The clinical effectiveness of the available anticancer drugs has been reduced due to the development of drug resistance and serious adverse effects, which have restricted chemotherapy for cancer. Therefore, there is a persistent need for new anticancer medications with reduced side effects. Medical researchers are pursuing various methods to find new, potent, specifically targeted molecules for cancer treatment. Through various techniques, numerous molecules are discovered. However, among them, acridine stands out as a promising heterocycle that has captured the interest of medicinal chemists and acquired significant pharmacological value. The synthetic adaptability of acridine has enabled the creation of numerous derivatives with a wide range of architectural properties, further accelerating this broad spectrum of pharmacological activities. Recent studies have looked at the mechanisms by which acridine and its analogs inhibit tyrosine kinases, topoisomerases, telomerase, and DNA repair interaction. We have compiled our knowledge of acridine compounds for their anticancer activities, mechanisms of action, structure-activity relationship (SAR), and selective, specific activity against different cancer drug targets, as well as in vitro and in vivo anticancer activities of acridine and its analogs from the perspective of cancer drug discovery, in this review.

Metastasis is one of the key factors of treatment failure in late-stage colorectal cancer (CRC). Metastatic CRC frequently develops resistance to chemotherapeutic agents. This study aimed to identify the novel regulators from \"hidden\" proteins encoded by long noncoding RNAs (lncRNAs) involved in tumor metastasis and chemoresistance. Methods: CRISPR/Cas9 library functional screening was employed to identify the critical suppressor of cancer metastasis in highly invasive CRC models. Western blotting, immunofluorescence staining, invasion, migration, wound healing, WST-1, colony formation, gain- and loss-of-function experiments, in vivo experimental metastasis models, multiplex immunohistochemical staining, immunohistochemistry, qRT-PCR, and RT-PCR were used to assess the functional and clinical significance of FOXP3, PRDM16-DT, HNRNPA2B1, and L-CHEK2. RNA-sequencing, co-immunoprecipitation, qRT-PCR, RT-PCR, RNA affinity purification, RNA immunoprecipitation, MeRIP-quantitative PCR, fluorescence in situ hybridization, chromatin immunoprecipitation and luciferase reporter assay were performed to gain mechanistic insights into the role of PRDM16-DT in cancer metastasis and chemoresistance. An oxaliplatin-resistant CRC cell line was established by in vivo selection. WST-1, colony formation, invasion, migration, Biacore technology, gain- and loss-of-function experiments and an in vivo experimental metastasis model were used to determine the function and mechanism of cimicifugoside H-1 in CRC. Results: The novel protein PRDM16-DT, encoded by LINC00982, was identified as a cancer metastasis and chemoresistance suppressor. The down-regulated level of PRDM16-DT was positively associated with malignant phenotypes and poor prognosis of CRC patients. Transcriptionally regulated by FOXP3, PRDM16-DT directly interacted with HNRNPA2B1 and competitively decreased HNRNPA2B1 binding to exon 9 of CHEK2, resulting in the formation of long CHEK2 (L-CHEK2), subsequently promoting E-cadherin secretion. PRDM16-DT-induced E-cadherin secretion inhibited fibroblast activation, which in turn suppressed CRC metastasis by decreasing MMP9 secretion. Cimicifugoside H-1, a natural compound, can bind to LEU89, HIS91, and LEU92 of FOXP3 and significantly upregulated PRDM16-DT expression to repress CRC metastasis and reverse oxaliplatin resistance. Conclusions: lncRNA LINC00982 can express a new protein PRDM16-DT to function as a novel regulator in cancer metastasis and drug resistance of CRC. Cimicifugoside H-1 can act on the upstream of the PRDM16-DT signaling pathway to alleviate cancer chemoresistance.

