• The Journal of the Korean Society for Microbiology
• /
• v.14 no.1
• /
• pp.27-37
• /
• 1979

Ninety-five strains of Shigella, 70 of Salmonella paratyphi A, and 230 of Salmonella typhi were tested for their resistance to drugs. Also studied was the inhibition and elimination of drug resistance. All except one strain of Shigella consisted of 79 Sh. flexneri and 16 Sh. sonnei were multiply resistant to chloramphenicol, tetracycline, streptomycin, and splfisomidine. Among them, 70 strains were resistant to ampicillin and carbenicillin, 80 to trimethoprim-sulfamethoxazole, 22 to nalidixic acid, and one to kanamycin, but strain resistant to gentamicin, cephaloridine, and rifampin was not encountered. All strains of S. paratyphi A and S. typhi were susceptible to drugs tested, except sulfisomidine and rifampin, for which all S. paratyphi A were slightly resistant to sulfisomidine and the majority of S. paratyphi A and S. typhi were slightly resistant to rifampin. Approximately 80% of multiply drug-resistant Shigella transferred their resistance to E. coli by conjugation, and the resistance was considered to be mediated by R plasmids. The frequency of transfer of drug resistance varied by donor strains and recipients, but not by selecting drugs. Resistance to nalidixic acid was not transferred by conjugation to the recipients. Drug-resistant Shigella strains successively subcultured in nutrient agar stabs contained clones resistant to drugs and those susceptible to drugs, but the ratio of resistant and susceptible clones varied by strains. The multiply drug-resistant S. typhi and Shigella strains were found to not lose completely their drug resistance by subculture in media. Acriflavine has some effect on the elimination of drug resistance mediated by R plasmids, but the effect varied markedly by strains. Atabrine has no effect among strains tested. The combination of drugs increased the drug actions in majority of cases with synergistic or additive effects.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.13
• /
• pp.5191-5197
• /
• 2015

A partial response or resistance to chemotherapeutic agents is considered as a main obstacle in treatment of patients with cancer, including breast cancer. Refining taxane-based treatment procedures using adjuvant or combination treatment is a novel strategy to increase the efficiency of chemotherapy. PPM1D is a molecule activated by reactive oxygen species. whose expression is reported to modulate the recruitment of DNA repair molecules. In this study we examined the impact of arsenic trioxide on efficacy of paclitaxel-induced apoptosis in paclitaxel-resistant MCF-7 cells. We also investigated the expression of PPM1D and TP53 genes in response to this combination treatment. Resistant cells were developed from the parent MCF-7 cell line by applying increasing concentrations of paclitaxel. MTT assays were applied to determine the rate of cell survival. DAPI staining using fluorescent microscopy was employed to study apoptotic bodies. Real-time RT-PCR analysis was also applied to determine PPM1D mRNA levels. Our results revealed that combination of arsenic trioxide and paclitaxel elevates the efficacy of the latter in induction of apoptosis in MCF-7/PAC resistant cells. Applying arsenic trioxide also caused significant decreases in PPM1D mRNA levels (p<0.05). Our findings suggest that arsenic trioxide increases paclitaxel-induced apoptosis by down regulation of PPM1D expression. PPM1D dependent signaling can be considered as a novel target to improve the efficacy of chemotherapeutic agents in resistant breast cancer cells.

• Korean Journal of Veterinary Research
• /
• v.17 no.2
• /
• pp.73-78
• /
• 1977

The distribution of coliform population and drug-resistant coliforms in Shinchun water during April to August in 1976 and R factors in resistant strains were studied. The mean coliform population in the stream water was 361 organisms per 0.1ml and 53.5% of total coliforms were fecal coliforms. Thritynine and a half percent of total coliforms were streptomycin (SM) resistant to one or more of following antibiotics; tetracycline (TC), chloramphenicol (CM), ampicillin (AP) and kanamycin (KM). The most frequent resistant pattern was triple resistance to SM, TC and AP (23.8%) and followed by quadruple one to SM, TC, CM and AP (17.5%). About 87 percent strains carried R factors which were transferable by conjugation to E. coli ML 1410 or S. typhimurium LT 2.

• Natural Product Sciences
• /
• v.24 no.4
• /
• pp.225-228
• /
• 2018

By activity-guided fractionation, gliotoxin was isolated as an antibacterial metabolite of the fungus Penicillium decumbens which was derived from the jellyfish Nemopilema nomurai. Gliotoxin was further evaluated for antibacterial activity against several piscine and human MDR (multidrug resistance) pathogens. Gliotoxin showed significant antibacterial activity against Gram-positive piscine pathogens such as Streptococcus iniae FP5228, Streptococcus iniae FP3187, Streptococcus parauberis FP3287, Streptococcus parauberis SPOF3K, S. parauberis KSP28, and Lactococcus garvieae FP5245. Gliotoxin showed strong activity especially against S. parauberis SPOF3K and S. iniae FP5228, which are resistant to oxytetracycline. It is noteworthy that gliotoxin effectively suppressed streptococci which are the major pathogens for piscine infection and mortality in aquaculture industry. Gliotoxin also showed strong antibacterial activity against multidrug- resistant human pathogens (MDR) including Enterococcus faecium 5270 and MRSA (methicillin-resistant Staphylococcus aureus) 3089.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.22
• /
• pp.9853-9857
• /
• 2014

