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Lung cancer remains a significant global health challenge, largely due to difficulties in early detection and the lack of effective therapeutic strategies for more advanced-stage disease. Elucidating the molecular mechanisms underlying lung carcinogenesis and identifying reliable biomarkers is of urgent importance. Long non-coding RNAs (lncRNAs), a class of transcripts of >200 nucleotides without protein-coding potential, have recently emerged as key regulators of tumor cell invasion, metastasis, proliferation, apoptosis and angiogenesis. Accumulating evidence suggests that lncRNAs hold notable promise as diagnostic and prognostic biomarkers in lung cancer. However, a comprehensive overview that integrates their mechanistic roles, clinical potential and the technological advances in their detection, while critically addressing the associated challenges, is lacking, to the best of the authors' knowledge. In the present review, a summary of recent advances in the mechanistic roles of lncRNAs during lung cancer progression and their involvement in therapy response and chemoresistance was provided, along with an up-to-date discussion of emerging detection technologies and their implications for clinical translation. The advantages, limitations and challenges of using lncRNAs as diagnostic or prognostic biomarkers in lung cancer are discussed. By synthesizing these aspects, the present review aimed to highlight the novel insights into lncRNAs and outline future research directions, thereby addressing a critical gap in the current literature.

Long non-coding RNAs (lncRNAs) have been reported to play vital roles in human lung cancer. In recent years, cancer/testis (CT) lncRNAs have been characterized as a novel class of lncRNA. However, this class of lncRNA remains to be thoroughly investigated. The present study identified long intergenic non-protein coding RNA 1635 (LINC01635), which was highly expressed in testis and in a broad range of human cancer types. Next, it was confirmed that LINC01635 was upregulated significantly in samples from patients with lung cancer and in non-small cell lung carcinoma (NSCLC) cell lines. Silencing LINC01635 suppressed the proliferation and metastasis of NSCLC cells in vitro and in vivo. Furthermore, it was found that LINC01635 could bind to microRNA (miRNA or miR)-455-5p and regulate the expression of a series of miR-455-5p-targeting tumor-related genes. Knockdown of miR-455-5p partially rescued the progression of lung cancer cells that was suppressed by LINC01635 silencing. Together, the current results demonstrated that LINC01635 may play important roles in NSCLC progression by targeting miR-455-5p, and that it could be a biomarker and therapeutic target for lung cancer.

Ovarian cancer (OV) is the fifth most common type of cancer affecting women worldwide. Long non-coding RNAs (lncRNAs) serve essential roles in the progression of OV. As such, the present study aimed to investigate the specific role of HAGLR opposite strand lncRNA (HAGLROS) in OV and the underlying mechanism of action through which HAGLROS exerts its effects on OV cells. In the present study, the expression of HAGLROS in several OV cell lines was first detected using reverse transcription-quantitative PCR. HAGLROS was then silenced to evaluate cell viability, proliferation and apoptosis, which were determined using Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Additionally, immunofluorescence staining and western blotting were used to confirm the expression profile of proliferation- and apoptosis-related proteins. Moreover, a dual luciferase reporter assay was used to verify the potential interactions between HAGLROS and microRNA (miR)-26b-5p. Subsequently, rescue assays were performed to investigate the effects of HAGLROS and miR-26b-5p on OV progression. The results indicated that HAGLROS was highly expressed in OV cells. Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. miR-26b-5p inhibitor transfection partially reversed the effects of HAGLROS knockdown on the proliferation and apoptosis of OV cells. In conclusion, the results of the present study suggested that interference of HAGLROS suppressed the proliferation and promoted the apoptosis of OV cells through regulating miR-26b-5p, indicating that HAGLROS may be a promising biomarker in OV diagnosis and treatment.

Cervical carcinoma expressed PCNA regulatory long non-coding (lnc)RNA (CCEPR) has recently been reported to play oncogenic roles in some common types of human cancer. However, the clinical significance of CCEPR mRNA expression levels in esophageal squamous cell carcinoma (ESCC) and the exact function of CCEPR in regulating the malignant phenotypes of ESCC cells have not been previously investigated. In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC. In vitro experiments showed that silencing CCEPR mRNA expression levels significantly suppressed the proliferation, migration, and invasion of ESCC cells, while inducing ESCC cell apoptosis. Furthermore, inhibition of CCEPR decreased the protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 and inhibited epithelial-mesenchymal transition in ESCC cells. In conclusion, the results showed that CCEPR plays an oncogenic role in ESCC and suggests that CCEPR could be used as a potential therapeutic target for ESCC treatment.