BACKGROUND: Cancer and infectious diseases are one of the greatest challenges of modern medicine. An unhealthy lifestyle, poor drug use, or drug misuse contribute to the rise in morbidity and mortality brought on by these illnesses. The inadequacies of the medications now being used to treat these disorders, along with the growing issue of drug resistance, have compelled researchers to look for novel compounds with therapeutic promise. The number of infections and diseases has significantly abated due to vaccine development and use over time, which is described in detail. Several novel vaccines can now be produced by manipulating Deoxyribonucleic acid (DNA), Ribonucleic acid (RNA), Messenger Ribonucleic acid (mRNA), proteins, viral vector Recombinant, and other molecules due to advances in genetic engineering and our understanding of the immune defense.
OBJECTIVE: The main topic of discussion is cancer-based vaccinations, which were developed less than a decade ago but have already been used to treat a wide range of both life-threatening and deadly diseases. It contains clinical studies for cancer vaccines against kidney, liver, prostate, cervix, and certain RNA-based cancer vaccines against breast and bladder cancer.
RESULTS: Numerous studies using various DNA and RNA-based methods have been conducted on the basis of cancer, with 9-10 diseases related to DNA and 8-9 diseases associated with RNA. Some of these studies have been completed, while others have been eliminated due to a lack of research; further studies are ongoing regarding the same.
CONCLUSIONS: This brief discussion of vaccines and their varieties with examples also discusses vaccine clinical trials in relation to cancer diseases in this DNA and RNA-based cancer vaccine that has had successful clinical trials like the cervical cancer drug VGX-3100, the kidney cancer drug Pembrolizumab, MGN-1601, the prostate cancer drug pTVG-HP with rhGM-CSF, the melanoma cancer drug proteasome siRNA, and the lung cancer drug FRAME-001.

BACKGROUND: Breast cancer (BC), as a heterogenous disease, is the most common cancer among women worldwide. Triple-negative breast cancer (TNBC) is the most aggressive and malignant subtype with a poor prognosis and a high rate of relapse and metastasis that is closely linked to epithelial-mesenchymal transition (EMT). It is well-documented that miRNAs play oncogenic (oncomiR) or tumor-suppressive (TS-miR) roles in controlling apoptosis (apoptomiR), differentiation, cell proliferation, invasion, migration, etc. Regarding the regulatory roles of miRNAs in the expression levels of various genes, dysfunction or deregulated expression of these molecules can lead to various disorders, including various types of cancers, such as BC. Many miRNAs have been identified with critical contributions in the initiation and development of different types of BCs due to their influence on the p53 signaling network.
OBJECTIVE: The aim of this review was to discuss several important deregulated miRNAs that are involved in the p53 signaling pathway in BC, especially the TNBC subtype. Finally, miRNAs\' involvement in tumor properties and their applications as diagnostic, prognostic, and therapeutic agents have been elaborated in detail.
RESULTS: The miRNA expression profile of BC is involved in tumor-grade estrogen receptor (ER) and progesterone receptor (PR) expression, and other pathological properties from luminal A to TNBC/basal-like subtypes via p53 signaling pathways.
CONCLUSIONS: Developing our knowledge about miRNA expression profile in BC, as well as molecular mechanisms of initiation and progression of BC can help to find new prognostic, diagnostic, and therapeutic biomarkers, which can lead to a suitable treatment for BC patients.

Glioma is a frequently occurring type of cancer that affects the central nervous system. Despite the availability of standardized treatment options including surgical resection, concurrent radiotherapy, and adjuvant temozolomide (TMZ) therapy, the prognosis for glioma patients is often unfavorable. Exosomes act as vehicles for intercellular communication, contributing to tissue repair, immune modulation, and the transfer of metabolic cargo to recipient cells. However, the transmission of abnormal substances can also contribute to pathologic states such as cancer, metabolic diseases, and neurodegenerative disorders. The field of exosome research in oncology has seen significant advancements, with exosomes identified as dynamic modulators of tumor cell proliferation, migration, and invasion, as well as angiogenesis and drug resistance. Exosomes have negligible cytotoxicity, low immunogenicity, and small size, rendering them an ideal therapeutic candidate for glioma. This comprehensive review discusses the dual effects of exosomes in glioma, with an emphasis on their role in facilitating drug resistance. Furthermore, the clinical applications and current limitations of exosomes in glioma therapy are also discussed in detail.

Cancer-associated fibroblasts (CAFs) as a major component of cancer stroma contribute to diverse procedures of most solid tumors and might be a targeted cancer therapy approach. Their specified features, related signaling pathways, distinct biomarkers, and sub-populations need to be deciphered. There is a need for CAF extraction or induction for in vitro investigations. Some miRNAs could activate CAF-like phenotype and they also interfere in CAF-mediated drug resistance, aggressiveness, and metastatic behaviors of several cancer cell types. Due to the complex relevance of miRNA and CAFs, these non-coding oligonucleotides may serve as attractive scope for anti-cancer targeted therapies, but the lack of an efficient delivery system is still a major hurdle. Here, we have summarized the investigated information on CAF features, isolation, and induction procedures, and highlighted the miRNA-CAF communications, providing special insight into nano-delivery systems.

