Dominant Inheritance of Field-Evolved Resistance to Fipronil in Plutella xylostella (Lepidoptera: Plutellidae).

A field-collected strain (HF) of Plutella xylostella (L.) showed 420-fold resistance to fipronil compared with a susceptible laboratory strain (Roth). The HF-R strain, derived from the HF strain by 25 generations of successive selection with fipronil in the laboratory, developed 2,200-fold resistance to fipronil relative to the Roth strain. The F(1) progeny of the reciprocal crosses between HF-R and Roth showed 640-fold (R♀ × S♂) and 1,380-fold (R♂ × S♀) resistance to fipronil, indicating resistance is inherited as an incompletely dominant trait. Analysis of progeny from a backcross (F1♂ × S♀) suggests that resistance is controlled by one major locus. The LC(50) of the R♂ × S♀ cross F(1) progeny is slightly but significantly higher than that of the R♀ × S♂ cross F(1) progeny, suggesting a minor resistance gene on the Z chromosome. Sequence analysis of PxGABARα1 (an Rdl-homologous GABA receptor gene of P. xylostella) from the HF-R strain identified two mutations A282S and A282G (corresponding to the A302S mutation of the Drosophila melanogaster Rdl gene), which have been previously implicated in fipronil resistance in several insect species including P. xylostella. PxGABARα1 was previously mapped to the Z chromosome of P. xylostella. In conclusion, fipronil resistance in the HF-R strain of P. xylostella was incompletely dominant, and controlled by a major autosomal locus and a sex-linked minor gene (PxGABARα1) on the Z chromosome.

Retraction Note to: Acetylshikonin inhibits in vitro and in vivo tumorigenesis in cisplatin-resistant oral cancer cells by inducing autophagy, programmed cell death and targeting m-TOR/PI3K/Akt signalling pathway.

Retraction of "Acetylshikonin inhibits in vitro and in vivo tumorigenesis in cisplatin-resistant oral cancer cells by inducing autophagy, programmed cell death and targeting m-TOR/PI3K/Akt signalling pathway", by Peng Wang, Weiyue Gao, Yibin Wang, Jun Wang. JBUON 2019;24(5):2062-2067; PMID: 31786876 Following the publication of the above article, readers drew to our attention that part of the data was unreliable. We requested the authors to provide the raw data to prove the originality. Then the corresponding author contacted with our journal and stated below: Our group tried to repeat the results presented in this paper, but found that some data was not able to be reproducible. The authors then asked to retract this article. At the same time, our journal's investigation into this article also showed that part of the results in this article can not be supported by the data. Given above, we decided to retract this article. All the authors were informed of the retraction. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

Molecular cloning, genomic structure, and genetic mapping of two Rdl-orthologous genes of GABA receptors in the diamondback moth, Plutella xylostella.

The Resistance to dieldrin (Rdl) gene encodes a subunit of the insect gamma-aminobutyric acid (GABA) receptor. Cyclodiene resistance in many insects is associated with replacement of a single amino acid (alanine at position 302) with either a serine or a glycine in the Rdl gene. Two Rdl-orthologous genes of GABA receptors (PxGABARalpha1 and PxGABARalpha2) were cloned and sequenced from a susceptible strain (Roth) of Plutella xylostella. PxGABARalpha1 and PxGABARalpha2 showed 84% and 77% identity with the Rdl gene of Drosophila melanogaster at an amino acid level, respectively. The coding regions of PxGABARalpha1 and PxGABARalpha2 both comprise ten exons, with two alternative RNA-splicing forms in exon 3 of both genes. At the orthologous position of alanine-302 in D. melanogaster Rdl, PxGABARalpha1 has a conserved alanine at position 282. PxGABARalpha2 has a serine instead of an alanine at the equivalent position. With two informative DNA markers, both PxGABARalpha1 and PxGABARalpha2 were mapped onto the Z chromosome of P. xylostella.

