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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.

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.

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.

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.

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.

Background CD90+ liver cancer cells have been described as cancer stem-cell-like (CSC), displaying aggressive and metastatic phenotype. Using two different in vitro models, already described as CD90+ liver cancer stem cells, our aim was to study their interaction with endothelial cells mediated by the release of exosomes. Methods Exosomes were isolated and characterized from both liver CD90+ cells and hepatoma cell lines. Endothelial cells were treated with exosomes, as well as transfected with a plasmid containing the full length sequence of the long non-coding RNA (lncRNA) H19. Molecular and functional analyses were done to characterize the endothelial phenotype after treatments. Results Exosomes released by CD90+ cancer cells, but not by parental hepatoma cells, modulated endothelial cells, promoting angiogenic phenotype and cell-to-cell adhesion. LncRNA profiling revealed that CD90+ cells were enriched in lncRNA H19, and released this through exosomes. Experiments of gain and loss of function of H19 showed that this LncRNA plays an important role in the exosome-mediated phenotype of endothelial cells. Conclusions Our data indicate a new exosome-mediated mechanism by which CSC-like CD90+ cells could influence their tumor microenvironment by promoting angiogenesis. Moreover, we suggest the lncRNA H19 as a putative therapeutic target in hepatocellular carcinoma.

With the development of proteomics and epigenetics, a large number of RNA‐binding proteins (RBPs) have been discovered in recent years, and the interaction between long non‐coding RNAs (lncRNAs) and RBPs has also received increasing attention. It is extremely important to conduct in‐depth research on the lncRNA‐RBP interaction network, especially in the context of its role in the occurrence and development of cancer. Increasing evidence has demonstrated that lncRNA‐RBP interactions play a vital role in cancer progression; therefore, targeting these interactions could provide new insights for cancer drug discovery. In this review, we discussed how lncRNAs can interact with RBPs to regulate their localization, modification, stability, and activity and discussed the effects of RBPs on the stability, transport, transcription, and localization of lncRNAs. Moreover, we explored the regulation and influence of these interactions on lncRNAs, RBPs, and downstream pathways that are related to cancer development, such as N6‐methyladenosine (m6A) modification of lncRNAs. In addition, we discussed how the lncRNA‐RBP interaction network regulates cancer cell phenotypes, such as proliferation, apoptosis, metastasis, drug resistance, immunity, tumor environment, and metabolism. Furthermore, we summarized the therapeutic strategies that target the lncRNA‐RBP interaction network. Although these treatments are still in the experimental stage and various theories and processes are still being studied, we believe that these strategies may provide new ideas for cancer treatment.

Cardiovascular diseases are a main cause of mortality whose prevalence continues to increase worldwide. Long non‐coding RNAs (lncRNAs) regulate a variety of biological processes by modifying and regulating transcription of coding genes, directly binding to proteins and even coding proteins themselves. LncRNAs play key roles in the occurrence and development of myocardial infarction, heart failure, myocardial hypertrophy, arrhythmias and other pathological processes that significantly affect the prognosis and survival of patients with cardiovascular diseases. We here review the latest research on lncRNAs in cardiovascular diseases as a basis to formulate future research on prevention and treatment of cardiovascular diseases.

Long non‐coding RNA (lncRNA) is an important regulatory factor in the development of lung adenocarcinoma, which is related to the control of autophagy. LncRNA can also be used as a biomarker of prognosis in patients with lung adenocarcinoma. Therefore, it is important to determine the prognostic value of autophagy‐related lncRNA in lung adenocarcinoma. In this study, autophagy‐related mRNAs‐lncRNAs were screened from lung adenocarcinoma and a co‐expression network of autophagy‐related mRNAs‐lncRNAs was constructed by using The Cancer Genome Atlas (TCGA). The univariate and multivariate Cox proportional hazard analyses were used to evaluate the prognostic value of the autophagy‐related lncRNAs and finally obtained a survival model composed of 11 autophagy‐related lncRNAs. Through Kaplan‐Meier analysis, univariate and multivariate Cox regression analysis and time‐dependent receiver operating characteristic (ROC) curve analysis, it was further verified that the survival model was a new independent prognostic factor for patients with lung adenocarcinoma. In addition, based on the survival model, gene set enrichment analysis (GSEA) was used to illustrate the function of genes in low‐risk and high‐risk groups. These 11 lncRNAs were GAS6‐AS1, AC106047.1, AC010980.2, AL034397.3, NKILA, AL606489.1, HLA‐DQB1‐AS1, LINC01116, LINC01806, FAM83A‐AS1 and AC090559.1. The hazard ratio (HR) of the risk score was 1.256 (1.196‐1.320) (P < .001) in univariate Cox regression analysis and 1.215 (1.149‐1.286) (P < .001) in multivariate Cox regression analysis. And the AUC value of the risk score was 0.809. The 11 autophagy‐related lncRNA survival models had important predictive value for the prognosis of lung adenocarcinoma and may become clinical autophagy‐related therapeutic targets.