This is about the GABRA3 gene.

I reached out to the lead researcher asking if specific subtypes over-express GABRA3.
His reply was: "The overexpression of GABRA3 in breast cancer is not subtype-specific. All subtypes have over-expression of GABRA3."

Here's the science version of the news: "The mRNA-edited form of GABRA3 suppresses GABRA3-mediated Akt activation and breast cancer metastasis."

Also, here's the important info from the media release:

The researchers analyzed The Cancer Genome Atlas (TCGA) and identified 41 genes inversely correlated with survival in breast cancer. Dr. Qihong Huang and colleagues focused on one gene in particular: GABAA receptor alpha3 (Gabra3). The gene was particularly intriguing, since prior to this study, researchers believed that Gabra3 was only found in brain tissue.

There were three main reasons the researchers determined it was worth studying.
- First, it's highly expressed in cancer tissues, but not in healthy breast tissues. [sounds like CD47]
- Second, it's a cell surface molecule and therefore something that could be potentially targeted by a drug.
- Finally, drugs that target Gabra3 are already available for treating other diseases like insomnia.
[See comments at very bottom of this post for examples of FDA approved drugs.]
The researchers showed that cells expressing Gabra3 were better at migrating and invading than their control counterparts, and Gabra3 showed metastasis-promoting activity in vivo, and animal models injected with the activated gene all developed metastatic lesions in their lungs. It does so by activating the AKT pathway, a cellular pathway essential to cell growth and survival in many types of cancer including breast cancer.

In some instances, though, certain types of Gabra3 are actually able to suppress breast cancer metastasis. This is closely linked to the RNA of the gene. RNA is a type of molecule similar to the DNA that encodes our genes, and recent discoveries have shown that RNA has a complex role in regulating how genes are turned on or off. In a phenomenon known as "RNA editing," small changes can be made to RNA nucleotide sequences even after they've been generated.

Huang and colleagues found that Gabra3 that had undergone RNA editing was found only in non-invasive breast cancers. When the RNA is edited, it suppressed the activation of the AKT pathway required for metastasis, meaning that breast cancer with this specific type of Gabra3 was unable to spread to other organs. This is particularly encouraging since signaling proteins called interferons can increase RNA editing activity and could therefore prevent Gabra3 from activating the AKT pathway.

"We believe this is the first time that anyone has demonstrated the importance of RNA editing in breast cancer," Huang said. "A combination strategy that that involves targeting Gabra3 while also upregulating the expression of RNA editing molecules could be an effective strategy for managing metastatic breast cancer."

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In terms of the FDA approved drugs, check this out:
Riluzole, an FDA-approved drug that inhibits the release of glutamate and is used for the treatment of amyotrophic lateral sclerosis has been shown to suppress GRM1 and the glutamate neurotransmission pathway, and decrease melanoma progression33, 34, 35. These results indicate that a gene that is specifically expressed in one tissue but aberrantly expressed in tumours of another tissue can play important roles in tumour development, and can thus serve as important therapeutic targets. Modulations of GABAA receptors are associated with sedation, ataxia, amnesia, anxiolytic and sleep activity36, 37 and there are a few GABAA receptor modulators currently used in clinic.
Flumazenil is a FDA-approved small molecule negative modulator of GABAA receptors, which targets GABRA1, 2, 3 and 5 (ref. 38). It is used to treat idiopathic hypersomnia and improve vigilance. It is worthwhile to determine whether flumazenil and other chloride channel blockers can be used as therapeutics to also treat breast cancer metastasis.

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Interferons upregulate the expression of ADAR1, which we have shown is responsible for Gabra3 editing in breast cancer cells^{45, 46, 47}. Recombinant interferon-β (IFN-β) has been shown in clinical trials to improve clinical benefits and overall survival in metastatic breast cancer patients with minimal residual disease after chemo or with disseminate disease non-progressing during endocrine therapy^{48, 49, 50}. Thus, the combination of targeting Gabra3 function and upregulating A-to-I editing of Gabra3 mRNAs may have the potential to further improve therapeutic effects as combination therapies.