| Abstrakt: |
Cancer is a disorder of growth control and cell differentiation caused by the abnormal expression of multiple genes. Long non-coding RNAs (lncRNAs) are critical regulators of numerous biological processes, especially in the development of diseases. Abnormal expression of some lncRNAs causes disease, especially cancer, and disease resistance. lncRNAs may act as oncogenes or tumor suppressors and can be used as diagnostic or prognostic markers, and may also have therapeutic potential in cancer treatment. Studies show that many lncRNAs have different effects on cell activity by regulating multiple downstream targets, such as signaling pathways that are signal transducers and activators of transcription 3 (STAT3). The STAT3 signaling pathway is one of the most critical pathways in developing various diseases, including cancer, which plays a vital role in cellular processes, disease onset and progression, and stem cell regeneration by regulating its target genes. STAT3 has been proven to be an anticancer target in various contexts. Types of genes can activate the STAT3 pathway in cancer. Many lncRNAs have been identified associated with the STAT3 pathway that is upstream or downstream. Oncogenic lncRNAs, including PVT1, HOTAIRM1, and MCM3AP-AS1, increase STAT3 expression, while tumor suppressor lncRNAs, such as TSLNC8, TPTEP1, and DILC decrease STAT3 expression. These lncRNAs can affect STAT3 signaling activity through numerous molecular mechanisms, including sponge of microRNAs, transcriptional activation/inhibition, and epigenetic alterations. Numerous studies show that targeting lncRNAs and molecules associated with the STAT3 signaling pathway are promising therapeutic strategies for various cancers. This review highlighted the mechanisms of the upstream lncRNAs of the STAT3 signaling pathway. [ABSTRACT FROM AUTHOR] |
