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- Proposal of Flavihumibacter fluvii sp. nov. as a replacement name for the effectively published but invalidated epithet Flavihumibacter fluminis Park et al. 2022
- Miri S. Park , Hyeonuk Sa , Ilnam Kang , Jang-Cheon Cho
- J. Microbiol. 2023;61(6):649-651. Published online June 12, 2023
- DOI: https://doi.org/10.1007/s12275-023-00057-1
- 55 View
- 0 Download
- 1 Web of Science
- 1 Crossref
-
Abstract
- The name Flavihumibacter fluminis Park et al. 2022, which was effectively published but invalidated, is an illegitimate homonymic epithet of Flavihumibacter fluminis Guo et al. 2023. The low 16S rRNA gene sequence similarity and genomic relatedness between the type strains IMCC34837T and RY-1T of the two homonymic species indicated that they are different species. To avoid further confusion, we propose a new name Flavihumibacter fluvii sp. nov. to replace the effectively published but invalidated homonymic epithet Flavihumibacter fluminis Park et al. 2022.
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Citations
Citations to this article as recorded by
- Validation List no. 214. Valid publication of new names and new combinations effectively published outside the IJSEM
Aharon Oren, Markus Göker
International Journal of Systematic and Evolutionary Microbiology .2023;[Epub] CrossRef
- Validation List no. 214. Valid publication of new names and new combinations effectively published outside the IJSEM
Journal Article
- 1Medical Convergence Materials Commercialization Center, Gyeongsan
- JaeJin An , Eun-Mi Ha
- J. Microbiol. 2020;58(11):967-977. Published online October 30, 2020
- DOI: https://doi.org/10.1007/s12275-020-0375-y
- 59 View
- 0 Download
- 20 Web of Science
- 17 Crossref
-
Abstract
-
Lactobacillus plantarum-derived metabolites (LDMs) increase
drug sensitivity to 5-FU and antimetastatic effects in 5-FUresistant
colorectal cancer cells (HCT-116/5FUR). In this
study, we evaluated the effects of LDMs on the regulation of
genes and proteins involved in HCT-116/5-FUR cell proliferation
and metastasis. HCT-116/5-FUR cells showed high
metastatic potential, significantly reduced tight junction (TJ)
integrity, including increased migration and paracellular permeability,
and upregulation of claudin-1 (CLDN-1). The genetic
silencing of CLDN-1 increased the sensitivity of HCT-
116/5FUR to 5-FU and inhibited its metastatic potential by
regulating the expression of epithelial-mesenchymal transition
(EMT) related genes. Co-treatment of HCT-116/5FUR
with LDMs and 5-FU suppressed chemoresistant and metastatic
behavior by downregulating CLDN-1 expression. Finally,
we designed LDMs-based therapeutic strategies to treatment
for metastatic 5-FU-resistant colorectal cancer cells. These
results
suggested that LDMs and 5-FU cotreatments can synergistically target 5-FU-resistant cells, making it a candidate strategy to overcome 5-FU chemoresistance improve anticancer drug efficacy. -
Citations
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