Effect of Botulinum Toxin A on Proliferation and Apoptosis in the T47D Breast Cancer Cell Line

Bandala, Cindy; Pérez-Santos, Martín; Lara‐Padilla, Eleazar; Lopez, Ma. Guadalupe Delgado; Anaya-Ruı́z, Maricruz

doi:10.7314/apjcp.2013.14.2.891

Cited by 47 publications

(30 citation statements)

References 21 publications

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“…BoNT/A induces apoptosis in cell cultures derived from prostate cancer and breast cancer (Bandala et al 2013;Karsenty et al, 2009;Proietti et al, 2012). Lack of neural elements in cell culture suggests that BoNT/A effect are mediated through mechanisms independent from neurotransmitter release.…”

Section: Possible Additional Targets Of Bont/a Action Other Than Snap-25mentioning

confidence: 99%

Botulinum toxin A, brain and pain

Matak

Lacković

2014

Progress in Neurobiology

149

114

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Section: Possible Additional Targets Of Bont/a Action Other Than Snap-25mentioning

confidence: 99%

Botulinum toxin A, brain and pain

Matak

Lacković

2014

Progress in Neurobiology

149

114

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“…Furthermore, other investigations imply that some bacterial toxins could be used in targeted-cancer therapy, and others synergistically promote the activity of the anticancer drugs (26, 27). Therefore, it is strongly proposed to complete additional supplementary studies to examine the synergistic activity of the enterotoxin with routine anticancer drugs.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Enterotoxin B Down-Regulates the Expression of Transforming Growth Factor-Beta (TGF-β) Signaling Transducers in Human Glioblastoma

Akbari

Farahnejad

Akhtari

et al. 2016

Jundishapur J Microbiol

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BackgroundIt has been revealed that Staphylococcus aureus enterotoxin B (SEB) may feature anti-cancer and anti-metastatic advantages due to its ability to modify cell immunity processes and signaling pathways. Glioblastoma is one of the most aggressive human cancers; it has a high mortality nature, which makes it an attractive area for the development of novel therapies.ObjectivesWe examined whether the SEB could exert its growth inhibitory effects on glioblastoma cells partially through the manipulation of a key tumor growth factor termed transforming growth factor-beta (TGF-β).Materials and MethodsA human primary glioblastoma cell line, U87, was treated with different concentrations of SEB. The cell quantity was measured by the MTT assay at different exposure times. For molecular assessments, total ribonucleic acid (RNA) was extracted from either non-treated or SEB-treated cells. Subsequently, the gene expression of TGF-β transducers, smad2/3, at the messenger RNA (mRNA) level, was analyzed via a quantitative real-time polymerase chain reaction (qPCR) using the SYBR Green method. Significant differences between cell viability and gene expression levels were determined (Prism 5.0 software) using one-way analyses of variance (ANOVA) test.ResultsWe reported that SEB could effectively down-regulate smad2/3 expression in glioblastoma cells at concentrations as quantity as 1 μg/mL and 2 μg/mL (P < 0.05 and P < 0.01, respectively). The SEB concentrations effective at regulating smad2/3 expression were correlated with those used to inhibit the proliferation of glioblastoma cells. Our results also showed that SEB was able to decrease smad2/3 expression at the mRNA level in a concentration- and time-dependent manner.ConclusionsWe suggested that SEB could represent an agent that can significantly decrease smad2/3 expression in glioblastoma cells, leading to moderate TGF-β growth signaling and the reduction of tumor cell proliferation.

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“…During the past decade, bacteria have extensively studied for their biomedical applications in cancer therapy (Bandala et al, 2013). Live and attenuated bacteria can all be antitumor agents that have been emerged as potential strategies (Bermudes et al, 2002).…”

Section: Discussionmentioning

confidence: 99%