Cellular signaling modulated by miRNA-3652 in ovarian cancer: unveiling mechanistic pathways for future therapeutic strategies.

MicroRNAs (miRNAs) are small non-coding RNA molecules that play pivotal roles in regulating gene expression and have been implicated in the pathogenesis of numerous cancers. miRNA-3652, though relatively less explored, has recently emerged as a potential key player in ovarian cancer's molecular landscape. This review aims to delineate the functional significance and tumor progression role of miRNA-3652 in ovarian cancer, shedding light on its potential as both a diagnostic biomarker and therapeutic target. A comprehensive literature search was carried out using established databases, the focus was on articles that reported the role of miRNA-3652 in ovarian cancer, encompassing mechanistic insights, functional studies, and its association with clinical outcomes. This updated review highlighted that miRNA-3652 is intricately involved in ovarian cancer cell proliferation, migration, and invasion, its dysregulation was linked to altered expression of critical genes involved in tumor growth and metastasis; furthermore, miRNA-3652 expression levels were found to correlate with clinical stages, prognosis, and response to therapy in ovarian cancer patients. miRNA-3652 holds significant promise as a vital molecular player in ovarian cancer's pathophysiology. Its functional role and impact on tumor progression make it a potential candidate for diagnostic and therapeutic applications in ovarian cancer. Given the pivotal role of miRNA-3652 in ovarian cancer, future studies should emphasize in-depth mechanistic explorations, utilizing advanced genomic and proteomic tools. Collaboration between basic scientists and clinicians will be vital to translating these findings into innovative diagnostic and therapeutic strategies, ultimately benefiting ovarian cancer patients. Video Abstract.

Potential involvement of mi-RNA 574-3p in progression of prostate cancer: A bioinformatic study.

Aberrant gene expression is a hallmark of prostate cancer (PCa), the second deadliest disease affecting males worldwide. Dysregulation of miRNA has been associated with the progression of PCa and in recent studies, miRNA 574-3p was found to be upregulated in cancerous prostate tissue. In this study, we characterize the effects of upregulated miRNA 574-3p on gene expression in the tumor microenvironment through different bioinformatic tools such as Diana-Tools, the KEGG Pathway Database, and the Reactome Database. We have identified nine regulatory genes that are targeted by miRNA 574-3p and downregulated in prostate cells. Pathway analysis of these genes shows that they are involved in the regulation of the Notch signaling pathway, Wnt signaling pathway, apoptosis, DNA damage response, G1 to S cell-cycle control, inflammatory response pathway, angiogenesis, translation factors, and the expression of oncogenes. Our results show the oncogenic potential of miRNA 574-3p in PCa progression and metastasis. Moreover, this study highlights the complex molecular mechanisms and pathways affected by the upregulation of miRNA 574-3p in prostate cells. In future studies, the presented data may aid in designing new therapies for PCa with improved efficacy.

In silico functional and tumor suppressor role of hypothetical protein PCNXL2 with regulation of the Notch signaling pathway.

Since the last decade, various genome sequencing projects have led to the accumulation of an enormous set of genomic data; however, numerous protein-coding genes still need to be functionally characterized. These gene products are called "hypothetical proteins". The hypothetical protein pecanex-like protein 2 Homo sapiens (PCNXL2) is found to be mutated in colorectal carcinoma with microsatellite instability; therefore, annotation of the function of PCNXL2 in tumorigenesis is very important. In the present study, bioinformatics analysis of PCNXL2 was performed at the molecular level to assess its role in the progression of cancer for designing new anti-cancer drugs. The retrieved sequence of PCNXL2 was functionally and structurally characterized through the web tools Pfam, Batch CD (conserved domain) search, ExPASy, COACH and I-TASSER directed for pathway analysis and design to explore the intercellular interactions of PCNXL2 involved in cancer development. The present study has shown that PCNXL2 encodes multi-pass transmembrane proteins whose tumor suppressor function may involve regulating Notch signaling by transporting protons across the membrane to provide suitable membrane potential for γ secretase function, which may liberate the Notch intracellular domain NICD from the receptor to inside the cell. Furthermore, domain A of PCNXL2 may exhibit nuclear transport activity of NICD from the cytoplasm to the nucleus through interaction with a nuclear localization signal that may act as an activator for Notch signaling in the nucleus. Conclusively, the tumor suppressor role of PCNXL2 by regulation of the Notch signaling pathway and its functional and structural characteristics are important findings. However, further studies are required to validate the putative role of PCNXL2 as a cancer biomarker in cancer development.