Bioelectonic Medicines Flashcards
What is a bio electronic medicine
A medicine that used electricity in order to have a therapeutic effect
Describe the differences between passive targeting, active targeting and triggered release
Passive targeting
Uses the body’s natural processes to deliver drugs
Drug carriers accumulate in diseased tissues
Relies on differences between healthy and diseased tissues
Examples include liposomes, polymeric nanoparticles, and metal oxide nanoparticles
Active targeting
Uses targeting agents to guide drug carriers to the target site
Involves external intervention
Targets specific markers in diseased cells such as receptors the drug is targeting
Examples include antibodies and receptor-like folate receptors
Triggered release
Uses a trigger that is specific to the target site
For example, nanoparticles can be made to release drugs when they encounter a specific pH. Tumour cells have a leaky vascular system so we can target this
What is the difference in terms of polarisation between healthy cells and cancer cells
Healthy cells are hyper-polarised and cancer cells are depolarised
What is resting potential
This is the membrane potential when the movement of ions is at equilibrium
What is the relationship between resting potential and cell proliferation
Increased cell proliferation in cell type = less negative membrane potential
What cell functions can changes in membrane potential influence
Gene expression and therefore protein expression
What influences membrane potential
The movement of ins through transport proteins - so if there are malfunctions in the proteins that control the movement of ions, the membrane potential will change and therefore influence gene and protein expression - this can lead to cancer.
FEEDBACK LOOP
Describe the feedback loop in bio electricity
Gene expression —> mRNA expression altered —> expression of channel proteins altered —> ion channels altered —> cell potential altered —> electrical activity altered —> gene expression altered
Stem cells and cancer cells tend to be ————
Depolarised (less negative potential)
What is an oncogene
A gene that induces or stops cell proliferation and when uncontrolled can lead to cancer
In mikes experiment, what was the effect when oncgenes were suppressed
The membranes became hyperpolarised = less proliferation
This is tumour surpression
What is the Warburg effect
the phenomenon in which cancer cells produce additional energy through increased oxygen-dependent glycolysis followed by lactic acid fermentation with secretion of lactate
What is tPMET
It is needed to convert NADPH to NADP+ (release electrons)
This is a way of cells creating energy through a redox reaction.
TPMET increase facilitates an increased rate of glycolysis by increasing rate of NADP+ regeneration.
What is glycolysis (simple terms)
Conversion of glucose to pyruvate
What happens when we knock down tPMET
Mitochondrial respiration is decreased.
What are tumour treating fields
Use of electrical fields to treat cancer
What are the 6 key mechanisms targeted in tumour treating fields
Anti-mitotic (MAIN), permeability of cells, anti-migratory, immunogenicity, DNA repair, Autophagic,
describe how bioelectricity can have an antimitotic effect
2 phases of mitosis can be effected:
- methaphase: Tumour treating fields interfere with mitotic spindle assembly - effecting the alighnemnt of tubulin
- telephase: change in cell shape and conformation, compromised polar elements= impared cell division
how can tumour treating fields effect DNA repair
downregulate BRCA and fanconi anaemia pathway genes = replication stress and increased double strand break formation and less repaie
how do TTF effect autophagy
inhibiory effects of a signalling pathway associated with autophagy - increased autophagy
what is autophagy
Autophagy is a natural cellular process that allows the body to degrade and recycle damaged or unnecessary components within cells.
how do TTF impact antitumour immunity
stimulate macrophages to secrete reactive oxygen species. nitric oxide and inflammatory cytokines = promotes cell death via dendritic cell recruitment and maturation = accumulation of T cells at tumour site
flagging of the tumour for immune response and destruction
how do TTF have an anti-migratory effect
reduce the capacity of cancer cells for migration and invasion
TTFields disrupt key molecular pathways inside the cancer cells:
📉 1. NF-κB Pathway
NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) controls the expression of genes that promote inflammation, survival, and mobility.
TTFields inhibit NF-κB, making cancer cells less able to invade surrounding tissues.
📉 2. MAPK Pathway
MAPK (Mitogen-Activated Protein Kinase) regulates cell growth, differentiation, and motility.
TTFields disrupt MAPK activity, reducing the signals that drive cell movement and invasiveness.
📉 3. PI3K/Akt Pathway
PI3K/Akt promotes cell survival, growth, and migration.
TTFields downregulate this pathway, which weakens the cancer cell’s ability to spread and resist death.
how do TTF impact cell membrane permeability
they increase cell membrane permeability - increasing number of holes and size of holes in cell membrane. This can enhance the sensitivity to chemotherapeutic drugs