Background: The morbidity and mortality rate of liver cancer continues to rise in China and advanced cases respond poorly to chemotherapy. Ribosomal protein L24 has been reported to be a potential therapeutic target whose depletion or acetylation inhibits polysome assembly and cell growth of cancer. Materials and Methods: Total RNA of cultured amycin-resistant and susceptible HepG2 cells was isolated, and real time quantitative RT-PCR were used to indicate differences between amycin-resistant and susceptible strains of HepG2 cells. Viability assays were used to determine amycin resistance in RPL24 transfected and control vector and null-transfected HepG2 cell lines. Results: The ribosomal protein L24 transcription level was 7.7 times higher in the drug-resistant HepG2 cells as compared to susceptible cells on quantitative RT-PCR analysis. This was associated with enhanced drug resistance as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions: The ribosomal protein L24 gene may have effects on drug resistance mechanisms in hepatocellular carcinoma HepG2 cells.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.1
• /
• pp.127-131
• /
• 2013

Trastuzumab is the first molecular targeting drug to increase the overall survival rate in advanced gastric cancer. However, it has also been found that a high intrinsic or primary trastuzumab resistance exists in some proportion of gastric cancer patients. In order to explore the mechanism of resistance to trastuzumab, firstly we investigated the expression of MUC1 (membrane-type mucin 1) in gastric cancer cells and its relationship with drug-resistance. Then using gene-silencing, we transfected a siRNA of MUC1 into drug-resistant cells. The results showed the MKN45 gastric cell line to be resistant to trastuzumab, mRNA and protein expression of MUC1 being significantly upregulated. After transfection of MUC1 siRNA, protein expression of MUC1 in MKN45cells was significantly reduced. Compared with the junk transfection and blank control groups, the sensitivity to trastuzumab under MUC1 siRNA conditions was significantly increased. These results imply that HER2-positive gastric cancer cell MKN45 is resistant to trastuzumab and this resistance can be cancelled by silencing expression of the MUC1 gene.

• Biomolecules & Therapeutics
• /
• v.26 no.3
• /
• pp.313-321
• /
• 2018

Anti-cancer drug resistance is a major problem in colorectal cancer (CRC) research. Although several studies have revealed the mechanism of cancer drug resistance, molecular targets for chemotherapeutic combinations remain elusive. To address this issue, we focused on the expression of cellular prion protein ($PrP^C$) in 5-FU-resistant CRC cells. In 5-FU-resistant CRC cells, $PrP^C$ expression is significantly increased, compared with that in normal CRC cells. In the presence of 5-FU, $PrP^C$ increased CRC cell survival and proliferation by maintaining the activation of the PI3K-Akt signaling pathway and the expression of cell cycle-associated proteins, including cyclin E, CDK2, cyclin D1, and CDK4. In addition, $PrP^C$ inhibited the activation of the stress-associated proteins p38, JNK, and p53. Moreover, after treatment of 5-FU-resistant CRC cells with 5-FU, silencing of $PrP^C$ triggered apoptosis via the activation of caspase-3. These results indicate that $PrP^C$ plays a key role in CRC drug resistance. The novel strategy of combining chemotherapy with $PrP^C$ targeting may yield efficacious treatments of colorectal cancer.

• Parasites, Hosts and Diseases
• /
• v.61 no.1
• /
• pp.78-83
• /
• 2023

The use of an effective antimalarial drug is the cornerstone of malaria control. However, the development and spread of resistant Plasmodium falciparum strains have placed the global eradication of malaria in serious jeopardy. Molecular marker analysis constitutes the hallmark of the monitoring of Plasmodium drug-resistance. This study included 96 P. falciparum PCR-positive samples from southern Somalia. The P. falciparum chloroquine resistance transporter gene had high frequencies of K76T, A220S, Q271E, N326S, and R371I point mutations. The N86Y and Y184F mutant alleles of the P. falciparum multidrug resistance 1 gene were present in 84.7 and 62.4% of the isolates, respectively. No mutation was found in the P. falciparum Kelch-13 gene. This study revealed that chloroquine resistance markers are present at high frequencies, while the parasite remains sensitive to artemisinin (ART). The continuous monitoring of ART-resistant markers and in vitro susceptibility testing are strongly recommended to track resistant strains in real time.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.11
• /
• pp.6757-6760
• /
• 2013

Gastric cancer is one of the most frequently occurring malignancies in the world. Development of multiple drug resistance (MDR) to chemotherapy is known as the major cause of treatment failure for gastric cancer. Multiple drug resistance 1/P-glycoprotein (MDR1/p-gp) contributes to drug resistance via ATP-dependent drug efflux pumps and is overexpressed in many solid tumors including gastric cancer. To investigate the role of MDR1 knockdown on drug resistance reversal, we knocked down MDR1 expression using shRNA in drug resistant gastric cancer cells and examined the consequences with regard to adriamycin (ADR) accumulation and drug-sensitivity. Two shRNAs efficiently inhibited mRNA and protein expression of MDR1 in SGC7901-MDR1 cells. MDR1 knockdown obviously decreased the ADR accumulation in cells and increased the sensitivity to ADR treatment. Together, our results revealed a crucial role of MDR1 in drug resistance and confirmed that MDR1 knockdown could reverse this phenotype in gastric cancer cells.

• Bulletin of the Korean Chemical Society
• /
• v.35 no.4
• /
• pp.1154-1158
• /
• 2014

Hsp90 is an ubiquitous molecular chaperone protein, which plays an important role in regulating maturation and stabilization of many oncogenic proteins. Due to its potential to simultaneously disable multiple signaling pathways, Hsp90 represents great promise as a therapeutic target of cancer. In this study, we synthesized flavokawain analogues and evaluated their biological activities against drug-resistant cancer cells. The study indicated that compound 1i impaired the growth of gefitinib-resistant non-small cell lung cancer (H1975), down-regulated the expression of Hsp90 client proteins including EGFR, Her2, Met, Akt and Cdk4, and upregulated the expression of Hsp70. The result strongly suggested that compound 1i inhibited the proliferation of cancer cells through Hsp90 inhibition. Overall, compound 1i could serve as a potential lead compound to overcome the drug resistance in cancer chemotherapy.