Registration for a live webinar on 'Neuroleptic malignant syndrome' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Talk outline
- Oxidative phosphorylation: ATP synthesis
- The H+-ATP synthase
- H+-ATP synthase is also an ATP hydrolase
- Role of mitochondria in cancer biology
- Cellular proliferation & aerobic glycolysis
- The bioenergetic signature of cancer
- Stage II colon cancer tissue microarrays
- Stage II colon cancer IHC & WB
- Low bioenergetic signature = worse prognosis
- β-F1-ATPase mRNA translation & localization
- Regulation of bioenergetic signature in cancer
- Purification / Identification of β-F1-ATPase
- Interaction of G3BP1 with β-F1-ATPase mRNA
- G3BP1 & β-F1 ATPase mRNA translation
- Functional role of G3BP1 in cancer
- Mechanisms that affect H+-ATP synthase
- ATPase inhibitory factor 1 (IF1)
- IF1 overexpression in human carcinomas
- Consequences of IF1/H49K overexpression
- Silencing of IF1 in HeLa cells
- Blockade of the ATP synthase
- IF1 overexpression triggers ROS signaling
- Mitochondrial ROS & NF-κB pathway in cancer
- Retrograde ROS signaling in colon cancer cells
- IF1-mediated retrograde signaling to nucleus
- The IF1 paradox in human tissues
- IF1 is phosphorylated in serine residues
- Phosphorylated IF1 in S39
- Dephospho-IF1 inhibits activity of enzyme
- Carcinomas overexpress dephosphorylated IF1
- Metabolism and cell cycle progression
- Mouse models of OXPHOS impairment
- Liver models: IF1-H49K expression & OXPHOS
- Overexpression of IF1-H49K in the liver
- Proliferation & apoptotic resistance
- IF1 & NFκB drive hepatocellular carcinoma
- High IF1 expression & breast cancer prognosis
- Phenotype of cancer cells overexpressing IF1
- Considerations
- Acknowledgements
Topics Covered
- Overview of oxidative phosphorylation
- ATP synthase and its regulation by IF1
- Functions of ATP synthase/hydrolase in cancer
- Aerobic glycolysis and cellular proliferation status
- Metabolic reprogramming in proliferation
- mRNA binding proteins in translation silencing & cancer progression
- Overexpression of IF1 in cancer
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Cuezva, J. (2018, October 31). Reprogramming oxidative phosphorylation in cancer [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 10, 2024, from https://doi.org/10.69645/CQAO8564.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. José Cuezva has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Cancer
Transcript
Please wait while the transcript is being prepared...
0:00
In this presentation, we will describe part of the mechanisms
that are involved in the reprogramming of oxidative phosphorylation in cancer.
0:10
The talk is going to be structured in four main parts.
First, we will look at the tight connection that exists between
oxidative phosphorylation and glycolysis to explain metabolic reprogramming in cancer.
Next, we will study the mechanisms that control
oxidative phosphorylation at the level of the ATP synthase in cancer.
And there are two main mechanisms;
by limiting the content of the ATP synthase,
and by inhibiting the activity of the ATP synthase,
by a small mitochondrial protein that is called IF1,
and it is the ATPase inhibitory factor one.
The third part of the talk,
will be devoted to the regulation of the activity of this inhibitor.
And finally, we will look at the role of the F1 ATPase in cancer progression,
and specifically focused on IF1.
1:07
Oxidative phosphorylation is the mitochondrial pathway
for obtaining biological energy in the form of ATP.
In this process, the electrons that have been obtained in the oxidation
of glucose and fatty acids are collected in NADH,
which is going to transfer the electrons to
the respiratory change that is placed in the inner mitochondrial membrane.
Electrons flow down through these complexes to
molecular oxygen to generate the water of respiration.
In this electron transfer through the respiratory complexes,
the proteins pump protons from
the matrix of the mitochondria into the intermembrane space,
generating what is called the proton electro-chemical gradient.
Another protein also placed in the inner mitochondrial membrane,
that is called the ATP synthase,
is going to utilize the proton gradient to generate the ATP that is used by the cell,
by the phosphorylation of the ADP and inorganic phosphate
that is made available to the matrix of the organelle by specific transporters.