Oral Delivery of Psoralidin by Mucoadhesive Surface-Modified Bilosomes Showed Boosted Apoptotic and Necrotic Effects against Breast and Lung Cancer Cells.

This study aims to design and optimize chitosan-coated bilosomal formulations loaded with psoralidin (Ps-CS/BLs) with improved physicochemical properties, oral bioavailability, and boosted apoptotic and necrotic effects. In this regard, uncoated bilosomes loaded with Ps (Ps/BLs) were nanoformulated using the thin-film hydration technique using different molar ratios of phosphatidylcholine (PC), cholesterol (Ch), Span 60 (S60), and sodium deoxycholate (SDC) (1:0.4:0.

miR-516a-3P, a potential circulating biomarker in hepatocellular carcinoma, correlated with polymorphism in .

The aim was to investigate the expression profile of miR-516a-3P and its correlation with the  polymorphism in Egyptian hepatitis C virus (HCV) and hepatocellular carcinoma (HCC) patients. miR-516a-3P was quantified and was genotyped by quantitative reverse transcription PCR. miR-516a-3P was significantly upregulated in HCC patients compared with HCV patients (p = 0.

miR-744/eNOS/NO axis: A novel target to halt triple negative breast cancer progression.

Background: Nitric oxide (NO) may have a dual role in cancer. At low concentrations, endogenous NO promotes tumor growth and proliferation. However, at very high concentrations, it mediates cancer cell apoptosis and inhibits cancer growth.

Targeting hydrogen sulphide signaling in breast cancer.

Introduction: Hydrogen sulphide (HS) has been established as a key member of the gasotransmitters family that recently showed a pivotal role in various pathological conditions including cancer.

Objectives: This study investigated the role of HS in breast cancer (BC) pathogenesis, on BC immune recognition capacity and the consequence of targeting HS using non-coding RNAs.

Methods: Eighty BC patients have been recruited for the study.

miRNA-506-3p Directly Regulates rs10754339 (A/G) in the Immune Checkpoint Protein B7-H4 in Breast Cancer.

Background: B7-H4 is a novel immune checkpoint protein that negatively regulates T cell activation and function. It is overexpressed in many malignant tumors, including Breast Cancer (BC). It was reported that the presence of the single nucleotide polymorphism rs10754339 (A/G) within the 3' UTR of the B7-H4 gene has a great influence on the risk and progression of BC as well as lymph node metastasis.

Why natural killer cells in triple negative breast cancer?

The triple-negative subtype of breast cancer (TNBC) has the bleakest prognosis, owing to its lack of either hormone receptor as well as human epidermal growth factor receptor 2. Henceforth, immunotherapy has emerged as the front-runner for TNBC treatment, which avoids potentially damaging chemotherapeutics. However, despite its documented association with aggressive side effects and developed resistance, immune checkpoint blockade continues to dominate the TNBC immunotherapy scene.

PNPLA3 and IL 28B signature for predicting susceptibility to chronic hepatitis C infection and fibrosis progression.

Background: Association studies identified genetic polymorphisms as predictive risk factors of rapid fibrosis progression in chronic hepatitis C (CHC). This study aims to assess the impact of IL28B rs8099917 polymorphism on CHC genotype 4 (G4) susceptibility and liver fibrosis progression individually; and in combination with PNPLA3 rs738409.

Patients And Methods: IL28B rs8099917 and PNPLA3 rs738409 were genotyped in 150 Egyptian CHC patients and 175 healthy controls using real-time PCR.

Epigallocatechin gallate (EGCG) and miR-548m reduce HCV entry through repression of CD81 receptor in HCV cell models.

Epigallocatechin gallate (EGCG) is the most abundant component in green tea extract, that has powerful antioxidant and antiviral effects. It has been previously reported to inhibit HCV entry via several mechanisms. Hence, this study aimed at further investigating the potential impact of EGCG on HCV entry through regulation of the expression of tetraspanin receptor CD81 by the novel predicted miR-548m.

Long non-coding RNAs: Functional regulatory players in breast cancer.

Historically, the long-held protein-centered bias has denoted 98% of the human genome as 'Junk' DNA. However, the current work has shifted the perception of such 'junk' transcriptional products to functional regulatory molecules. The recent surveillance of the human transcriptome has highlighted the pivotal role of such non-coding RNA (ncRNA) molecules in diverse physiological and pathological conditions.

A methoxylated quercetin glycoside harnesses HCC tumor progression in a TP53/miR-15/miR-16 dependent manner.

This study focused on studying the impact of flavonoids isolated from on HCC cell lines and to further unveil their possible impact on TP53 and its downstream tumor suppressor miRNAs. Three flavonol glycosides were isolated from namely, Isorhamnetin-3-O-β-D-glucoside Quercetin-3`-methoxy-3-O-(4``-acetylrhamnoside)-7-O-α-rhamnoside and Kaempferol-4`-methoxy-3,7-O-dirhamnoside They showed a concentration and time dependent reduction in cellular viability and anchorage-independent growth of HCC cells. Moreover, they exhibited a decrease in the migrating capacity of HepG2 cells in a pattern similar to positive control cells.

A novel role of sONE/NOS3/NO signaling cascade in mediating hydrogen sulphide bilateral effects on triple negative breast cancer progression.

Hydrogen sulphide (HS) gas has been recognized as an intracellular mediator influencing an array of signaling pathways. Yet, the role of HS in cancer progression has been controversial. This study aims to unravel the role of exogenous HS in triple negative breast cancer (TNBC) and to further investigate any possible association of HS mediated actions with the endogenous production of nitric oxide (NO) gas.

MiR-615-5p depresses natural killer cells cytotoxicity through repressing IGF-1R in hepatocellular carcinoma patients.

miR-615-5p was characterized by our group as a tumour suppressor. IGF-1 R activates a downstream signalling pathway, well characterized in liver cells, however, its role in immunity especially Natural Killer cells (NKs) remains vague. This study aimed at investigating the regulatory role of miR-615-5p on IGF signalling and its impact on NKs cytotoxicity in HCC.

MicroRNA-486-5p enhances hepatocellular carcinoma tumor suppression through repression of IGF-1R and its downstream mTOR, STAT3 and c-Myc.

The insulin-like growth factor (IGF)-axis has been paradigmatically involved in hepatocellular carcinoma (HCC) tumor initiation, progression and drug resistance. Consequently, members of the IGF-axis and most importantly, IGF-1 receptor (IGF-1R) have been considered as intriguing targets for HCC therapy. Few miRNAs have been recently reported to be associated with IGF-1R regulation.

Contradicting interplay between insulin-like growth factor-1 and miR-486-5p in primary NK cells and hepatoma cell lines with a contemporary inhibitory impact on HCC tumor progression.

In this study, an impaired natural killer (NK) cell cytolytic activity in 135 hepatocellular carcinoma (HCC) patients parallel to a reduced expression level of insulin-like growth factor (IGF)-1 in NK cells of HCC patients has been revealed. Ectopic expression of miR-486-5p, a direct upstream regulator of IGF-1, restored the endogenous level of IGF-1 in NK cells of HCC patients, thus augmenting its cytolytic activity against Huh7 cells in an opposite manner to the IGF-1 siRNAs. Unorthodoxly, over-expression of miR-486-5p in target hepatocytes resulted in the repression of IGF-1, suppression of Huh7 cells proliferation and viability in a similar pattern to the IGF-1 siRNAs.