• Microbiology and Biotechnology Letters
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• v.23 no.2
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• pp.178-186
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• 1995

Streptomyces albus wild type ATCC 21838 produced salinomycin, polyether antibiotic. To clone genes related salinomycin production, a genomic library was screened using actI as a DNA hybridization probe. pWHM 210 was isolated, which contained an approximately 24 kb of insert DNA. A 3.8 kb region in the 24 kb insert DNA was hybridized to actI and the nucleotide sequence of this region was determinied. Two open reading frames found in the same direction were homologous to genes for $\beta$-keto acyl synthase/acyl transferase and chain length determining factor in type II PKS (polyketide synthase). The genes were components of minimal type II PKS genes, highly conserved and showed the strong simiarity to other type II PKS genes known today.

• Journal of Microbiology
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• v.45 no.1
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• pp.6-10
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• 2007

Culture broth of a streptomycete isolate, Streptomyces sp. CS684 showed antibacterial activity on methicilin resistant Staphylococcus aureus (MRSA) and vancomycin resistant enterococci (VRE). Among purified substances from the organism, CSU-1, which is active against MRSA and VRE, is a $C_{37}H_{62}O_{12}Na\;(M^+,721.3875)$, and identified as laidlomycin. The anti-MRSA and anti-VRE activity of CSU-1 was stronger than oxacillin and vancomycin. Phylogenetic analysis showed that strain CS684 is very similar to Streptomyces ardus NRRL $2817^T$, whereas the ability of Streptomyces sp. CS684 to produce laidlomycin was shown to be unique.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.1
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• pp.21-30
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• 2024

The challenging clinical outcomes associated with advanced cervical cancer underscore the need for a novel therapeutic approach. Monensin, a polyether antibiotic, has recently emerged as a promising candidate with anti-cancer properties. In line with these ongoing efforts, our study presents compelling evidence of monensin's potent efficacy in cervical cancer. Monensin exerts a pronounced inhibitory impact on proliferation and anchorage-independent growth. Additionally, monensin significantly inhibited cervical cancer growth in vivo without causing any discernible toxicity in mice. Mechanism studies show that monensin's anti-cervical cancer activity can be attributed to its capacity to inhibit the Wnt/β-catenin pathway, rather than inducing oxidative stress. Monensin effectively reduces both the levels and activity of β-catenin, and we identify Akt, rather than CK1, as the key player involved in monensin-mediated Wnt/β-catenin inhibition. Rescue studies using Wnt activator and β-catenin-overexpressing cells confirmed that β-catenin inhibition is the mechanism of monensin's action. As expected, cervical cancer cells exhibiting heightened Wnt/β-catenin activity display increased sensitivity to monensin treatment. In conclusion, our findings provide pre-clinical evidence that supports further exploration of monensin's potential for repurposing in cervical cancer therapy, particularly for patients exhibiting aberrant Wnt/β-catenin activation.

• Korean Journal of Poultry Science
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• v.12 no.2
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• pp.127-134
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• 1985

Battery trial with 240 broiler chicks of Hubbard strain was conducted for a period of 2 weeks in order to compare the anticoccidical efficacy of polyether ionophorous antibiotics ; Maduramicin ammonium, Monensin and Salinomyc in sodium. The criteria used in these anticoccidial efficacy studies were anticoccidial index, growth rate, feed efficiency, mortality, lesion score and the number of oocysts produced after artificial inoculation with 70,000 sporulated oocysts of Eimeria tenella(90%) and E.necatrix (10%) to each bird. The result obtained are summarized as follow: 1. All groups medicated anticoccidial feed additives improved body weight gain and feed efficiency. However, it was found that the group medicated with Maduramicin showed better body weight gain (352.5 and 648.8 g) and feed efficiency(1.603 and 1.680) during the first and the second week experiments, 2. The mortality rate(4.2%) and lesion scores (1.72) of Maduramicin medicated group, from artificial coccidiosis were comparatively lower than those of other two medicated groups, 3. It was also found that oocyst output (0.25 ${\times}$ 10$^4$) in Maduramicin medicated group were lower than those of other two groups. 4. Anticoccidial indexes during the first week were 177.9 in Maduramicin medica-group, 158.7 in Salinomycin medicated group, 141.6 in Monensin medicated group and 78.0 in infected, nonmedicated group as compared with 200.0 in noninfected, nonmedicated group (NNC) 5. Anticoccidial indexes during the second week were 201.1 in Maduramicin group 184.0 in infected, nonmedicated group as compared with 200.0 in noninfected, nonmedicated group (NNC).

• Tuberculosis and Respiratory Diseases
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• v.75 no.1
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• pp.9-17
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• 2013

Background: In cancer cells, autophagy is generally induced as a pro-survival mechanism in response to treatment-associated genotoxic and metabolic stress. Thus, concurrent autophagy inhibition can be expected to have a synergistic effect with chemotherapy on cancer cell death. Monensin, a polyether antibiotic, is known as an autophagy inhibitor, which interferes with the fusion of autophagosome and lysosome. There have been a few reports of its effect in combination with anticancer drugs. We performed this study to investigate whether erlotinib, an epidermal growth factor receptor inhibitor, or rapamycin, an mammalian target of rapamycin (mTOR) inhibitor, is effective in combination therapy with monensin in non-small cell lung cancer cells. Methods: NCI-H1299 cells were treated with rapamycin or erlotinib, with or without monensin pretreatment, and then subjected to growth inhibition assay, apoptosis analysis by flow cytometry, and cell cycle analysis on the basis of the DNA contents histogram. Finally, a Western blot analysis was done to examine the changes of proteins related to apoptosis and cell cycle control. Results: Monensin synergistically increases growth inhibition and apoptosis induced by rapamycin or erlotinib. The number of cells in the sub-$G_1$ phase increases noticeably after the combination treatment. Increase of proapoptotic proteins, including bax, cleaved caspase 3, and cleaved poly(ADP-ribose) polymerase, and decrease of anti-apoptotic proteins, bcl-2 and bcl-xL, are augmented by the combination treatment with monensin. The promoters of cell cycle progression, notch3 and skp2, decrease and p21, a cyclin-dependent kinase inhibitor, accumulates within the cell during this process. Conclusion: Our findings suggest that concurrent autophagy inhibition could have a role in lung cancer treatment.