Novel antimicrobial method to tackle drug-resistant bacteria

COVID-19 has further highlighted the importance of effective treatments for different conditions. Together, researchers have developed vaccines for COVID-19 that will save countless lives by preventing infection. Antibiotics are an example of another revolutionary and life-saving medical development. However, antibiotic resistance is on the rise, with drug-resistant bacteria becoming less responsive to antibiotics. This is a serious problem that requires urgent solutions. Associate Professor Mitsuoki Kawano, Department of Human Nutrition, Chugokugakuen University, Japan, is working to develop a novel antimicrobial method to tackle Antimicrobial resistance (AMR). He and his team are developing a technology that uses antisense RNA to control bacterial gene expression. Kawano also wishes to limit the damage caused to indigenous bacteria and intestinal flora by existing antibacterial drugs, To do this, he and the team are developing a method that can prevent the transmissive plasmid from being transmitted to other bacteria. The researchers have developed a system that can inhibit cell growth by suppressing the synthesis of proteins that are essential for bacterial growth through the action of antisense RNA transcribed from phagemid nucleic acid introduced into bacteria by phage infection.

hsa_circ_0008234 inhibits the progression of lung adenocarcinoma by sponging miR-574-5p

AbstractcircRNAs are a novel type of noncoding RNA (ncRNA) that have been identified as an important regulator of gene expression and play a part in the progression of various diseases. However, the function of circ_0008234 in lung adenocarcinoma (LUAC) remains unknown. Through the GEO (Gene Expression Omnibus) database, circ_0008234 was first found to be downregulated in LUAC tissues. It could inhibit cell growth and accelerate apoptosis in vitro and in vivo. In terms of its possible mechanism, circ_0008234 mainly was present in the cytoplasm and competed with miR-574-5p to regulate RND3 (Rho family GTPase 3). Our results revealed that circ_0008234 inhibited the progression of LUAC through a competing endogenous RNA (ceRNA)-based mechanism and provided potential biomarkers and therapeutic targets for LUAC treatment.

RNAi Targeting-STIL Suppresses Cell Growth and Induces Apoptosis of Lung Cancer NCI-H1299 Cells via Inactivation of Akt/SAPK/TAK1 Pathways

Background: Gradually emerged studies demonstrated that SCL/TAL1 interrupting locus (STIL or SIL) is upregulated in multiple kinds of fatal tumors; at present, there is no clean understanding about the role of STIL in lung adenocarcinoma cells. This study aimed to discover the significance of STIL in lung adenocarcinoma, so as to find a potential gene target for diagnosis and therapy. Methods: STIL expression in lung adenocarcinoma tissue and clinical pathological characteristic was analyzed using the online databases, UALCAN and GEPIA. Lentivirus STIL-shRNA was manufactured and transducted into lung adenocarcinoma cells to seek and analyze the effects on tumor phenotype. The cell proliferation was assessed using Cellomics Array Scan imaging assay, and colony-formation assay, respectively. The apoptosis was detected by flow cytometry assay. Moreover, the antibody array of PathScan Cancer Phenotype, PathScan stress and apoptosis pathway was used to explore relevant molecular mechanisms following STIL knockdown in NCI-H1299 cells. Results: The clinical pathological characteristic assay showed that STIL is upregulated in lung adenocarcinoma tissues, and this trend was associated with cancer stage1 and histological subtypes. Silencing experiment showed that downregulation of STIL could inhibit cell growth and colony formation, induce cell apoptosis, and a G2 phase arrest effect significantly, and antibody array detection revealed that p-Bad were upregulated, and p-Akt, p-Bad, p-HSP27, p-SAPK/JNK, p-TAK1, Vimentin, CD45, PCNA and Ki-67 were downregulated significantly after STIL silenced in NCI-H1299 cells.Conclusions: In conclusion, STIL is overexpressed in lung adenocarcinoma tissues compared with normal lung tissue. Knockdown of STIL could inhibit cell growth and colony formation ability, promote apoptosis via Akt/SAPK/TAK1 signal pathways inactivation.

