Advances in the role of miRNAs in the occurrence and development of osteosarcoma

Osteosarcoma (OS) is the most common primary malignant tumor of the skeleton system in the clinic. This mainly occurs in adolescent patients and the pathogenesis of this disease is very complicated. A distant metastasis can occur in the early stages, and the prognosis is bad. Microrna (MIRNAS) is a non-coding RNA around 18-25 NT long involved in post-transcription gene regulation. MIRNAS can regulate the expression of target genes by promoting MRNAS degradation targets or inhibiting the translation process, thus OS cell proliferation can be inhibited and apoptosis can be promoted; In this way, MIRNAS can affect OS cell metabolism and can also participate in the occurrence, invasion, metastasis, and recurrence of OS.

Some MIRNAs have been found closely related to the prognosis of patients with the OS. Unlike other reviews, this review summarizes Mirna molecules closely related to development, diagnosis, prognosis, and OS treatment in recent years. The expression and influence of mircular molecules in the OS are discussed in detail, and the progress of related research is summarized to provide new research directives for early diagnosis and OS treatment.

Comparison between the effects of excessive expression of MIRNA-16 and MIRNA-34A in the development of cell cycles of mesothelioma cell lines and in their cisplatin sensitivity

The prognosis of patients affected by mesotheloma pleural malignant (MPM) is currently bad and there is no therapeutic strategy that increases their survival. The introduction of mirna mimics to restore their functionality reduced or non-existent in cancer cells is considered an important opportunity and the combination of Mir may be even more effective. In this study, MIR-16 and MIR-34A were translated, in a single and in combination, in the cell line MPM H2052 and H28, and the effect on cell proliferation and sensitivity to Cisplatin was reported.

Interestingly, excessive expression of Mir, itself or combined, slows the development of cell cycles, modulates P53 expression and HMGB1 and increases cell sensitivity to Cisplatein, resulting in significant cell proliferation and strengthening the effects of apoptosis of the drug. However, the co-overexpression of two mirs produces more effectively in the regulation of cell cycles, but does not increase the sensitivity of MPM cells to Cisplatin. As a result, despite the potential of MIR-16 and MIR-34A confirmed, we must conclude that their combination does not increase MPM’s response to chemotherapy.

The Role of Mirnas in the Development of Colorectal Cancer and Kimuadiotherapy

Colorectal cancer (CRC) is known as the third most common cancer and the fourth most deadly cancer throughout the world. CRC accounts for around 10% of all new cancer cases globally, the remaining causes are most often from cancer-related deaths. Micrornas (MIRNAS) is a small non-class RNA class that can affect various cellular and molecular targets. Depending on the cell environment where the information is expressed, MIRAS can function as a crc or promoter suppressor and play an important role in several biological processes. In this review, we summarize the relationship between MIRNAS and proliferation, metastasis, angiogenesis, autophagy, apoptosis, and CRC chemoarotherapy, revealing that the relevant MIRNA can function as a potential target for CRC therapy.

Exosomal Mirna-16-5p comes from M1 Macrophags increasing the immune response depending on cells by regulating PD-L1 in gastric cancer

Macrophages have affinity to develop tumors and have been proven to play a role in tumor battles and immune supervision. However, the exact mechanism in which macrophages participate in anti-tumor immune responses is still unclear. Therefore, the current study aims to identify the effects of macrophages in gastric cancer cells (GC) through Exosom.

Paired cancer, adjacent tumor, and non-cancerous abdominal tissue at first from 68 GC patients. T cells are isolated from peripheral blood mononuclear cells (PBMC) obtained from GC patients and healthy donors. Furthermore, exosom is isolated from LPS and IFN-INDUCCED PBMCS (M1 Macrophages) and cultured along with human GC cells. Other culture systems consisting of CD3 + T cells and GC cells treated with exosomes are then carried out. Balb / c and Nude NOD / SCID rats are prepared for the exosomal effect of MIR-16-5P on the growth of tumors and anti-tumor immune responses in Vivo.

The relationship between M1 macrophages and the survival of poor GC patients was identified, while they issued an exosong to inhibit the development of GC and activate the immune response depending on cells. Our results reveal that MIR-16-5P transferred Inter-cellular from M1 macrophages to GC cells through the exosomes and targeted PD-L1. M1 Exosom Macrophag derivatives containing MIR-16-5P are found triggering T cell immune response which inhibits the formation of tumors either in vitro and in vivo by reducing the expression of PD-L1.

Taken together, the main findings of the current research show that the exosom derivative of M1 macrophages which brought MIR-16-5P mobilized the effects of inhibition in the development of GC through the activation of the T-cell immune response through PD-L1. Our research highlights the promise of M1 macrophage as potential cell-based therapy for GC treatment by increasing MIR-16-5P in exosom.

Overexpression MIRNA-3613-3P enhances the sensitivity of breast cancer three negative triple to CDK4 / 6 inhibitors Palbociclib

Triple negative breast cancer (TNBC) is characterized by a lack of expression of estrogen receptors and progesterone and HER2, which is a target of general therapy. CDK4 / 6 inhibitors Palbociclib has been approved as an anti-cancer agent for breast cancer. However, identifying biomarkers who predict response to Palbociclib has always been a challenge for molecular target therapy. In this study, we identified Michorna as a typical feature in TNBC patients and explores whether MIR-3613-3P might function as a tumor suppressor biomarker for three-duplicate breast cancer patients and if the excessive expression of MIR-3613P can increase the sensitivity of TNBC cells for Palbociclib.

We indicate that MIR3613-3P expressions are arranged in tumors and TNBC cells, and excessive expressions of MIR-3613P on patient tumor tissue clinically and pathologically correlates with a favorable prognosis, such as smaller and lower tumors. Ki-67. In vitro, overexpression MIR-3613-3P proliferation of blocking cells, due to the capture of the G1 cell cycle, and increases the sensitivity of TNBC cells to the treatment of Palbociclib. In the Vivo study revealed that the excess expression of the MIR-3613-3P inhibits Tumnbc tumorigenesis and provides a significant inhibition effect from Palbociclib in MDA-MB-231 cells.

Mechanically, SMAD2 and EZH2 are found as two direct targets of MIR-3613P and mediate the proliferation of TNBC cells and cell sensitivity to Palbociclib through cellular aging inducing. Our findings suggest that MIR-3613-3P acts as a mirna cancer suppressor in TNBC. In addition, our research shows that MIR-3613-3P can be used as a predictive biomarker for TNBC response to Palbociclib.

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