RESUMO
Lung cancer holds the position of being the primary cause of cancer-related fatalities on a global scale. Furthermore, it exhibits the highest mortality rate among all types of cancer. The survival rate within a span of 5 years is less than 20%, primarily due to the fact that the disease is often diagnosed at an advanced stage, resulting in less effective treatment options compared to earlier stages. There are two main types of primary lung cancer: nonsmall-cell lung cancer, which accounts for approximately 80%-85% of all cases, and small-cell lung cancer, which is categorized based on the specific type of cells in which the cancer originates. The understanding of the biology of this disease and the identification of oncogenic driver alterations have significantly transformed the landscape of therapeutic approaches. Long noncoding RNAs (lncRNAs) play a crucial role in regulating various physiological and pathological processes through diverse molecular mechanisms. Among these lncRNAs, lncRNA H19, initially identified as an oncofetal transcript, has garnered significant attention due to its elevated expression in numerous tumors. Extensive research has confirmed its involvement in tumorigenesis and malignant progression by promoting cell growth, invasion, migration, epithelial-mesenchymal transition, metastasis, and therapy resistance. This comprehensive review aims to provide an overview of the aberrant overexpression of lncRNA H19 and the molecular pathways through which it contributes to the advancement of lung cancer. The findings of this review highlight the potential for further investigation into the diagnosis and treatment of this disease, offering promising avenues for future research.
Assuntos
Neoplasias Pulmonares , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/diagnóstico , Transição Epitelial-Mesenquimal , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Regulação Neoplásica da Expressão GênicaRESUMO
Colorectal cancer (CRC) involves various genetic alterations, with liver metastasis posing a significant clinical challenge. Furthermore, CRC cells mostly show an increase in resistance to traditional treatments like chemotherapy. It is essential to investigate more advanced and effective therapies to prevent medication resistance and metastases and extend patient life. As a result, it is anticipated that small interfering RNAs (siRNAs) would be exceptional instruments that can control gene expression by RNA interference (RNAi). In eukaryotes, RNAi is a biological mechanism that destroys specific messenger RNA (mRNA) molecules, thereby inhibiting gene expression. In the management of CRC, this method of treatment represents a potential therapeutic agent. However, it is important to acknowledge that siRNA therapies have significant issues, such as low serum stability and nonspecific absorption into biological systems. Delivery mechanisms are thus being created to address these issues. In the current work, we address the potential benefits of siRNA therapy and outline the difficulties in treating CRCby focusing on the primary signaling pathways linked to metastasis as well as genes implicated in the multi-drug resistance (MDR) process.
RESUMO
Transcripts longer than 200 nucleotides that are not translated into proteins are known as long non-coding RNAs, or lncRNAs. Now, they are becoming more significant as important regulators of gene expression, and as a result, of many biological processes in both healthy and pathological circumstances, such as blood malignancies. Through controlling alternative splicing, transcription, and translation at the post-transcriptional level, lncRNAs have an impact on the expression of genes. In multiple myeloma (MM), the majority of lncRNAs is elevated and promotes the proliferation, adhesion, drug resistance and invasion of MM cells by blocking apoptosis and altering the tumor microenvironment (TME). To control mRNA splicing, stability, and translation, they either directly attach to the target mRNA or transfer RNA-binding proteins (RBPs). By expressing certain miRNA-binding sites that function as competitive endogenous RNAs (ceRNAs), most lncRNAs mimic the actions of miRNAs. Here, we highlight lncRNAs role in the MM pathogenesis with emphasize on their capacity to control the molecular mechanisms known as "hallmarks of cancer," which permit earlier tumor initiation and progression and malignant cell transformation.
Assuntos
Mieloma Múltiplo , RNA Longo não Codificante , Mieloma Múltiplo/genética , Mieloma Múltiplo/patologia , Humanos , RNA Longo não Codificante/genética , Regulação Neoplásica da Expressão Gênica , Microambiente Tumoral/genéticaRESUMO
Fibrosarcoma is a challenging cancer originating from fibrous tissues, marked by aggressive growth and limited treatment options. The discovery of non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and small interfering RNAs (siRNAs), has opened new pathways for understanding and treating this malignancy. These ncRNAs play crucial roles in gene regulation, cellular processes, and the tumor microenvironment. This review aims to explore the impact of ncRNAs on fibrosarcoma's pathogenesis, progression, and resistance to treatment, focusing on their mechanistic roles and therapeutic potential. A comprehensive review of literature from databases like PubMed and Google Scholar was conducted, focusing on the dysregulation of ncRNAs in fibrosarcoma, their contribution to tumor growth, metastasis, drug resistance, and their cellular pathway interactions. NcRNAs significantly influence fibrosarcoma, affecting cell proliferation, apoptosis, invasion, and angiogenesis. Their function as oncogenes or tumor suppressors makes them promising biomarkers and therapeutic targets. Understanding their interaction with the tumor microenvironment is essential for developing more effective treatments for fibrosarcoma. Targeting ncRNAs emerges as a promising strategy for fibrosarcoma therapy, offering hope to overcome the shortcomings of existing treatments. Further investigation is needed to clarify specific ncRNAs' roles in fibrosarcoma and to develop ncRNA-based therapies, highlighting the significance of ncRNAs in improving patient outcomes in this challenging cancer.