As a critical internal RNA modification in higher eukaryotes, N⁶-methyladenosine (m⁶A) has become the hotspot of epigenetics research in recent years. Extensive studies on messenger RNAs have revealed that m⁶A affects RNA fate and cell functions in various bioprocesses, such as RNA splicing, export, translation, and stability, some of which seem to be directly or indirectly regulated by noncoding RNAs. Intriguingly, abundant noncoding RNAs such as microRNAs, long noncoding RNAs, circular RNAs, small nuclear RNAs, and ribosomal RNAs are also highly modified with m⁶A and require m⁶A modification for their biogenesis and functions. Here, we discuss the interaction between m⁶A modification and noncoding RNAs by focusing on the functional relevance of m⁶A in cancer progression, metastasis, drug resistance, and immune response. Furthermore, the investigation of m⁶A regulatory proteins and its inhibitors provides new opportunities for early diagnosis and effective treatment of cancer, especially in combination with immunotherapy.

Lung cancer leads to the highest mortality among all cancer types in the world, and non–small‐cell lung cancer (NSCLC) occupies over 80% of the lung cancer cases. Numerous studies have demonstrated that long non‐coding RNA (lncRNA) is involved in various human diseases including cancer. LncRNA FTX was firstly identified in Xist gene locus and was dysregulated in many human cancers. However, the function of FTX in NSCLC is still unclear. Here, we report that long non‐coding RNA FTX expression level is down‐regulated in NSCLC clinical tissue samples and cell lines. Ectopic expression of FTX inhibits proliferation and metastasis of lung cancer cells in vitro and in vivo. Furthermore, we find that FTX overexpression activates the expression of transcription factor FOXA2, an important regulator in lung cancer progression, and we reveal a novel FTX/miR‐200a‐3p/FOXA2 competing endogenous RNA regulatory axis in lung cancer cells. Our results provide new insights and directions for exploring the function of FTX in lung cancer progression.

The tRNA-derived fragments (tRFs) and tRNA halves (tiRNAs) are newly discovered noncoding RNAs in recent years. They are derived from specific cleavage of mature and pre-tRNAs and expressed in various cancers. They enhance cell proliferation and metastasis or inhibit cancer progression. Many studies have investigated their roles in the diagnosis, progression, metastasis, and prognosis of various cancers, but the mechanisms through which they are involved in resistance to cancer treatment are unclear. This review outlines the classification of tRFs and tiRNAs and their mechanisms in cancer drug resistance, thus providing new ideas for cancer treatment.

Adenosine deaminases acting on RNA (ADARs) catalyze the conversion of adenosine (A) to inosine (I) in double-stranded RNA, which can change the codons after transcription. Abnormal ADAR editing is present in a variety of cancers. However, the study of the biological effects of ADARs in cancer is not very deep. Here, we review current important ADAR-mediated editing events, related carcinogenic mechanisms and applications in clinical medicine. Further exploration in ADARs can provide a new direction for cancer treatment.

Non-small cell lung cancer (NSCLC) has the highest morbidity and mortality worldwide among malignant tumors. NSCLC is a great threat to health and well-being. Biopsy is the gold standard to diagnose lung cancer, but traditional biopsy methods cannot fully reflect the true condition of tumors. There is growing evidence that a single-point biopsy fails to reveal the complete landscape of the tumor due to intratumor heterogeneity, but it is impractical to complete multiple biopsies that are separated both spatially and temporally. Liquid biopsy heralds that a new era is coming. Circulating tumor cells (CTCs) are tumor cells that circulate in the peripheral blood after being shed from primary or metastatic tumors. CTCs constitute a considerable portion of a liquid biopsy, which contributes to the diagnosis, assessment of prognosis, and therapy of NSCLC. Herein, this review discusses the technologies for detection and enrichment of CTCs as well as clinical applications involving CTCs.

Background: Circular RNAs (circRNAs), which are a new type of single-stranded circular RNA, have significant involvement in progression of many diseases, including tumors. Currently, multiple circRNAs have been identified in hepatocellular carcinoma (HCC). Our study aims to investigate the function and mechanism of circDCAF8 in HCC. Methods: The expression of circDCAF8 (hsa_circ_0014879) in HCC and para-carcinoma tissue samples was determined using quantitative real-time polymerase chain reaction (qRT-PCR). The biological function of circDCAF8 in HCC was confirmed by experiments conducted both in vitro and in vivo. And the relationship between circDCAF8, miR-217 and NAP1L1 was predicted by database and verified using qRT-PCR, RNA-binding protein immunoprecipitation (RIP) and dual-luciferase reporter assays. Exosomes isolated from HCC cells were utilized to assess the connection of exosomal circDCAF8 with HCC angiogenesis and regorafenib resistance. Results: CircDCAF8 is upregulated in HCC tissues and cell lines, and is linked to an unfavourable prognosis for HCC patients. Functionally, circDCAF8 was proved to facilitate proliferation, migration, invasion and Epithelial-Mesenchymal Transformation (EMT) in HCC cells. Animal examinations also validated the tumor-promoting characteristics of circDCAF8 on HCC. Besides, exosomal circDCAF8 promoted angiogenesis in HUVECs. Mechanistically, circDCAF8 interacted with miR-217 and NAP1L1 was a downstream protein of miR-217. CircDCAF8 promoted NAP1L1 expression by sponging miR-217. In addition, exosomes may transfer circDCAF8 from regorafenib-resistant HCC cells to sensitive cells, where it would confer a resistant phenotype. Conclusion: CircDCAF8 facilitates HCC proliferation and metastasis via the miR-217/NAP1L1 axis. Meanwhile, circDCAF8 can promote angiogenesis and drive resistance to regorafenib, making it a viable therapeutic target for HCC patients.