A review on the role of LINC00467 in the carcinogenesis.

LINC00467 is an example of long intergenic non-coding RNAs whose roles in human disorders are being identified. This gene coding LINC00467 is located on chromosome 1: 211,382,736 - 211,435,570 forward strand. This lncRNA has been firstly recognized through a microarray-based lncRNA profiling as an N-Myc target in neuroblastoma cells. Further studies have shown up-regulation of LINC00467 in different cancer including those originated from brain, gastrointestinal tract, lung and breast. It acts as a molecular sponge for miR-339, miR-138-5p, miR-107, miR-133b, miR-451a, miR-485-5p, miR-7-5p, miR-485-5p, miR-339-3p, miR-200a, miR-1285-3p, miR-299-5p, miR-509-3p, miR-18a-5p, miR-9-5p and miR-20b-5p. LINC00467 can regulate activity of NF-κB, STAT1, Wnt/b-catenin, Akt and ERK1/2 signaling pathways. Accumulating evidence indicates oncogenic role of LINC00467. The current review article aims at providing an overview of LINC00467 in the carcinogenesis.

LINC00467: an oncogenic long noncoding RNA.

Long non-coding RNAs (lncRNAs) have been found to play essential roles in the cell proliferation, fission and differentiation, involving various processes in humans. Recently, there is more and more interest in exploring the relationship between lncRNAs and tumors. Many latest evidences revealed that LINC00467, an oncogenic lncRNA, is highly expressed in lung cancer, gastric cancer, colorectal cancer, hepatocellular carcinoma, breast cancer, glioblastoma, head and neck squamous cell carcinoma, osteosarcoma, and other malignant tumors. Besides, LINC00467 expression was linked with proliferation, migration, invasion and apoptosis via the regulation of target genes and multiple potential pathways. We reviewed the existing data on the expression, downstream targets, molecular mechanisms, functions, relevant signaling pathways, and clinical implications of LINC00467 in various cancers. LINC00467 may serve as a novel biomarker or therapeutic target for the diagnosis and prognosis of various human tumors.

LncRNA LINC00467 acted as an oncogene in esophageal squamous cell carcinoma by accelerating cell proliferation and preventing cell apoptosis via the miR-485-5p/DPAGT1 axis.

BACKGROUND AND AIM: Esophageal carcinoma has been regarded as one of the top 10 common malignancies globally. Esophageal squamous cell carcinoma (ESCC) is an important subtype of esophageal carcinoma with approximately 20% survival rate. Long noncoding RNAs were documented to regulate the occurrence or progression of several tumors. However, neither the biological role nor the molecular mechanism of LINC00467 has been explored. This research is aimed to investigating the regulatory mechanism of LINC00467 in ESCC. METHODS: In this study, a series of experiments including reverse transcription-quantitative polymerase chain reaction, Cell Counting Kit-8, luciferase reporter, western blot, and RNA immunoprecipitation were designed and conducted to explore the potential function and mechanism of LINC00467 in ESCC. RESULTS: According to experimental results, we found out upregulated LINC00467 improved cell proliferation, but hindered cell apoptosis. In mechanism, miR-485-5p was predicted, screened out, and validated to combine with LINC00467, which displayed lower expression in ESCC. Additionally, miR-485-5p negatively regulated and directly targeted DPAGT1. Rescue assays suggested that DPAGT1 amplification was able to recover the influence of LINC00467 deficiency on cell proliferation and apoptosis. Furthermore, knockdown of LINC00467 suppressed tumor growth in vivo. CONCLUSION: We proved that LINC00467 acted as an oncogene in ESCC by accelerating cell proliferation and preventing cell apoptosis via miR-485-5p/DPAGT1 axis. This may provide a potential diagnostic marker for ESCC treatment.

Long non-coding RNA LINC00467 drives hepatocellular carcinoma progression via inhibiting NR4A3.

