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Electrospun membranes have the potential to act as an effective barrier for wounds from the external environment to prevent pathogens. In addition, materials with good antibacterial properties can effectively fight off the invading pathogens. In this paper, we report the development of a novel electrospun polyvinyl alcohol (PVA) membrane containing biosynthesized silver nanoparticle (bAg) for wound dressing applications. Plant extract from a medicinal plant Mimosa pudica was utilized for the synthesis of bAg. Synthesized bAg were characterized by Ultraviolet-Visible (UV) Spectroscopy and Fourier Transform Infrared Spectroscopy (FTIR). The morphology of bAg was obtained from Transmission Electron Microscopy (TEM) and found that they were spherical in morphology with average particle size 7.63 ± 1.2 nm. bAg nanoparticles incorporated PVA membranes were characterized using several physicochemical techniques such as Scanning Electron Microscopy (SEM), Energy Dispersive X-Ray Spectroscopy (EDS) and X-Ray Diffraction (XRD) analysis. Experimental results confirmed the successful incorporation of bAg in PVA fibers. PVA nanofiber membranes incorporated with bAg showed good mechanical strength, excellent exudate uptake capacity, antibacterial activity, blood compatibility and cytocompatibility.

Human epidermal growth factor receptor 2 (HER2) is a subtype of breast cancer that is associated with poor prognosis and low survival rates. The discovery of novel anti-cancer agents to manage this subtype of cancer is still needed. Ziziphus spina-christi (ZSC) is a plant species that is native to Qatar. It exerts various biological activities, including cytotoxicity as it contains different essential bioactive constituents, mainly rutin and quercetin. To examine the outcome of ZSC on HER2-positive breast cancer, we standardized the ZSC methanolic leaves extracted by Reverse Phase High-Performance Liquid Chromatography (RP-HPLC) analysis using the flavonoids rutin and quercetin as marker compounds. Here we used two HER2-positive breast cancer cell lines, ZR-75-1 and SK-BR-3, and the chorioallantoic membrane as an angiogenesis model. We found that ZSC extract significantly reduces viability, alters the normal morphological phenotype of HER2-positive breast cancer cells, and inhibits cell migration as well as colony formation; this is accompanied by deregulating different apoptotic markers such as Bax/Bcl-2 and NF-κB in both cell lines. Additionally, ZSC methanolic extract significantly represses the angiogenesis of the chorioallantoic membrane model. Moreover, the molecular pathway investigations pointed out that ZSC extract represses the activity of HER2 and p38 MAPK which could be the main pathways behind the effect of ZSC in HER2-positive cells. Collectively, our results support the potential role of ZSC in the management of HER2-positive breast cancer and form the basis for future investigations.

Colorectal cancer (CRC) is the third most common cause of cancer-related deaths worldwide. Human papillomaviruses (HPVs) and Epstein–Barr virus (EBV) have been reported to be present in different types of human cancers, including CRCs, where they can play a key role in the onset and/or progression of these cancers. Thus, we herein explored the prevalence of high-risk HPVs and EBV in a cohort of 94 CRC tissue samples and 13 colorectal normal tissues from the Lebanese population using polymerase chain reaction, immunohistochemistry, and tissue microarray methodologies. We found that high-risk HPVs are present in 64%, while EBV is present in 29% of our CRC samples. Additionally, our data showed that high-risk HPV types (16, 18, 35, 58, 51, 45, 52, 31, and 33) are the most frequent in CRC in the Lebanese cohort, respectively. Our data point out that HPVs and EBV are copresent in 28% of the samples. Thus, this study clearly suggests that high-risk HPVs and EBV are present/copresent in CRCs, where they could play an important role in colorectal carcinogenesis. Nevertheless, further investigations using a larger cohort are needed to elucidate the possible cooperation between these oncoviruses in the development of CRC.

