Spinal diseases, including intervertebral disc degeneration (IDD), ankylosing spondylitis, spinal cord injury and other non‑infectious spinal diseases, severely affect the quality of life of patients. Current treatments for IDD and other spinal diseases can only relieve symptoms and do not completely cure the disease. Therefore, there is an urgent need to explore the causes of these diseases and develop new treatment approaches. Long non‑coding RNA (lncRNA), a form of non‑coding RNA, is abundant in diverse sources, has numerous functions, and plays an important role in the occurrence and development of spinal diseases such as IDD. However, the mechanism of action of lncRNAs has not been fully elucidated, and significant challenges remain in the use of lncRNAs as new therapeutic targets. The present article reviews the sources, classification and functions of lncRNAs, and introduces the role of lncRNAs in spinal diseases, such as IDD, and their therapeutic potential.

Esophageal squamous cell carcinoma (ESCC) is a prevalent and deadly malignancy of the digestive tract. Recent research has identified long non‑coding RNAs (lncRNAs) as crucial regulators in the pathogenesis of ESCC. These lncRNAs, typically exceeding 200 nucleotides, modulate gene expression through various mechanisms, including the competing endogenous RNA (ceRNA) pathway and RNA‑protein interactions. The current study reviews the multifaceted roles of lncRNAs in ESCC, highlighting their involvement in processes such as proliferation, migration, invasion, epithelial‑mesenchymal transition, cell cycle progression, resistance to radiotherapy and chemotherapy, glycolysis, apoptosis, angiogenesis, autophagy, tumor growth, metastasis and the maintenance of cancer stem cells. Specific lncRNAs like HLA complex P5, LINC00963 and non‑coding repressor of NFAT have been shown to enhance resistance to radio‑ and chemotherapy by modulating pathways such as AKT signaling and microRNA interaction, which promote cell survival and proliferation under therapeutic stress. Furthermore, lncRNAs like family with sequence similarity 83, member A antisense RNA 1, zinc finger NFX1‑type containing 1 antisense RNA 1 and taurine upregulated gene 1 are implicated in enhancing invasive and proliferative capabilities of ESCC cells through the ceRNA mechanism, while interactions with RNA‑binding proteins further influence cancer cell behavior. The comprehensive analysis underscores the potential of lncRNAs as biomarkers for prognosis and therapeutic targets in ESCC, suggesting avenues for future research focused on elucidating the detailed molecular mechanisms and clinical applications of lncRNAs in ESCC management.

Even under aerobic conditions, tumor cells can reprogram their metabolism to preferentially metabolize glucose into lactic acid. This abnormal metabolic pattern, known as the \'Warburg\' effect or aerobic glycolysis, promotes cancer progression. Long non‑coding RNAs (lncRNAs) are RNAs that are >200 nucleotides in length and do not have protein‑coding capabilities. However, these RNAs play a key role in tumor development. There is increasing evidence to indicate that lncRNAs regulate glucose metabolism in tumor cells by affecting metabolic enzymes and some signaling pathways, thereby regulating the occurrence and progression of hepatocellular carcinoma (HCC). Therefore, it is crucial to understand which lncRNAs play a regulatory role in HCC glycolysis and to determine the related molecular mechanisms. The present review summarized and discussed the functions of lncRNAs, focusing on the regulatory mechanisms of lncRNAs in the process of glycolysis in HCC. In addition, the present review suggests the importance of lncRNAs as future therapeutic targets for antitumor cell metabolism.

Nuclear receptors (NRs) are transcriptional regulators involved in different aspects of normal cell physiology. Their deregulation is associated with aberrant expression, gene mutations and/or epigenetic alterations that can be related to the pathogenesis of various human diseases, and especially in cancer. In particular, a complex genomic network involved in the development and progression of NR‑mediated cancer has been highlighted. Advanced genomic technologies have made it possible to understand that the expression of any particular NR in a given cancer subtype is only one component of a larger transcriptional machinery that is controlled by multiple associated NRs and transcription factors. Additionally, their ability to regulate and to be regulated by molecules of non‑coding RNAs, microRNAs as well as long non‑coding RNAs, is opening new scenarios for understanding the role of NRs in cancer initiation and progression. In the present review, the authors aimed to outline the reciprocal interactions that exist between the main NRs and long non‑coding RNAs in different tumor diseases, to suggest new diagnostic biomarkers as well as therapeutic strategies for these tumors.

