Botulinum neurotoxin type A inhibits synaptic vesicle 2 expression in breast cancer cell lines.
OBJECTIVE
It is known that botulinum neurotoxin type A (BoNTA) improves some kinds of cancer (e.g. prostate) and that synaptic vesicle glycoprotein 2 (SV2) is the molecular target of this neurotoxin. Besides having potential therapeutic value, this glycoprotein has recently been proposed as a molecular marker for several types of cancer. Although the mechanisms of cancer development and the improvement found with botulinum treatment are not well understood, the formation of the botulinum-SV2 complex may influence the presence and distribution of SV2 and the function of vesicles. To date, there are no reports on the possible effect of botulinum on breast cancer of unknown causes, which have a great impact on women's health. Thus we determined the presence of SV2 in three breast cancer cell lines and the alterations found with botulinum application.


METHODS
With and without adding 10 units of botulinum, SV2 protein expression was determined by optical densitometry in T47D, MDA-MB-231 and MDA-MB-453 cell lines and the distribution of SV2 was observed with immunochemistry (hematoxylin staining).


RESULTS
The SV2 protein was abundant in the cancer cells herein tested, and maximally so in T47D. In all three cancer cell lines botulinum diminished SV2 expression, which was found mostly in the cell periphery.


CONCLUSIONS
SV2 could be a molecular marker in breast cancer. Its expression and distribution is regulated by botulinum, suggesting an interesting control mechanism for SV2 expression and a possible alternative therapy. Further studies are needed in this sense.
Research Support Group, INR Mexico.
C
C
Bandala
Laboratory of Molecular Oncology and Oxidative Stress, Medical School, IPN Mexico.
A L
AL
Cortés-Algara
Laboratory of Molecular Oncology and Oxidative Stress, Medical School, IPN Mexico.
C M
CM
Mejía-Barradas
Laboratory of Molecular Oncology and Oxidative Stress, Medical School, IPN Mexico.
I
I
Ilizaliturri-Flores
Research Support Group, INR Mexico.
R
R
Dominguez-Rubio
Laboratory of Cell Biology, CINVESTAV Mexico.
C I
CI
Bazán-Méndez
SEDENA Mexico.
E
E
Floriano-Sánchez
Laboratory of Cell Biology, CINVESTAV Mexico.
J P
JP
Luna-Arias
Laboratory of Cell Biology CIBIOR, IMSS Puebla, Mexico.
M
M
Anaya-Ruiz
Laboratory of Molecular Oncology and Oxidative Stress, Medical School, IPN Mexico.
E
E
Lara-Padilla
D000970:Antineoplastic Agents / Q000494:pharmacology*; D014408:Biomarkers, Tumor / Q000378:metabolism*; D019274:Botulinum Toxins, Type A / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D015536:Down-Regulation; D005260:Female; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D060066:Protein Interaction Maps
D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D008562:Membrane Glycoproteins; D009419:Nerve Tissue Proteins; C076414:SV2A protein, human; D019274:Botulinum Toxins, Type A
BoNTA; SV2; breast cancer; protein expression