mutated gene samples; highly mutated genes are selected for the enrichment analysis. Due to certain interactions with each other the interaction network model for the hub genes is developed and simulations are produced to determine the levels of expression. For the array analyses, a total of 100 tumor specimens are collected. Cell cultures are prepared, RNA is extracted, cDNA arrays probes are generated, and the expressions analysis of Hub genes is determined. RESULTS: Out of cDNA array findings, only 7 genes: CDKN2A, AKT1, NRAS, PIK3CA, RB1, BRAF, and TP53 are differentially expressed and shown as significant in the development of bone tumors, approximately 15 pathways have been identified, including pathways for non-small cell lung cancer, prostate cancer, pancreatic cancer, chronic myeloid leukemia, and glioma, consisting of all the identified 7 genes. After clinical validations of tumor samples, the IDH1 and TP53 gene revealed significant number of mutations similar to other genes. Specimens analysis showed that RB1, P53, and NRAS are amplified in brain tumor, while BRAF, CDKN2A, and AKT1 are amplified in sarcoma. Maximum deletion mutations of the PIK3CA gene are observed in leukemia. CDKN2A gene amplifications have been observed in virtually all tumor specimens. CONCLUSION: This study points to a recognizable evidence of novel superimposed pathways mechanisms strongly linked to cancer.