The term autophagy describes a process that supports nutrient cycling and metabolic adaptation that is accomplished via multistep lysosomal degradation. These activities modulate cell, tissue and internal environment stability, and can also affect the occurrence and development of cancer. Previous studies have mostly described autophagy as having dual effects in cancer, serving to limit tumorigenesis in the early stages of cancer, but promoting tumor progression in certain types of cancer. There have been indications in recent years that microRNAs (miRNAs/miRs) and long non‑coding RNAs (lncRNAs), as types of non‑coding RNAs, play major roles in the occurrence, invasion, development and drug resistance of hepatocellular carcinoma (HCC) and in the migration of HCC cells by governing HCC cell autophagy. Therefore, understanding which miRNAs and lncRNAs play such roles and the relevant molecular mechanisms is critical. The present review highlights the significant functions of miRNAs and lncRNAs in the regulation of autophagy in HCC and the relevant mechanisms, aiming to provide novel insight into HCC therapeutics.

Resistance to stress is a feature of cancer cells. Cellular stress includes oxidative, metabolic and genotoxic stress conditions, which under normal conditions lead to cell death. However, in contrast to normal cells, cancer cells overcome the checkpoints that normally restrict growth, and are able to resist cellular stress and subsequent cell death through a variety of mechanisms, which include several non‑coding RNAs (ncRNAs). Within this context, long ncRNAs (lncRNAs) and microRNAs (miRNAs/miRs) are the main categories of ncRNAs that have been shown in the literature to function as regulators of stress resistance pathways in cancer. miRNAs play a key role in the majority of biological pathways, as they regulate the expression of hundreds of target genes, including genes involved in stress response and cell death, oncogenes, or tumor suppressor genes, by inhibiting protein translation or promoting the degradation of mRNAs. Respectively, lncRNAs are epigenetic regulators, which are also involved in cancer progression, stress response and metabolic pathways by promoting or inhibiting the transcription, splicing, translation and modulation of protein function. Thus, the present review summarizes recent knowledge related to the role of these molecules in the cancer response to stress, highlighting the ability of these non‑coding molecules to be effective drug targets and biomarkers in cancer treatment.

Gliomas are a primary types of intracranial malignancies and are characterized by a poor prognosis due to aggressive recurrence profiles. Temozolomide (TMZ) is an auxiliary alkylating agent that is extensively used in conjunction with surgical resection and forms the mainstay of clinical treatment strategies for gliomas. However, the frequent occurrence of TMZ resistance in clinical practice limits its therapeutic efficacy. Accumulating evidence has demonstrated that long non‑coding RNAs (lncRNAs) can play key and varied roles in glioma progression. lncRNAs have been reported to inhibit glioma progression by targeting various signaling pathways. In addition, the differential expression of lncRNAs has also been found to mediate the resistance of glioma to several chemotherapeutic agents, particularly to TMZ. The present review article therefore summarizes the findings of previous studies in an aim to report the significance and function of lncRNAs in regulating the chemoresistance of gliomas. The present review may provide further insight into the clinical treatment of gliomas.

