Commentary - International Journal of Pure and Applied Zoology (2021) Volume 9, Issue 5

PRINCIPLES OF STEM-CELL BIOLOGY TO CANCER AND REGULATORS

Amani Paul^*

Department of Zoology, Andhra University, Visakhapatnam, India

Corresponding Author:

Amani Paul
Department of Zoology, Andhra University, Visakhapatnam, India
E-mail: amanipaul@gmail.com

Received: 6th August, 2021; Accepted: 20th August, 2021; Published: 27th August, 2021

Description

The stem cell/material interface may be a complex, dynamic microenvironment during which the cell and therefore the material cooperatively dictate one another's fate: the cell by remodelling its surroundings, and therefore the material through its inherent properties (such as adhesivity, stiffness, nanostructure or degradability). Stem cells in touch with materials are ready to sense their properties, integrate cues via signal propagation and ultimately translate parallel signalling information into cell fate decisions. However, discovering the mechanisms by which stem cells answer inherent material characteristics is challenging due to the highly complex, multicomponent signalling milieu present within the somatic cell environment. During this review, we discuss recent evidence that shows that inherent material properties could also be engineered to dictate somatic cell fate decisions, and overview a subset of the operative signal transduction mechanisms that have begun to emerge. Further developments in somatic cell engineering and mechanotransduction are poised to possess substantial implications for somatic cell biology and regenerative medicine.

• A subset of cancer cells have the properties of cancer stem cells, which self-renew to get additional cancer stem cells and differentiate to get phenotypically diverse cancer cells with limited proliferative potential. Cancer stem cells are highly enriched for the power to make tumours following transplantation relative to bulk tumour cells or non-tumorigenic cancer cells.

• Cancer stem cells are characterized within the context of human acute myeloid leukaemia, carcinoma and glioblastoma. In each case, surface markers are identified that distinguish cancer stem cells from cancer cells with more limited proliferative potential, allowing the potential identification of cancer stem cells.

• In some cases, cancer stem cells might arise from the mutational transformation of normal stem cells, whereas in other cases mutations might cause restricted progenitors or differentiated cells to accumulate properties of cancer stem cells like self-renewal potential.

• The neoplastic proliferation of cancer stem cells is probably going to be driven by mutations that inappropriately activate pathways that promote the self-renewal of normal stem cells. Samples of these pathways include the WNT, and BMI1-dependent pathways that regulate the self-renewal of haematopoietic stem cells and neural stem cells.

• Further characterization of cancer stem cells might cause improved diagnostics and therapies by allowing us to raised identify and target cancer stem cells. To cure cancer it's necessary to kill, differentiate or prevent the metastasis of cancer stem cells.

• We are currently facing an unprecedented level of public interest in research on embryonic stem cells, a biomedical research that until recently was small, highly specialized and of limited interest to anyone but experts within the field.

Real and imagined possibilities for the treatment of degenerative and other diseases are of interest to our rapidly ageing population; real and imagined associations of stem cells to cloning, embryos and reproduction stir deeply held beliefs and prejudices. The conjunction of those factors could explain the recent sudden interest in embryonic stem cells but we need to remember that this research features a long and convoluted history, which the findings described today within the scientific and popular press are firmly grounded in research that has been happening for several decades.