Cancer, the STRA6 “receptors” and Insulin

In my recent Obesity Causation v 2.0 blog post discussing the connection between insulin resistance and obesity I shared my theory on the key role played by the STRA6 “receptors”.  I thought I’d add to it here and highlight the similar connections with cancer.  Once again, I used Claude.ai from Anthropic to speed up the discussion.

Grant:

In cellular biology there is what’s called the STRA6 etc. receptors. Is there a known relationship between these receptors and cancer cells?

Claude.ai:

Yes, there are known relationships between STRA6 (Stimulated by Retinoic Acid 6) and cancer. STRA6 is primarily known as a vitamin A/retinol transporter, but research has shown several important connections to cancer:

1. STRA6 has been found to be overexpressed in several types of cancers, including:
   • Colorectal cancer
   • Breast cancer
   • Certain types of leukemia
2. The receptor functions as more than just a transporter – it can activate JAK2/STAT3 signalling pathways, which are known to promote:
   • Cell proliferation
   • Cell survival
   • Cancer cell migration
   • Drug resistance
3. High STRA6 expression has been correlated with poorer prognosis in some cancer types, suggesting it may play a role in cancer progression.

However, I should note that while these relationships have been documented in research literature, my knowledge cutoff means I may not be aware of the most recent findings. Given this is an active area of research, I’d recommend checking recent publications for the latest understanding of STRA6’s role in cancer biology.

Grant:

Is it correct that in some types of cancer cells insulin metabolism is dysregulated, and more specifically that those cells can take up glucose without the action of insulin?

Claude.ai:

Yes, that’s correct! This is actually one of the hallmark metabolic changes in cancer cells, often called the “Warburg Effect” after Otto Warburg who first described it. Here are the key points:

1. Normal cells typically require insulin signalling to efficiently take up glucose through GLUT4 transporters
2. Cancer cells often exhibit what’s called “insulin-independent glucose uptake” through several mechanisms:
   • Overexpression of GLUT1 transporters (which don’t require insulin)
   • Constitutive activation of the PI3K/AKT pathway
   • Mutations that keep glucose uptake mechanisms permanently “switched on”
3. This metabolic reprogramming allows cancer cells to:
   • Maintain high glucose uptake regardless of insulin levels
   • Support their high energy demands
   • Feed their preference for aerobic glycolysis over oxidative phosphorylation
4. This altered metabolism has become an important diagnostic tool:
   • It’s the basis for PET scanning using radioactive glucose analogs (FDG-PET)
   • Cancer cells show up as “hot spots” because they rapidly take up the glucose tracer independent of insulin

This metabolic independence from insulin is one reason why cancer cells can maintain their high energy consumption even under conditions where normal cells would reduce their glucose uptake.

Grant:

Is mutated DNA and / or chromosomes one of the other key hallmarks of cancer cells?

Claude.ai:

Yes, genomic instability and mutation is one of the key hallmarks of cancer cells. This includes:

1. Point mutations in critical genes:
   • Oncogenes (e.g., RAS)
   • Tumor suppressor genes (e.g., p53)
2. Chromosomal abnormalities:
   • Aneuploidy (incorrect chromosome numbers)
   • Translocations
   • Deletions
   • Duplications
3. DNA repair defects:
   • Impaired DNA damage response
   • Microsatellite instability
   • Increased mutation rates

These genetic changes enable cancer cells to evade normal growth controls and accumulate additional mutations that promote their survival and spread.

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Now combine the above information with what I’ve shared in my eBooks regarding cancer causation.  Specifically, my analysis of this study:

And, of course this little ditty from my diabetes blog post on RA, the so-called “active form of vitamin A”, fracturing our DNA.

DNA fragmentation induced by all-trans retinoic acid and its steroidal analogue EA-4 in C2C12 mouse and HL-60 human leukemic cells in vitro
Raghda S. Alakhrasa, Georgia Stephanoua, Nikos A. Demopoulosa*,
Konstantinos Grintzalisa, Christos D. Georgioua and Sotirios S. Nikolaropoulosb

Abstract:
We have recently shown that retinoic acid induces micronucleation mainly via chromosome breakage.

Likewise, all of the information in my Breast Cancer eBook also very strongly implicates so called “vitamin A” in causing the disease.

I’ve now had multiple reports from relatively young people who were regularly eating liver develop cancer. So, to all the folks still clinging to the belief that liver is a “super food”, give your head a shake and wake up.  Consuming liver is no doubt “super effective” in causing cancer in addition to a bunch of other horrible disease conditions. It’s just a matter of time…. you’ve been warned.

Although here in this article and in my Breast Cancer eBook I make a strong case for vA being an important factor in causing cancer there’s very little hope that a low vA diet can reverse it, most certainly not in the near term. Meaning, once the disease is initiated it is going to be very difficult to naturally reverse it.

Cancer is an extremely serious disease. If it’s not treated early then there’s the additional risk of metastasis, and that could be fatal. I can’t give medical advice, and even if I could I wouldn’t have any recommendations for following a natural healing path as I sure don’t know of anything that’s proven effective.