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When the expression levels of metastasis suppressor-1 (MTSS1) were discovered to be downregulated in a metastatic cancer cell line in 2002, it was proposed that MTSS1 functioned as a suppressor of metastasis. The 755 amino acid long protein MTSS1 connects to actin and organizes the cytoskeleton. Its gene is located on human chromosome 8q24. The suppressor of metastasis in metastatic cancer was first found to be MTSS1. Subsequent reports revealed that MTSS1 is linked to the prevention of metastasis in a variety of cancer types, including hematopoietic cancers like diffuse large B cell lymphoma and esophageal, pancreatic, and stomach cancers. Remarkably, conflicting results have also been documented. For instance, it has been reported that MTSS1 expression levels are elevated in a subset of melanomas, hepatocellular carcinoma associated with hepatitis B, head and neck squamous cell carcinoma, and lung squamous cell carcinoma. This article provides an overview of the pathological effects of lncRNA MTSS1 dysregulation in cancer. In order to facilitate the development of MTSS1-based therapeutic targeting, we also shed light on the current understanding of MTS1. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is the most prevalent aggressive malignant tumor in women worldwide and develops from breast tissue. Although cutting-edge treatment methods have been used and current mortality rates have decreased, BC control is still not satisfactory. Clarifying the underlying molecular mechanisms will help clinical options. Extracellular vesicles known as exosomes mediate cellular communication by delivering a variety of biomolecules, including proteins, oncogenes, oncomiRs, and even pharmacological substances. These transferable bioactive molecules can alter the transcriptome of target cells and affect signaling pathways that are related to tumors. Numerous studies have linked exosomes to BC biology, including therapeutic resistance and the local microenvironment. Exosomes' roles in tumor treatment resistance, invasion, and BC metastasis are the main topics of discussion in this review. [ABSTRACT FROM AUTHOR]

Despite the development of numerous therapies, cancer remains an incurable disease due to various factors, including drug resistance produced by cancer cells. MicroRNAs (miRNAs) regulate different target genes involved in biological and pathological processes, including cancer, through post-transcriptional mechanisms. The development of drug resistance in cancer treatment is a significant barrier because it decreases drug uptake, cellular transport, and changes in proteins involved in cell proliferation, survival, and apoptotic pathways. Numerous studies have found a connection between miRNAs and the development of drug resistance in cancer cells. This paper provides a broad overview of how miRNAs regulate signaling pathways and influence treatment resistance in different cancers. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) are non-coding RNAs that were transcribed from the human genome and have become important regulators in a number of cellular activities, mostly via controlling gene expression. A growing body of evidence shows that lncRNAs regulate various factors to impact various biological activities that are related to tumorigenesis, including the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. lncRNAs influence the JAK-STAT signaling pathway either by directly targeting or via indirectly modulating other upstream or downstream pathways' components like members of the suppressor of cytokine signaling (SOCS) family, and other genes that regulate cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition. Furthermore, lncRNAs can act as downstream effectors of the JAK-STAT pathway and mediates tumorigenesis. The relationship between JAK-STAT signaling and lncRNAs differs among various types of cancers. Besides, lncRNAs, as biological molecules, have been shown to play a dual role in either tumorigenesis or tumor suppression in various cancers. In this review, we focus on the reciprocated regulation and functions of lncRNAs and the JAK-STAT signaling pathway in cancer, as well as narrate the latest research progress on this association. A deeper understanding of this correlation may simplify the recognition of potential targets for clinical therapeutics. [ABSTRACT FROM AUTHOR]