Abstract

The cell is the smallest unit of life. It is a structure that maintains order through self-organization, characterized by a high level of dynamism, which in turn is characterized by work. For this work to take place, a continuous high flow of energy is necessary. However, a focused view of the physical relationship between energy and work is inadequate for describing complex biological/medical mechanisms or systems. In this review, we try to make a connection between the fundamental laws of physics and the mechanisms and functions of biology, which are characterized by self-organization. Many different physical work processes (work) in human cells are called cell work and can be grouped into five forms: synthetic, mechanical, electrical, concentration, and heat generation cell work. In addition to the flow of energy, these cell functions are based on fundamental processes of self-organization that we summarize with the term Entirety of molecular interaction (EoMI). This illustrates that cell work is caused by numerous molecular reactions, flow equilibrium, and mechanisms. Their number and interactions are so complex that they elude our perception in their entirety. To be able to describe cell functions in a biological/medical context, the parameters influencing cell work should be summarized in overarching influencing variables. These are “biological” energy, information, matter, and cell mechanics (EMIM). This makes it possible to describe and characterize the cell work involved in cell systems (e.g., respiratory chain, signal transmission, cell structure, or inheritance processes) and to demonstrate changes. If cell work and the different influencing parameters (EMIM influencing variables) are taken as the central property of the cell, specific gene mutations cannot be regarded as the sole cause for the initiation and progression of cancer. This reductionistic monocausal view does not do justice to the dynamic and highly complex system of a cell. Therefore, we postulate that each of the EMIM influencing variables described above is capable of changing the cell work and thus the order of a cell in such a way that it can develop into a cancer cell.

Highlights

  • The continuous changes produced by cell work necessitate a constant influx of biological energy

  • Molecular biology has suggested that the processes required for this are primarily regulated by genes. This view does not do justice to the complex events that take place; cell work can be described by four overarching EMIM influencing variables

  • Cell work is based on the mechanisms and processes of the entity of molecular interactions, which are characterized by complex molecular interactions and biophysical influences

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Summary

INTRODUCTION

Since the discovery of oncogenes and tumor suppressor genes, modern cancer research has assumed that gene mutations alone are responsible for the initiation and progression of cancer (somatic mutation theory; Weinberg, 2014). This biophysical parameter is suitable for describing cell functions and examining and explaining them in the context of biological systems, such as functional substructures, organelles, and cells Against this background, we will discuss that cellular work is influenced and possibly disturbed by one variable, namely genes (information) and their derivatives, and by other factors, such as energy, matter/milieu, and mechanics. We will discuss that cellular work is influenced and possibly disturbed by one variable, namely genes (information) and their derivatives, and by other factors, such as energy, matter/milieu, and mechanics This approach makes it clear that the cause of cancer can be initiated and driven by parameters other than genes

Cell Mechanics
Biological Systems
Entirety of Molecular Interaction
Cell work is the Central Hallmark of
Cell work and the EMIM Influencing Variables
THE ROLE OF THE GENOME
The Complex
EXAMPLES FOR BIOPHYSICAL INFLUENCING MECHANISMS
ATP as a Biological Aggregation Inhibitor
Intrinsically Disordered Proteins, Liquid-Liquid Phase Separation, and EMIM
SUMMARY
DATA AVAILABILITY STATEMENT
Full Text
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