Colorectal cancer (CRC), the third most common type of cancer, is the second leading cause of cancer-related mortality rates worldwide. Although modern research was able to shed light on the pathogenesis of CRC and provide enhanced screening strategies, the prevalence of CRC is still on the rise. Studies showed several cellular signaling pathways dysregulated in CRC, leading to the onset of malignant phenotypes. Therefore, analyzing signaling pathways involved in CRC metastasis is necessary to elucidate the underlying mechanism of CRC progression and pharmacotherapy. This review focused on target genes as well as various cellular signaling pathways including Wnt/β-catenin, p53, TGF-β/SMAD, NF-κB, Notch, VEGF, and JAKs/STAT3, which are associated with CRC progression and metastasis. Additionally, alternations in methylation patterns in relation with signaling pathways involved in regulating various cellular mechanisms such as cell cycle, transcription, apoptosis, and angiogenesis as well as invasion and metastasis were also reviewed. To date, understanding the genomic and epigenomic instability has identified candidate biomarkers that are validated for routine clinical use in CRC management. Nevertheless, better understanding of the onset and progression of CRC can aid in the development of early detection molecular markers and risk stratification methods to improve the clinical care of CRC patients.

DNA damage is well recognized as a critical factor in cancer development and progression. DNA lesions create an abnormal nucleotide or nucleotide fragment, causing a break in one or both chains of the DNA strand. When DNA damage occurs, the possibility of generated mutations increases. Genomic instability is one of the most important factors that lead to cancer development. DNA repair pathways perform the essential role of correcting the DNA lesions that occur from DNA damaging agents or carcinogens, thus maintaining genomic stability. Inefficient DNA repair is a critical driving force behind cancer establishment, progression and evolution. A thorough understanding of DNA repair mechanisms in cancer will allow for better therapeutic intervention. In this review we will discuss the relationship between DNA damage/repair mechanisms and cancer, and how we can target these pathways.

Natural chalcones possess antitumor properties and play a role as inducers of apoptosis, antioxidants and cytotoxic compounds. We recently reported that novel nitrogen chalcone-based compounds, which were generated in our lab, have specific effects on triple-negative breast cancer cells. However, the outcome of these two new compounds on human epidermal growth factor receptor 2 (HER2)-positive breast cancer remains nascent. Thus, we herein investigated the effects of these compounds (DK-13 and DK-14) on two HER2-positive breast cancer cell lines, SKBR3 and ZR75. Our data revealed that these compounds inhibit cell proliferation, deregulate cell-cycle progression and significantly induce cell apoptosis in both cell lines. Furthermore, the two chalcone compounds cause a significant reduction in the cell invasion ability of SKBR3 and ZR75 cancer cells. In parallel, we found that DK-13 and DK-14 inhibit colony formation of both cell lines in comparison to their matched controls. On the other hand, we noticed that these two compounds can inhibit angiogenesis in the chorioallantoic membrane model. The molecular pathway analysis of chalcone compounds exposed cells revealed that these compounds inhibit the expression of both JNK1/2/3 and ERK1/2, the major plausible molecular pathways behind these events. Our findings implicate that DK-13 and DK-14 possess effective chemotherapeutic outcomes against HER2-positive breast cancer via the ERK1/2 and JNK1/2/3 signaling pathways.

Human coronaviruses, especially SARS-CoV-2, are emerging pandemic infectious diseases with high morbidity and mortality in certain group of patients. In general, SARS-CoV-2 causes symptoms ranging from the common cold to severe conditions accompanied by lung injury, acute respiratory distress syndrome in addition to other organs’ destruction. The main impact upon SARS-CoV-2 infection is damage to alveolar and acute respiratory failure. Thus, lung cancer patients are identified as a particularly high-risk group for SARS-CoV-2 infection and its complications. On the other hand, it has been reported that SARS-CoV-2 spike (S) protein binds to angiotensin-converting enzyme 2 (ACE-2), that promotes cellular entry of this virus in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2). Today, there are no vaccines and/or effective drugs against the SARS-CoV-2 coronavirus. Thus, manipulation of key entry genes of this virus especially in lung cancer patients could be one of the best approaches to manage SARS-CoV-2 infection in this group of patients. We herein provide a comprehensive and up-to-date overview of the role of ACE-2 and TMPRSS2 genes, as key entry elements as well as therapeutic targets for SARS-CoV-2 infection, which can help to better understand the applications and capacities of various remedial approaches for infected individuals, especially those with lung cancer.