Redox homeostasis is essential for keeping our bodies healthy, but it also helps breast cancer cells grow, stay alive, and resist treatment. Changes in the redox balance and problems with redox signaling can make breast cancer cells grow and spread and make them resistant to chemotherapy and radiation therapy. Reactive oxygen species/reactive nitrogen species (ROS/RNS) generation and the oxidant defense system are out of equilibrium, which causes oxidative stress. Many studies have shown that oxidative stress can affect the start and spread of cancer by interfering with redox (reduction-oxidation) signaling and damaging molecules. The oxidation of invariant cysteine residues in FNIP1 is reversed by reductive stress, which is brought on by protracted antioxidant signaling or mitochondrial inactivity. This permits CUL2FEM1B to recognize its intended target. After the proteasome breaks down FNIP1, mitochondrial function is restored to keep redox balance and cell integrity. Reductive stress is caused by unchecked amplification of antioxidant signaling, and changes in metabolic pathways are a big part of breast tumors\' growth. Also, redox reactions make pathways like PI3K, PKC, and protein kinases of the MAPK cascade work better. Kinases and phosphatases control the phosphorylation status of transcription factors like APE1/Ref-1, HIF-1, AP-1, Nrf2, NF-B, p53, FOXO, STAT, and - catenin. Also, how well anti-breast cancer drugs, especially those that cause cytotoxicity by making ROS, treat patients depends on how well the elements that support a cell\'s redox environment work together. Even though chemotherapy aims to kill cancer cells, which it does by making ROS, this can lead to drug resistance in the long run. The development of novel therapeutic approaches for treating breast cancer will be facilitated by a better understanding of the reductive stress and metabolic pathways in tumor microenvironments.

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UNASSIGNED: Wound treatment comprises a substantial portion of the healthcare budgets in developed countries. Studies suggest that about 50% of patients admitted to hospitals have wounds, while 1%-2% of the general population in the developed world suffers from chronic wounds. Chronic wounds fail to repair themselves within the expected period of 30 days. Technologies have been developed to address challenges encountered during wound care with the aim of alleviating pain, promoting healing, or controlling wound infections.
UNASSIGNED: The objective of this study was to explore the technological improvements that have been made in this field over time.
UNASSIGNED: To gain insight into the future of wound management, a systematic review of literature on the subject was conducted in scientific databases (PubMed, Scopus, Web of Science, Medline, and Clinical Trials).
UNASSIGNED: Results indicate that wound dressings have evolved from the traditional cotton gauze to composite materials embedded with appropriate ingredients such as metal-based nanoparticles. Studies on biodegradable dressing materials are also underway to explore their applicability in dressing large and irregular wounds. On the other hand, conventional drugs and traditional formulations for the management of pain, inflammation, infections, and accelerating healing have been developed. However, more research needs to be carried out to address the issue of microbial resistance to drugs. Drugs for managing other ailments also need to be designed in such a way that they can augment wound healing. In addition, it has been demonstrated that a coordinated integration of conventional and traditional medicine can produce laudable results in chronic wound management.
UNASSIGNED: Accordingly, collaborative efforts and ingenuity of all players in the field can accelerate technological advances in the wound care market to the benefit of the patients.

BACKGROUND: Onychomycosis, also called tinea unguium, is a common fungal infection affecting the nails. After dermatophytes, Candida species are recognized as second-line pathogens responsible for this infection. The treatment of onychomycosis requires a long time and is associated with high rates of recurrence. Antifungal medicines conjugated with gold (Au-NP) nanoparticle are the possible platforms for the reduction of drug resistance.
METHODS: In the present study, we reported the in-vitro antifungal activity of itraconazole (ITZ) - Au conjugates, time-kill studies, and biofilm-producing ability of six ITZ-resistant C. glabrata.
RESULTS: 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium bromide (MTT) quantitative results revealed that four out of six resistant isolates studied able to form biofilms in vitro. ITZ-Au conjugates were more effective than ITZ or Au nanoparticle alone, and the time-kill tests pointed to the suitable effect of ITZ-Au conjugate.
CONCLUSIONS: The present study concluded that ITZ-Au conjugates have an inhibitory effect on the biofilm of resistant C. glabrata isolates. Further studies are needed to compare the ex-vivo onychomycosis model.