Following the publication of the above paper, the authors have realized that the cell apoptosis and cell proliferation assays in Fig. 8 were poorly presented, which made the interpretation of the data difficult. Furthermore, a change was also required to the text concerning the description of Fig. 8: The sentence starting on p. 517, left‑hand column, line 7 (\'The fraction of apoptotic cells was 22.41±2.596 in the lncENST00000444102-overexpressing SKM‑1 cells, and 8.650±0.889 in the negative control; the fraction of apoptotic cells was 20.58±2.190 in the lncENST00000444102‑overexpressing THP‑1 cells and 8.192±0.997 in the negative control group (P<0.001, Fig. 8B)\' should be replaced with the following text: \'Flow cytometry showed that the fraction of apoptotic cells increased in the lncENST00000444102‑overexpressing SKM‑1 and THP‑1 cells, as determined by Annexin V‑APC/7-AAD staining at 48 h (P<0.05; Fig. 8B)\'. A revised version of Fig. 8, presenting the results of the flow cytometric analysis more clearly, is shown on the next page. Note that the revisions made to this figure have not had a major impact on the reported results, and do not affect the overall conclusions reported in the study. All the authors agree to the publication of this corrigendum. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize for any inconvenience caused to the readership of the Journal. [Oncology Reports 42: 509‑520, 2019; DOI: 10.3892/or.2019.7175].

Long non‑coding RNAs (lncRNAs) feature prominently in pancreatic carcinoma progression. The present study aimed to clarify the biological functions, clinical significance and underlying mechanism of lncRNA CTBP1 antisense RNA 2 (CTBP1‑AS2) in pancreatic carcinoma. Reverse transcription‑quantitative PCR was performed to assess the expression levels of CTBP1‑AS2, microRNA (miR)‑141‑3p and ubiquitin‑specific protease 22 (USP22) mRNA in pancreatic carcinoma tissues and cell lines. Western blotting was used to examine USP22 protein expression in pancreatic carcinoma cell lines. Loss‑of‑function experiments were used to analyze the regulatory effects of CTBP1‑AS2 on proliferation, apoptosis, migration and invasion of pancreatic carcinoma cells. Dual‑luciferase reporter assay was used to examine the binding relationship between CTBP1‑AS2 and miR‑141‑3p, as well as between miR‑141‑3p and USP22. It was demonstrated that CTBP1‑AS2 expression was markedly increased in pancreatic carcinoma tissues and cell lines. High CTBP1‑AS2 expression was associated with advanced clinical stage and lymph node metastasis of patients. Functional experiments confirmed that knocking down CTBP1‑AS2 significantly inhibited pancreatic carcinoma cell proliferation, migration and invasion, and promoted cell apoptosis. In terms of mechanism, it was found that CTBP1‑AS2 adsorbed miR‑141‑3p as a molecular sponge to upregulate the expression level of USP22. In conclusion, lncRNA CTBP1‑AS2 may be involved in pancreatic carcinoma progression by regulating miR‑141‑3p and USP22 expressions; in addition, CTBP1‑AS2 may be a diagnostic biomarker and treatment target for pancreatic carcinoma.

Cervical cancer is the fourth most common female malignancy for both incidence and mortality worldwide and is one of the major threats to women\'s health. The role of long non‑coding RNAs (lncRNAs) in cervical cancer remains largely unknown. In the present study, the differentially expressed lncRNAs in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) tissues were retrieved form The Cancer Genome Atlas (TCGA) and were analyzed. The expression analysis of related genes was performed with GEPIA. The proliferation and migratory and invasive abilities of MIR205HG knockdown CESC cells were analyzed using Cell Counting Kit‑8 and transwell assays. The expression of Ki‑67 and p16 was detected by immunofluorescence. A total of 203 differentially expressed lncRNAs were identified. The results demonstrated that MIR205HG was overexpressed in CESC tissues. Furthermore, the genes related to MIR205HG were enriched in cancer‑related pathways. MIR205HG knockdown significantly decreased the proliferation and migratory and invasive abilities of CESC cells. In addition, silencing of MIR205HG significantly decreased the expression of p16 in C‑33 A cells. The expression of fibroblast growth factor receptor 3, thymidine phosphorylase and GTPase HRas was downregulated in MIR205HG knockdown CESC cells. These findings revealed some potential lncRNA candidates for cervical cancer research and suggested that MIR205HG may have a pro‑tumor role in CESC.