Acetylshikonin inhibits in vitro and in vivo tumorigenesis in cisplatin-resistant oral cancer cells by inducing autophagy, programmed cell death and targeting m-TOR/PI3K/Akt signalling pathway.

PURPOSE: Oral cancer causes considerable mortality across the globe, mainly due development of chemoresistance and lack of efficient chemotherapeutic agents. In the current study the anticancer potential of Acetylshikonin was examined against KB-R cisplatin-resistant oral cancer cells along with evaluation of in vitro and in vivo modes of action. METHODS: The proliferation rate of the oral cancer cells was checked by MTT assay. Autophagy was detected by electron microscopy. Apoptotic cell death was assessed by DAPI and annexin V/propidium iodide (PI) staining. Protein expression was determined by immunoblotting. Xenografted mice models were used for in vivo evaluation of Acetylshikonin. RESULTS: The results revealed that Acetylshikonin could significantly inhibit the proliferation of all the oral cancer cells with lower cytoxicity compared with the normal cells. The anticancer activity of Acetylshikonin against the KB-R cisplatin-resistant cells was found to be due to induction of autophagy and apoptosis. The Acetylshikonin prompted apoptosis and autophagy was also associated with alteration in the apoptosis and autophagy-related protein expression. Furthermore, it was observed that Acetylshikonin could inhibit the mTOR/PI3K/AKT signalling pathway in the cisplatin-resistant KB-R oral cancer cells. The effects of the Acetylshikonin were also examined in vivo in xenografted mice models and it was observed that Acetylshikonin inhibited the growth of xenografted tumors. CONCLUSIONS: These results suggest that Acetylshikonin considerably suppresses the growth of cisplatin-resistant oral cancer in vitro and in vivo and may prove beneficial in the treatment of drug-resistant oral cancer.

[The capacity of proliferation and migration is higher in Tca8113 cells with up-regulated TNFSF14 expression].

OBJECTIVE: To construct a lentiviral vector carrying tumor necrosis factor superfamily member 14 (TNFSF14) gene, infect tongue cancer Tca8113 cells in vitro, and observe the effect on infected Tca8113 cells. METHODS: A lentiviral vector containing TNFSF14 gene was constructed and used to infect the Tca8113 cells. After selected by puromycin, the level of TNFSF14 mRNA in Tca8113 cells was detected by real-time quantitative PCR. Cell proliferation activity and cell circle were determined respectively by MTT assay and flow cytometry (FCM). And the cell migration ability was measured by Transwell(TM) assay. RESULTS: Compared with the control group, the expression of TNFSF14 mRNA increased in the infected cells. MTT assay and FCM showed TNFSF14 promoted the proliferation of Tca8113 cells. Transwell™ assay showed TNFSF14 boosted the migration ability of Tca8113 cells. CONCLUSION: The proliferation and migration would be enhanced in Tca8113 cells with over-expressed TNFSF14.

Effects of ginsenoside Rg-1 on the proliferation and osteogenic differentiation of human periodontal ligament stem cells.

OBJECTIVE: To evaluate the effects of ginsenoside Rg-1 on the proliferation and osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) and to explore the possible application on the alveolar bone regeneration. METHODS: To determine the optimum concentration, the effects of ginsenoside Rg-1 ranging from 10 to 100 µmol/L were evaluated by 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide, alkaline phosphatase activity and calcium deposition. Expressions of runt-related transcription factor 2, collagen alpha-2(I) chain, osteopontin, osteocalcin protein were examined using real-time polymerase chain reaction. RESULTS: Compared with the control group, a certain concentration (10 µmol/L) of the Rg-1 solution significantly enhanced the proliferation and osteogenic differentiation of hPDLSCs (P<0.05). However, concentrations that exceeds 100 µmol/L led to cytotoxicity whereas concentrations below 10 nmol/L showed no significant effect as compared with the control. CONCLUSION: Ginsenoside Rg-1 can enhance the proliferation and osteogenic differentiation of hPDLSCs at an optimal concentration of 10 µmol/L.