Ultrastructure Microscopic Characterization of Apoptosis in Myelomoncytic Leukemia Cell Line Treated with Velogenic Viscerotropic Newcastle Disease Virus Strain AF 2240.

OBJECTIVE: Leukemia is a group of hematologic malignancies in the bonemarrow that arise from the dysfunctional proliferation of developing leukocytes. It is classified as either acute or chronic based on the rapidity of proliferation and as myelocytic or lymphocytic based on the cell of origin. Newcastle Disease Virus (NDV) is an avian paramyxovirus, which has been demonstrated to possess significant oncolytic activity against mammalian cancers because its ability to kill tumor cells with limited toxicity to normal cells. METHODS:  In this study, the morphophical changes and apoptosis induction of WEHI 3B leukemia cell line treated with NDV strain AF2240 were studied by scanning electron microscopes and  transmission electron microscopes techniques. RESULT: Electron microscopy indicated that NDV strain AF 2240 significantly altered cell morphology and reduced cell viability. Furthermore,  early apoptosis was observed 6 h post-inoculation by fluorescence microscope. CONCLUSION: Our results suggest that NDV has ability to induce significant apoptoic structural changes in WEHI 3B leukemia cell line. These findings provide new insights into the mechanism of action of NDV virotherapy and could lead to the development of more effective treatments for leukemia.

Molecular Regulatory Roles of Long Non-coding RNA HOTTIP: An Overview in Gastrointestinal Cancers.

Gastrointestinal (GI) cancers presented an alarmingly high number of new cancer cases worldwide and are highly characterised by poor prognosis. The poor overall survival is mainly due to late detection and emerging challenges in treatment, particularly chemoresistance. Thus, the identification of novel molecular targets in GI cancer is highly regarded as the main focus. Recently, long non-coding RNAs (lncRNAs) have been discovered as potential novel molecular targets for combating cancer, as they are highly associated with carcinogenesis and have a great impact on cancer progression. Amongst lncRNAs, HOTTIP has demonstrated a prominent oncogenic regulation in cancer progression, particularly in GI cancers, including oesophageal cancer, gastric cancer, hepatocellular carcinoma, pancreatic cancer, and colorectal cancer. This review aimed to present a focused update on the regulatory roles of HOTTIP in GI cancer progression and chemoresistance, as well as deciphering the associated molecular mechanisms underlying their impact on cancer phenotypes and chemoresistance and the key molecules involved. It has been reported that it regulates the expression of various genes and proteins in GI cancers that impact cellular functions, including proliferation, adhesion, migration and invasion, apoptosis, chemosensitivity, and tumour differentiation. Furthermore, HOTTIP was also discovered to have a higher diagnostic value as compared to existing diagnostic biomarkers. Overall, HOTTIP has presented itself as a novel therapeutic target and potential diagnostic biomarker in the development of GI cancer treatment.

Molecular and Epigenetic Basis of Extracellular Vesicles Cell Repair Phenotypes in Targeted Organ-specific Regeneration.

Extracellular vesicles (EVs), which are released by most of the cells, constitute a new system of cell-cell communication by transporting DNA, RNA, and proteins in various vesicles namely exosomes, apoptotic bodies, protein complexes, high-density lipid (HDL) microvesicles, among others. To ensure accurate regulation of somatic stem cell activity, EVs function as an independent metabolic unit mediating the metabolic homeostasis and pathophysiological of several diseases such as cardiovascular diseases, metabolic diseases, neurodegenerative diseases, immune diseases, and cancer. Whist examining the EV biomolecules cargos and their microenvironments that lead to epigenetic alteration of the cell in tissue regeneration, studies have gained further insights into the biogenesis of EVs and their potential roles in cell biology and pathogenicity. Due to their small size, non-virulence, flexibility, and ability to cross biological barriers, EVs have promising therapeutic potentials in various diseases. In this review, we describe EV's mechanism of action in intercellular communication and transfer of biological information as well as some details about EVinduced epigenetic changes in recipient cells that cause phenotypic alteration during tissue regeneration. We also highlight some of the therapeutic potentials of EVs in organ-specific regeneration.