RESUMEN
The overuse of antibiotics has caused the emergence of antibiotic-resistant strains, such as multidrug-resistant, extensively drug-resistant, and pandrug-resistant bacteria. The treatment of infections caused by such strains has become a formidable challenge. In the post-antibiotic era, phage therapy is an attractive solution for this problem and some successful phase 1 and 2 studies have demonstrated the efficacy and safety of phage therapy over the last decade. It is a form of evolutionary medicine, phages exhibit immunomodulatory and anti-inflammatory properties. However, phage therapy is limited by factors, such as the narrow spectrum of host strains, the special pharmacokinetics and pharmacodynamics in vivo, immune responses, and the development of phage resistance. The aim of this minireview was to compare the potencies of lytic phages and chemical antibiotics to treat bacterial infections. The advantages of phage therapy has fewer side effects, self-replication, evolution, bacterial biofilms eradication, immunomodulatory and anti-inflammatory properties compared with chemical antibiotics. Meanwhile, the disadvantages of phage therapy include the narrow spectrum of available host strains, the special pharmacokinetics and pharmacodynamics in vivo, immune responses, and phage resistance hurdles. Recently, some researchers continue to make efforts to overcome these limitations of phage therapy. Phage therapy will be a welcome addition to the gamut of options available for treating antibiotic-resistant bacterial infections. We focus on the advantages and limitations of phage therapy with the intention of exploiting the advantages and overcoming the limitations.
RESUMEN
Drug resistance remains a challenge in ovarian cancer. In addition to aberrant activation of relevant signaling pathways, the adaptive stress response is emerging as a new spotlight of drug resistance in cancer cells. Stress granules (SGs) are one of the most important features of the adaptive stress response, and there is increasing evidence that SGs promote drug resistance in cancer cells. In the present study, we compared two types of ovarian cancer cells, A2780 and SKOV3, using the dual PI3K/mTOR inhibitor, PKI-402. We found that SGs were formed and SGs could intercept the signaling factor ATF5 and regulate the mitochondrial unfolded protein response (UPRmt) in A2780 cells. Therefore, exploring the network formed between SGs and membrane-bound organelles, such as mitochondria, which may provide a new insight into the mechanisms of antitumor drug functions.