Ready for a deep dive into how to kill cancer with peptides? This is real and it’s coming on the scene soon. Very exciting.
First, we have to start with how cancer cells become cancer cells. A normal cell develops, does its function, then gets out of the way with an organized, sensible collapse of the mitochondria. That leads to the term apoptosis, or cell death of the whole cell. When it’s done properly, it makes no inflammation and the cell gets “processed”. It is then replaced with a new baby stem cell of the same tissue. The gene that mediates that is the p53 gene. The p53 gene is essentially your watchdog for DNA damage that gets activated when the cell DNA gets too far broken and sets in motion a process of making the mitochondria get leaky. In swoops p53, the cell dies in an orderly fashion and the whole organism survives. You get a new liver cell, heart cell, skin cells, white blood cell….. and life goes on.
In cancer, something else happens. Cancers aren’t a problem because they are multiplying too fast. (Well, they do in some circumstances but bear with me.) The real problem with cancer is that the cancer cells live too long. Way too long. And just about every cancer depends on an “altered” p53 gene as part of its tool kit to live forever. We actually know down to the molecule how that happens in the majority of cancer cells. You read language like: “sequestration of the p53 in the cytoplasmic body correlates with the ability of the E18 55-kDa to repress p53-dependent apoptosis.”
Did you get that? Cancers all have a broken p53 system. What would happen if we repair it? What would happen if we put a proper p53 back into place? There’s a peptide for that! It’s actually probably all about protein folding and shape that gets us what we want. Cellular origami, if you will. You gotta know when to “hold em, and when to fold em“.
I don’t want to kill you off trying to explain it but it comes down to a tumor gene called Mdm2 that suppresses our friend p53. There is a binding site on Mdm2 that attaches and inactivates p53. It happens to have a peptide that fits right into it. Disrupt Mdm2 binding to p53. p53 refolds itself properly. It goes to work. It discovers all the broken DNA in the cancer cell and gets to work killing it. Cancer cell dies. Viola!
Ok. Get to the point. How do I get the peptide into the cancer cell? PNC-27. It’s actually a fragment of the Mdm2 protein. That’s what peptides are; fragments and pieces of bigger proteins that fit into the molecular lock and activate it.
There is a peptide called penetratin with a peptide sequence, KKWKMRRNQF- WVKVQRG. (Pronounce that for me.) Add that to the Mdm2 fragment so you can transport it into the cell, and lookout cancer! All with no toxicity to normal cells. p53 is your friend. Activating it is no big deal if your cells are normal.
There must be a fly in the ointment somewhere. There is. It takes 72 hours of continuous exposure to kill the ALL the cancer cells. How to do that? Tricky. Inject it into the tumor? Nope. The cancer is in too many places. Get it past your gut with a very slow-release form? That may be possible. Sound exciting? Hold on. The FDA has issued a warning about the premature enthusiasm. But there are clinics in Mexico administering it. There is experimental evidence it kills breast cancer in 30 minutes. Pancreatic cancer may need longer. The problem is not with the peptide. It’s the wild cat labs making the polluted or adulterated stuff that has it contaminated and has given some folks sepsis. What would you do?
WWW: What will work for me. I’m all over this with interest. If it causes no toxicity, and you are in a tough spot, would you try it? Do you have the right to do it? This is all sufficient material for a graduate course in medical ethics. Is there hope for the future? You bet. Would I try it on myself if I were in that spot? Anyone not caught up with the awful disease cancer can’t tell folks who are what they should do. My opinion. Some of the best research out there is with pancreatic cancer, one of the worst.
- What is the name of your own natural cancer cell killer protein? Answer. P53. Your friend.
- What happens in most human cancers that make p53 unavailable? Answer: It gets “sequestered” and refolded or attached to another cancer-associated protein called MdM2. In any case, it isn’t there to do the job of killing off a cell with too many DNA mutations.
- What is PNC-27? Answer: It is a fragment of Mdm2 that is the binding part
to p-53. That appears to release P53 from its clutches so it can do its job of initiating cell death.
- What is the key peptide discovery to get PNC-27 to where it needs to do its job? Answer: Scientists had to find a way to get the blocking fragment into the cell through the cancer cell wall. They did that with a transporting peptide called KKWKMRRNQF- WVKVQRG. (Save that spelling for your next Scrabble)
- How quickly does PNC-27 work in lab samples? Answer. Between 30 minutes with some breast cancer lines. 72 hours for other cancers.
- Would you sign up for a 3 day IV of a drug that has zero toxicity to human cells if you had a wicked, aggressive cancer? Answer: You talk here.
- The FDA has issued warnings about PNC-27 because? Answer: there are so many desperate folks that crooks are taking advantage and selling awful, adulterated stuff and some folks have gotten sepsis.