Is a Synthetic Cell the same as Synthetic Life ?

 

From  a bioRxiv preprint , “Here we demonstrate a complete cell cycle for a synthetic cell undergoing selection, with genome replication, growth, resource acquisition via feeding, and genetically encoded division” from “A Chemically Defined Synthetic Cell Capable Of Growth And Replication”, Gaut et al., 2026.

Link: https://www.biorxiv.org/content/10.64898/2026.07.01.735724v1#:~:text=Here%20we%20demonstrate%20a%20complete,feeding%2C%20and%20genetically%20encoded%20division

The question I ask is a synthetic cell =synthetic life ? The answer is a resounding no. The hallmark of biological organisms, higher up the hierarchy of the tree of life is multicellularity followed by self-organization. Single cells survive in specific environments and are more primitive. So until the single cell shows potential for multicellularity and organization into colonies,clusters,tissues, it will be a bottleneck for synthesizing “living organisms” from scratch.

During the synthesis of  an artificial cell, it remains to be seen, that information coded in the molecular components or sub-structures sufficient for the derivation of a cell in a fluid environment; or does information encoded in the environment required ? A cell develops in a fluid environment as its cytoplasm is gel-like and not in a solid such as sand. Presumably, mobility of molecular components occur in a fluid. Maybe exchange of  information encoded in molecular components and the fluid environment via molecule-environment interactions lead to the emergence of a cell. The environment then becomes indispensable for higher-order organization. So under controlled laboratory conditions, the milieu for organization of cells into higher-order living structures, could be derived from natural environments such as  wetlands, marshes, hydrothermal vents as they will encode the environmental information.

Does Cancer Metastasis Occur via a Quorum-Sensing-Like Mechanism?

 

Does Cancer Metastasis Occur via a Quorum-Sensing-Like Mechanism?

 

In February, The Hindu published an article titled “Bacteria Can Talk to Each Other and Are Multilingual, Says Biologist.” The biologist in question is Bonnie Bassler, who runs a laboratory at Princeton University and has spent her career studying a process called quorum sensing in bacteria. Quorum sensing is the mechanism by which bacteria communicate and coordinate group behavior based on population density. They do this by continuously secreting and detecting chemical signaling molecules known as autoinducers. Once the bacterial population reaches a critical threshold, the resulting concentration of autoinducers triggers the synchronized activation of specific genes.

After listening to a conversation with Bassler on physicist Sean Carroll's podcast, Mindscape, I found myself wondering whether metastasis — the spread of cancer to distant organs — might occur through a similar, quorum-sensing-like mechanism.

Metastasis involves a step called the epithelial-to-mesenchymal transition (EMT), in which stationary, polarized epithelial cells lose their cell-to-cell adhesion and acquire migratory, invasive properties, becoming mesenchymal cells. This same process also plays a crucial role in embryonic development and wound healing. Within the primary tumor, cells proliferate uncontrollably and secrete enzymes called matrix metalloproteinases (MMPs), such as MMP2 and MMP9. These enzymes initiate and sustain EMT by breaking down basement membranes, degrading adhesion molecules like E-cadherin, and releasing pro-EMT signaling factors such as TGF-β from the extracellular matrix. Together, these actions drive cancer invasion and metastasis.

If quorum sensing is indeed involved in EMT, it may work as follows: in the primary tumor, cells divide uncontrollably and release MMPs, which act much like autoinducers. As the tumor cells multiply, MMP concentration rises in step with them, and once the tumor reaches a critical size, this rising concentration of MMPs triggers the synchronized activation of EMT genes. This remains a hypothesis, however, and would need to be tested directly in primary tumor cells through wet-lab experiments in tissue culture.