RESUMEN
N6-methyladenosine (m6A) is one of the most common internal modifications in eukaryotic RNA. The presence of m6A on transcripts can affect a series of fundamental cellular processes, including mRNA splicing, nuclear transportation, stability, and translation. The m6A modification is introduced by m6A methyltransferases (writers), removed by demethylases (erasers), and recognized by m6A-binding proteins (readers). Current research has demonstrated that m6A methylation is involved in the regulation of malignant phenotypes in tumors by controlling the expression of cancer-related genes. Non-coding RNAs (ncRNAs) are a diverse group of RNA molecules that do not encode proteins and are widely present in the human genome. This group includes microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and PIWI interaction RNAs (piRNAs). They function as oncogenes or tumor suppressors through various mechanisms, regulating the initiation and progression of cancer. Previous studies on m6A primarily focused on coding RNAs, but recent discoveries have revealed the significant regulatory role of m6A in ncRNAs. Simultaneously, ncRNAs also exert their influence by modulating the stability, splicing, translation, and other biological processes of m6A-related enzymes. The interplay between m6A and ncRNAs collectively contributes to the occurrence and progression of malignant tumors in humans. This review provides an overview of the interactions between m6A regulatory factors and ncRNAs and their impact on tumors.
RESUMEN
Background: Pulmonary sarcomatoid carcinoma (PSC) is a rare disease which is highly malignant with a poor prognosis. PSC is highly resistant to chemotherapy and radiotherapy and is prone to recurrence even after surgery. Most of what is known about PSC comes from limited single-center, retrospective studies. There is still no standard international clinical guideline for PSC. Limited case reports have shown that PSC patients with driver gene mutations and high programmed death-ligand 1 (PD-L1) expression have good responses to molecular targeted therapy and immune checkpoint inhibitor (ICI) immunotherapy, respectively. Therefore, current first-line chemotherapy, targeted therapy and immunotherapy play a leading role in the diagnosis and treatment of advanced PSC patients. Case Description: We report a 42-year-old male who was diagnosed with PSC [stage IVB (T4N2M1)] and treated at our department (Department of Radiation Oncology, The Affiliated Hospital of Soochow University). The initial computed tomography (CT) scan of the chest showed a large mass (159 mm × 112 mm) which on needle biopsy showed sarcomatoid carcinoma histology. The patient received 8 cycles of abraxane plus cisplatin chemotherapy combined with anlotinib and immunotherapy, followed by immunotherapy and anlotinib for >1 year. Finally, the local tumor was well controlled, and no obvious drug-related adverse reactions were observed. The large lesions in the lung remained in complete response for >24 months. Conclusions: To our knowledge, this is the first reported case of an advanced PSC patient showing a good response to the treatment consisting of anlotinib combined with sintilimab and platinum-doublet chemotherapy. This case suggests that chemotherapy combined with antiangiogenic therapy and immunotherapy may benefit patients with advanced PSC. Long-term immunotherapy and anlotinib maintenance therapy has been safe and effective in our case. However, randomized controlled clinical studies are needed to confirm the efficacy and safety of these treatment options.