Long non‐coding RNAs (lncRNAs) are well known as crucial regulators to breast cancer development and are implicated in controlling autophagy. LncRNAs are also emerging as valuable prognostic factors for breast cancer patients. It is critical to identify autophagy‐related lncRNAs with prognostic value in breast cancer. In this study, we identified autophagy‐related lncRNAs in breast cancer by constructing a co‐expression network of autophagy‐related mRNAs‐lncRNAs from The Cancer Genome Atlas (TCGA). We evaluated the prognostic value of these autophagy‐related lncRNAs by univariate and multivariate Cox proportional hazards analyses and eventually obtained a prognostic risk model consisting of 11 autophagy‐related lncRNAs (U62317.4, LINC01016, LINC02166, C6orf99, LINC00992, BAIAP2‐DT, AC245297.3, AC090912.1, Z68871.1, LINC00578 and LINC01871). The risk model was further validated as a novel independent prognostic factor for breast cancer patients based on the calculated risk score by Kaplan‐Meier analysis, univariate and multivariate Cox regression analyses and time‐dependent receiver operating characteristic (ROC) curve analysis. Moreover, based on the risk model, the low‐risk and high‐risk groups displayed different autophagy and oncogenic statues by principal component analysis (PCA) and Gene Set Enrichment Analysis (GSEA) functional annotation. Taken together, these findings suggested that the risk model of the 11 autophagy‐related lncRNAs has significant prognostic value for breast cancer and might be autophagy‐related therapeutic targets in clinical practice.

Melanoma is a rare malignancy in China and the treatment outcomes are generally satisfactory. However, postoperative recurrence can be life-threatening. The current study aimed to investigate the involvement of long intergenic non-protein coding RNA 1638 (LINC01638) long non-coding RNA (lncRNA) in the recurrence of melanoma. Expression of LINC01638 lncRNA in skin biopsies and plasma of patients with melanoma, patients with benign skin lesions and healthy controls was detected by reverse transcription-quantitative polymerase chain reaction. Diagnostic values of LINC01638 lncRNA for melanoma were analyzed by receiver operating characteristic curve analysis. The association between LINC01638 lncRNA and clinicopathological data of patients with melanoma was analyzed by χ2 test. All patients were followed up for five years to record recurrence. LINC01638 lncRNA expression vectors and shRNAs were transfected into human melanoma cell lines and the effects of LINC01638 lncRNA overexpression and knockdown on cell proliferation were analyzed by cell counting kit-8 assay. LINC01638 lncRNA was significantly upregulated in patients with melanoma compared with the other two groups of patients, and upregulation of LINC01638 lncRNA distinguished patients with melanoma from patients with benign skin lesions and healthy controls. LINC01638 lncRNA expression was significantly associated with tumor size but not with other patient clinical data. Plasma levels of LINC01638 lncRNA were further increased during follow-up in patients with local recurrence but not in patients without recurrence. LINC01638 lncRNA overexpression promoted, while knockdown inhibited proliferation of cells of melanoma cell lines, C32 and SK-MEL-28, in vitro. The upregulation of LINC01638 lncRNA was likely associated with the local recurrence of melanoma following surgical resection.

Oral squamous cell carcinoma (OSCC), the eighth most prevalent cancer in the world, arises from the interaction of multiple factors including tobacco, alcohol consumption, and betel quid. Chemotherapeutic agents such as cisplatin, 5‐fluorouracil, and paclitaxel have now become the first‐line options for OSCC patients. Nevertheless, most OSCC patients eventually acquire drug resistance, leading to poor prognosis. With the discovery and identification of non‐coding RNAs (ncRNAs), the functions of dysregulated ncRNAs in OSCC development and drug resistance are gradually being widely recognized. The mechanisms of drug resistance of OSCC are intricate and involve drug efflux, epithelial‐mesenchymal transition, DNA damage repair, and autophagy. At present, strategies to explore the reversal of drug resistance of OSCC need to be urgently developed. Nano‐delivery and self‐cellular drug delivery platforms are considered as effective strategies to overcome drug resistance due to their tumor targeting, controlled release, and consistent pharmacokinetic profiles. In particular, the combined application of new technologies (including CRISPR systems) opened up new horizons for the treatment of drug resistance of OSCC. Hence, this review explored emerging regulatory functions of ncRNAs in drug resistance of OSCC, elucidated multiple ncRNA‐meditated mechanisms of drug resistance of OSCC, and discussed the potential value of drug delivery platforms using nanoparticles and self‐cells as carriers in drug resistance of OSCC. The mechanisms of drug resistance are intricate and involve drug efflux, epithelial mesenchymal transition, DNA damage repair, and autophagy. Nano‐delivery and self‐cellular drug delivery platforms have a broad prospective for alleviating OSCC drug resistance. In particular, the combined application of new technologies (including CRISPR systems) opens up new horizons for treatment of OSCC drug resistance.

