RESUMO
Sugarcane borers are economically damaging insects with species that vary in distribution patterns both geographically and temporally, and vary based on ecological niche. Currently, identification of sugarcane borers is mostly based on morphological characters. However, morphological identification requires taxonomic expertise. An alternative method to identify sugarcane borers is the use of molecular data. DNA barcoding based on partial cytochrome c oxidase subunit 1 (COI) sequences has proven to be a useful tool for rapid and accurate species determination in many insect taxa. This study was conducted to test the effectiveness of DNA barcodes to discriminate among sugarcane borer species in China. Partial sequences of the COI gene (709 bp) were obtained from six species collected from different geographic areas. Results showed that the pairwise intraspecies genetic distance was < 0.02, whereas the interspecies genetic distance ranged from 0.117 to 0.182. Results from a neighbor-joining tree showed that the six sugarcane borer species were certainly separated. These results suggested that the partial COI sequences had high barcoding resolution in discriminating among sugarcane borer species. Our study emphasized the use of DNA barcodes for identification of the analyzed sugarcane borer species and represents an important step for building a comprehensive barcode library for sugarcane borers in China.
Assuntos
Código de Barras de DNA Taxonômico , Lepidópteros/classificação , Filogenia , Saccharum , Animais , China , DNA Mitocondrial/genética , HerbivoriaRESUMO
PURPOSE: Biological effects of low-dose radiation (LDR) are distinguishable from those of high-dose radiation. Adaptive response is an important biological effect following low-dose radiation. Cancer stem cells (CSCs) have self-renewal and multidirectional differentiation potency which results in relapse and metastasis of cancer. In this study, we aimed to examine whether adaptive response could be induced in CSCs by LDR. METHODS: Parental cells of three colon cancer cell lines (HRT18, HT29, and HCT116) and CSCs of these three cell lines were irradiated with LDR (i.e., D1) and then high-dose radiation (HDR) of X-rays (i.e., D1 + D2) or only HDR (D2 alone), followed by examination of adaptive response. RESULTS: Adaptive response was not observed either in the three tumor parental cells lines or in three CSCs lines following LDR, due to the lack of resistance to subsequent D2-induced cell growth inhibition. CONCLUSION: These results suggested that LDR may not induce adaptive response in colon cancer cells or colon CSCs under in vitro conditions. Our study provided experimental and clinical foundations for the application of LDR in the treatment of colon cancers.
Assuntos
Sobrevivência Celular/efeitos da radiação , Neoplasias do Colo/patologia , Células-Tronco Neoplásicas/patologia , Tolerância a Radiação , Neoplasias do Colo/radioterapia , Relação Dose-Resposta à Radiação , Humanos , Células-Tronco Neoplásicas/efeitos da radiação , Células Tumorais Cultivadas , Raios XRESUMO
Overexpression of cytokine-induced apoptosis inhibitor 1 (CIAPIN1) contributes to multidrug resistance (MDR) in breast cancer. This study aimed to evaluate the potential of CIAPIN1 gene silencing by RNA interference (RNAi) as a treatment for drug-resistant breast cancer and to investigate the effect of CIAPIN1 on the drug resistance of breast cancer in vivo. We used lentivirus-vector-based RNAi to knock down CIAPIN1 in nude mice bearing MDR breast cancer tumors and found that lentivirus-vector-mediated silencing of CIAPIN1 could efficiently and significantly inhibit tumor growth when combined with chemotherapy in vivo. Furthermore, Western blot analysis showed that both CIAPIN1 and P-glycoprotein expression were efficiently downregulated, and P53 was upregulated, after RNAi. Therefore, we concluded that lentivirus-vector-mediated RNAi targeting of CIAPIN1 is a potential approach to reverse MDR of breast cancer. In addition, CIAPIN1 may participate in MDR of breast cancer by regulating P-glycoprotein and P53 expression.
Assuntos
Animais , Feminino , Humanos , Antibióticos Antineoplásicos/uso terapêutico , Neoplasias da Mama/tratamento farmacológico , Doxorrubicina/uso terapêutico , Resistencia a Medicamentos Antineoplásicos/genética , Inativação Gênica , Peptídeos e Proteínas de Sinalização Intracelular/genética , Western Blotting , Neoplasias da Mama/genética , Carcinoma/tratamento farmacológico , Carcinoma/genética , Modelos Animais de Doenças , Genes MDR , Vetores Genéticos/genética , Inibidores do Crescimento/genética , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Lentivirus/genética , Camundongos Endogâmicos BALB C , Camundongos Nus , Membro 1 da Subfamília B de Cassetes de Ligação de ATP/efeitos dos fármacos , Interferência de RNA , RNA Interferente Pequeno/genética , /efeitos dos fármacosRESUMO
Overexpression of cytokine-induced apoptosis inhibitor 1 (CIAPIN1) contributes to multidrug resistance (MDR) in breast cancer. This study aimed to evaluate the potential of CIAPIN1 gene silencing by RNA interference (RNAi) as a treatment for drug-resistant breast cancer and to investigate the effect of CIAPIN1 on the drug resistance of breast cancer in vivo. We used lentivirus-vector-based RNAi to knock down CIAPIN1 in nude mice bearing MDR breast cancer tumors and found that lentivirus-vector-mediated silencing of CIAPIN1 could efficiently and significantly inhibit tumor growth when combined with chemotherapy in vivo. Furthermore, Western blot analysis showed that both CIAPIN1 and P-glycoprotein expression were efficiently downregulated, and P53 was upregulated, after RNAi. Therefore, we concluded that lentivirus-vector-mediated RNAi targeting of CIAPIN1 is a potential approach to reverse MDR of breast cancer. In addition, CIAPIN1 may participate in MDR of breast cancer by regulating P-glycoprotein and P53 expression.