Background Colorectal cancer (CRC) represents a major fraction of the total cancer burden worldwide. It has been recently identified that various high‐risk Human Papillomaviruses (HPVs) are present in human CRCs, where they play a critical role in the development and progression of the cancer. Aims In this study, we explored the synergistic effect of the E6/E7 viral oncoproteins of the two most frequently observed HPV types (16 and 18) on KRAS and TP53 mutant CRC cell models. Methods We performed an experimental in vitro study utilizing lipofection to transfect KRAS and TP53 mutant CRC cell models (HCT 116 and HT‐29 respectively) with E6/E7 oncoproteins of HPV types 16 and 18 individually and in combination. Subsequently, we assessed their synergistic effect on cell proliferation, invasion, migration, and survival. In addition, we also compared the protein expression patterns of key epithelial‐mesenchymal transition (EMT) biomarkers like E‐cadherin, fascin, and vimentin among transfected, co‐transfected, and wild‐type cells. Results We found that the co‐expression of E6/E7 of HPV types 16 and 18 enhanced cell proliferation, invasion, migration, and survival in both cell models. Interestingly, this was also accompanied by the deregulation of all three EMT biomarkers, E‐cadherin, fascin, and vimentin. The synergistic effect of the viral oncoproteins in promoting cancer was more pronounced in TP53 mutant cells (HT‐29) as compared to KRAS mutant cells (HCT 116). We also report that HPV type 18 can induce a greater and more sustained oncogenic outcome as compared to HPV type 16. Conclusion Our data indicate that co‐expression of the E6/E7 oncoproteins of HPV types 16 and 18 can enhance oncogenic processes in CRC, especially TP53 mutant CRC.

Gold nanorods (AuNRs) were synthesized by the seed-mediated wet chemical method using a binary surfactant system. AuNRs were stabilized with polyethylene glycol, then functionalized with 4-mercaptophenol (4-MPH) ligand by surface ligand exchange. The surface-functionalized AuNRs (4-MPH-AuNRs) exhibited a typical UV–vis spectrum of AuNRs with a slightly shifted longitudinal peak. Furthermore, 4-MPH-AuNRs demonstrated a similar Fourier-Transformed Infrared spectrum to 4-MPH and a fading of the thiol band, which suggests a successful functionalization through thiol-gold binding. The antibacterial and antibiofilm activities of 4-MPH-AuNRs were evaluated against a clinical isolate of Methicillin-Resistant Staphylococcus aureus (MRSA). The results indicate that 4-MPH-AuNRs exhibit a bactericidal activity with a minimum inhibitory concentration (MIC) of ~ 6.25  μ g/mL against a planktonic suspension of MRSA. Furthermore, 4-MPH-AuNRs resulted in a 1.8–2.9 log-cycle reduction of MRSA biofilm viable count over a concentration range of 100–6.0  μ g/mL. The bacterial uptake of the surface-modified nanorods was investigated by inductively coupled plasma-optical emission spectroscopy (ICP-OES) and scanning electron microscopy (SEM) imaging; the results reveal that the nanorods were internalized into the bacterial cells after 6 h (h) of exposure. SEM imaging revealed a significant accumulation of the nanorods at the bacterial cell wall and a possible cellular internalization. Thus, 4-MPH-AuNRs can be considered a potential antibacterial agent, particularly against MRSA strain biofilms.

There is a lack of predictive markers for early and rapid identification of disease progression in COVID-19 patients. Our study aims at identifying microRNAs (miRNAs)/small nucleolar RNAs (snoRNAs) as potential biomarkers of COVID-19 severity. Using differential expression analysis of microarray data (n = 29), we identified hsa-miR-1246, ACA40, hsa-miR-4532, hsa-miR-145-5p, and ACA18 as the top five differentially expressed transcripts in severe versus asymptomatic, and ACA40, hsa-miR-3609, ENSG00000212378 (SNORD78), hsa-miR-1231, hsa-miR-885-3p as the most significant five in severe versus mild cases. Moreover, we found that white blood cell (WBC) count, absolute neutrophil count (ANC), neutrophil (%), lymphocyte (%), red blood cell (RBC) count, hemoglobin, hematocrit, D-Dimer, and albumin are significantly correlated with the identified differentially expressed miRNAs and snoRNAs. We report a unique miRNA and snoRNA profile that is associated with a higher risk of severity in a cohort of SARS-CoV-2 infected patients. Altogether, we present a differential expression analysis of COVID-19-associated microRNA (miRNA)/small nucleolar RNA (snoRNA) signature, highlighting their importance in SARS-CoV-2 infection.