Since comprehensive analysis of the mammalian genome revealed that the majority of genomic products are transcribed in long non‐coding RNA (lncRNA), increasing attention has been paid to these transcripts. The applied next‐generation sequencing technologies have provided accumulating evidence of dysregulated lncRNA in cancer. The implication of this finding can be seen in many forms and at multiple levels. With impacts ranging from integrating chromatin remodeling complexes to regulating transcription and post‐transcriptional processes, aberrant expression of lncRNA may have repercussions in cell proliferation, tumor progression or metastasis. lncRNA may act as enhancers, scaffolds or decoys by physically interacting with other RNA species or proteins, resulting in a direct impact on cell signaling cascades. Even though their functional classification is well‐established in the context of cancer, clearer characterization in terms of their phenotypic outputs is needed to optimize and identify suitable candidates that enable the development of new therapeutic strategies and the design of novel diagnostic approaches. The present article aims to outline different cancer‐associated lncRNA according to their contribution to tumor suppression or tumor promotion based on their most current functional annotations. lncRNAs involved in tumor plasticity. Aberrantly expressed lncRNAs may have an important impact in the EMT‐MET processes by interacting with diverse signaling cascades.

Long non‐coding RNAs (lncRNAs) are a numerous class of newly discovered genes in the human genome, which have been proposed to be key regulators of biological processes, including stem cell pluripotency and neurogenesis. However, at present very little functional characterization of lncRNAs in human differentiation has been carried out. In the present study, we address this using human embryonic stem cells (hESCs) as a paradigm for pluripotency and neuronal differentiation. With a newly developed method, hESCs were robustly and efficiently differentiated into neurons, and we profiled the expression of thousands of lncRNAs using a custom‐designed microarray. Some hESC‐specific lncRNAs involved in pluripotency maintenance were identified, and shown to physically interact with SOX2, and PRC2 complex component, SUZ12. Using a similar approach, we identified lncRNAs required for neurogenesis. Knockdown studies indicated that loss of any of these lncRNAs blocked neurogenesis, and immunoprecipitation studies revealed physical association with REST and SUZ12. This study indicates that lncRNAs are important regulators of pluripotency and neurogenesis, and represents important evidence for an indispensable role of lncRNAs in human brain development. An array‐based approach identifies hESC‐specific novel long non‐coding RNAs (lncRNAs) that are essential for the maintenance of pluripotency and indispensable for neuronal differentiation. A number of these lncRNAs directly interact with the pluripotency regulators SOX2 and PRC2.

Cancer constitutes a significant public health concern, and addressing the challenge of cancer holds paramount importance and requires immediate attention. Epigenetic alterations, encompassing DNA methylation, have emerged as pivotal contributors to the development of diverse cancer types. These modifications exert their influence by modulating chromatin structure, gene expression patterns and other nuclear processes, thereby influencing cancer pathogenesis. Over the last two decades, an increasing body of evidence has established the involvement of DNA methyltransferase 1 (DNMT1) in various aspects of cancer development, including tumorigenesis, aggressiveness and treatment response. Furthermore, non‐coding RNAs (ncRNAs), such as microRNAs (miRNAs) and long non‐coding RNAs (lncRNAs), are increasingly recognised as significant modulators in diverse biological processes, encompassing metastasis, apoptosis, cell proliferation and differentiation. Several recent studies have elucidated the intricate relationship between epigenetic machinery, specifically DNMT1, and the expression of ncRNAs in the context of cancer. In this review, we provide a comprehensive overview of the interaction between DNMT1 and ncRNAs in cancer pathogenesis. Furthermore, we discuss the important role of the ncRNAs‐DNMT1 axis in cancer stem cells and cancer therapy resistance as critical issues in cancer therapy. Finally, we demonstrate that herbal medicine and synthetic RNA molecules regulate DNMT1 activity and hold great promise in cancer treatment.