Signaling crosstalk between mesenchymal stem cells and tumor cells: Implications for tumor suppression or progression.

Mesenchymal stem cells (MSCs) have been extensively used in various therapeutic applications over the last two decades, particularly in regenerative medicine and cancer treatment. MSCs have the ability to differentiate into mesodermal and non-mesodermal lineages, which makes them a popular choice in tissue engineering and regenerative medicine. Studies have shown that MSCs have inherent tumor-suppressive properties and can affect the behavior of multiple cells contributing to tumor development. Additionally, MSCs possess a tumor tropism property and have a hypoimmune nature. The intrinsic features of MSCs along with their potential to undergo genetic manipulation and be loaded with various anticancer therapeutics have motivated researchers to use them in different cancer therapy approaches without considering their complex dynamic biological aspects. However, despite their desirable features, several reports have shown that MSCs possess tumor-supportive properties. These contradictory results signify the sophisticated nature of MSCs and warn against the potential therapeutic applications of MSCs. Therefore, researchers should meticulously consider the biological properties of MSCs in preclinical and clinical studies to avoid any undesirable outcomes. This manuscript reviews preclinical studies on MSCs and cancer from the last two decades, discusses how MSC properties affect tumor progression and explains the mechanisms behind tumor suppressive and supportive functions. It also highlights critical cellular pathways that could be targeted in future studies to improve the safety and effectiveness of MSC-based therapies for cancer treatment. The insights obtained from this study will pave the way for further clinical research on MSCs and development of more effective cancer treatments.

Non-coding RNAs enhance the apoptosis efficacy of therapeutic agents used for the treatment of glioblastoma multiform.

The treatment of brain tumours remains a challenge despite progress in surgical techniques and radio/chemotherapy. The therapeutic outcomes for glioblastoma multiform (GBM) have not been satisfactory and result in median overall survival (12-18 months). GBM displays both intra- and inter-tumour heterogeneity, causing resistance and eventually tumour recurrence. In this review, we address molecular events responsible for the dysregulation of apoptosis and introduce newly discovered non-coding RNAs (MicroRNAs and Long non-coding RNAs) that regulate tumour growth and enhance therapeutic outcomes in GBM. The combinatory use of MicroRNAs and Long non-coding RNAs with chemotherapeutic compounds, as well as the induction of suicide genes, provide an innovative therapeutic approach for the management of GBM. The understanding of GBM pathogenesis, intrinsic drug resistance mechanism, and targetable oncogenic pathways could lead to establishing novel approaches and techniques to combat GBM.

BAZ1B the Protean Protein.

The bromodomain adjacent to the zinc finger domain 1B (BAZ1B) or Williams syndrome transcription factor (WSTF) are just two of the names referring the same protein that is encoded by the WBSCR9 gene and is among the 26-28 genes that are lost from one copy of 7q11.23 in Williams syndrome (WS: OMIM 194050). Patients afflicted by this contiguous gene deletion disorder present with a range of symptoms including cardiovascular complications, developmental defects as well as a characteristic cognitive and behavioral profile. Studies in patients with atypical deletions and mouse models support BAZ1B hemizygosity as a contributing factor to some of the phenotypes. Focused analysis on BAZ1B has revealed this to be a versatile nuclear protein with a central role in chromatin remodeling through two distinct complexes as well as being involved in the replication and repair of DNA, transcriptional processes involving RNA Polymerases I, II, and III as well as possessing kinase activity. Here, we provide a comprehensive review to summarize the many aspects of BAZ1B function including its recent link to cancer.