Water-Soluble Pristine C60 Fullerene Inhibits Liver Alterations Associated with Hepatocellular Carcinoma in Rat

Excessive production of reactive oxygen species is the main cause of hepatocellular carcinoma (HCC) initiation and progression. Water-soluble pristine C60 fullerene is a powerful and non-toxic antioxidant, therefore, its effect under rat HCC model and its possible mechanisms were aimed to be discovered. Studies on HepG2 cells (human HCC) demonstrated C60 fullerene ability to inhibit cell growth (IC50 = 108.2 μmol), to induce apoptosis, to downregulate glucose-6-phosphate dehydrogenase, to upregulate vimentin and p53 expression and to alter HepG2 redox state. If applied to animals experienced HCC in dose of 0.25 mg/kg per day starting at liver cirrhosis stage, C60 fullerene improved post-treatment survival similar to reference 5-fluorouracil (31 and 30 compared to 17 weeks) and inhibited metastasis unlike the latter. Furthermore, C60 fullerene substantially attenuated liver injury and fibrosis, decreased liver enzymes, and normalized bilirubin and redox markers (elevated by 1.7–7.7 times under HCC). Thus, C60 fullerene ability to inhibit HepG2 cell growth and HCC development and metastasis and to improve animal survival was concluded. C60 fullerene cytostatic action might be realized through apoptosis induction and glucose-6-phosphate dehydrogenase downregulation in addition to its antioxidant activity.

Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN

ABSTRACTNeuroblastoma cell identity depends on a core regulatory circuit (CRC) of transcription factors that collaborate with MYCN to drive the oncogenic gene expression program. For neuroblastomas dependent on the adrenergic CRC, treatment with retinoids can inhibit cell growth and induce differentiation in both primary neuroblastomas and cell lines; however, the underlying mechanisms remain unclear. Here we show that when MYCN-amplified neuroblastomas cells are treated with all-trans retinoic acid (ATRA), histone H3K27 acetylation and methylation become redistributed to decommission super-enhancers driving the expression of PHOX2B and GATA3, together with the activation of new super-enhancers that drive high levels of MEIS1, HIC1 and SOX4 expression. These findings indicate that treatment with ATRA can reprogram the enhancer landscape to collapse the adrenergic CRC, resulting in downregulation of MYCN expression, while upregulating a new retino-sympathetic CRC that causes proliferative arrest and sympathetic differentiation. Thus, we provide mechanisms that account for the beneficial effects of retinoids against high-risk neuroblastoma and explain the rapid downregulation of expression of MYCN despite massive levels of gene amplification.

The importance of silver nanoparticles in human life

One nanomaterial that is having an early impact in health care product is nano-silver. Silver has been used for the treatment of medical ailments for over 100 years due to its natural antibacterial and antifungal properties. The nano silver particles typically measure 25nm. They have extremely large relatively surface area, increasing their contact with bacteria or fungi, and vastly improving its bactericidal and fungicidal effectiveness. The nano silver when in contact with bacteria and fungus will adversely affect cellular metabolism and inhibit cell growth. The nano silver suppresses respiration, basal metabolism of electron transfer system, and transport of substrate in the microbial cell membrane. The nano silver inhibits multiplication and growth of those bacteria and fungi which cause infection, odor, itchiness and sores. Nano Silver can be applied to range of other healthcare products such as dressings for burns, scald, skin donor and recipient sites; acne and cavity wounds; and female hygiene products – panty liners, sanitary towels and pants.

Tubeimoside-1 Inhibits Glioblastoma Growth, Migration, and Invasion via Inducing Ubiquitylation of MET

Tubeimoside-1 (TBMS1) is one of the extracts of rhizoma bolbostemmae, which has remarkable anti-cancer function in the treatment of esophagus and gastric cancer in traditional Chinese medicine. However the mechanisms of its anti-cancer function is remain unclear. In this study, we demonstrate that TBMS1 could inhibit cell growth and metastasis in glioblastoma. MET is a member of the receptor tyrosine kinase family, which amplifies frequently in various human cancers. As an important proto-oncogene, multiple inhibitors have been developed for the therapy of cancers. Here, we found TBMS1 could reduce/decrease the protein level of MET via increasing its Ubiquitination degradation. Therefore, TBMS1 is a promising compound for the treatment of glioblastoma and an inhibitor of MET.