Hepatocellular carcinoma (HCC) is a main cause of cancer-related deaths globally. Long non-coding RNAs (lncRNAs) play important roles in diverse cancers. Our previous microarray-based lncRNA profiling showed that LINC00467 was highly expressed in HCC. Here, we further explored the expression, role and functional mechanism of lncRNA LINC00467 in HCC. Our findings revealed that LINC00467 was up-regulated in HCC tissues and HCC cell lines. Increased expression of LINC00467 was positively associated with tumour size and vascular invasion. In vitro functional experiments revealed that LINC00467 accelerated HCC cell proliferation, cell cycle progression and migration and reduced HCC cell apoptosis. In vivo functional assays revealed that LINC00467 drove HCC xenograft growth and HCC cell proliferation and repressed HCC cell apoptosis in vivo. Moreover, LINC00467 inhibited NR4A3 post-transcriptionally via interacting with NR4A3 mRNA to form double-stranded RNA, which was further degraded by Dicer. The expression of NR4A3 was inversely associated with LINC00467 in HCC tissues. Functional rescue assays found that restore of NR4A3 expression blocked the oncogenic roles of LINC00467 in HCC. Taken together, our results demonstrated that lncRNA LINC00467 was a novel highly expressed and oncogenic lncRNA in HCC via inhibiting NR4A3. Targeting LINC00467 or enhancing NR4A3 may be potential therapeutic strategies against HCC.

LINC00467 promotes cell proliferation and stemness in lung adenocarcinoma by sponging miR-4779 and miR-7978.

Lung adenocarcinoma (LAD), as one of the most common types of lung tumors, is lethal and malignant. Long noncoding RNAs (lncRNAs) play important roles in various cancers according to many previous studies. LINC00467 was proposed to be a tumor promoter. Despite the validated promotive effect of LINC00467 on neuroblastoma progression, its regulatory mechanism in LAD remains unclear. In this study, LINC00467 expressed higher in LAD tissues and cell lines, and increased LINC00467 indicated a poor prognosis. Knockdown of LINC00467 inhibited cell proliferation, the expressions of tumor stem cell-related genes, and cell spheroid formation ability, while it promoted cell apoptosis. miR-4779 and miR-7978 were reported to play antitumor roles in several cancers before. LINC00467 could combine with miR-4779 and miR-7978, and negatively regulated miR-4779 and miR-7978. miR-4779 and miR-7978 inhibitor could partly rescue the LINC00467 knockdown-induced influence on cell proliferation, apoptosis, and stemness. In a word, this study innovatively investigated the mechanism of LINC00467 in LAD and verified LINC00467 exerted its carcinogenesis function by sponging miR-4779 and miR-7978, which may become a catalyst for generating new therapeutic targets for LAD treatment.

Long noncoding RNA linc00467 plays an oncogenic role in hepatocellular carcinoma by regulating the miR-18a-5p/NEDD9 axis.

Increasing evidence has shown that numerous long noncoding RNAs (lncRNAs) play critical roles in tumorigenesis. Herein, we investigated the biological role of lncRNA linc00467 in the cancer biology of hepatocellular carcinoma (HCC). We observed that linc00467 was upregulated in HCC tissues and cells. Silencing of linc00467 using small interfering RNA interference significantly inhibited the growth and motility of HCC cells, and increased cell apoptosis through regulating the Bcl-2/Bax axis and the caspase cascade, suggesting that linc00467 exerted oncogenic functions in the progression of HCC. Moreover, we found that linc00467 could target miR-18a-5p, and NEDD9 was a target for miR-18a-5p in HCC cells. Furthermore, either the miR-18a-5p inhibitor or upregulation of NEDD9 could recover the inhibitory effects caused by silencing of linc00467. In conclusion, our data highlighted the oncogenic role of linc00467 in HCC progression by regulating the miR-18a-5p/NEDD9 axis.

LINC00467 enhances head and neck squamous cell carcinoma progression and the epithelial-mesenchymal transition process via miR-299-5p/ubiquitin specific protease-48 axis.

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) has attracted the attention of researchers as a result of its high incidence around the world. This malignancy occurs in the oral cavity, pharynx and larynx in most cases. A number of lncRNAs have been revealed to regulate the malignant neoplasia of several cancers. Nevertheless, the effects of lncRNA LINC00467 in HNSCC have not yet been reported. METHODS: The expression of LINC00467, miR-299-5p and ubiquitin specific protease-48 (USP48) in HNSCC cells was quantified by a quantitative reverse transcriptase-polymerase chain reaction. The influences of LINC00467 deficiency on HNSCC progression were reflected by cell counting kit-8, colony formation, ethynyl-2-deoxyuridine, wound healing and western blot assays. RIP and luciferase reporter assays were conducted to confirm the interaction among LINC00467, miR-299-5p and USP48. RESULTS: LINC00467 was considerably upregulated in HNSCC cells, and an absence of LINC00467 suppressed cell growth, cell migration and the epithelial-mesenchymal process in HNSCC. In addition, miR-299-5p expression was notably downregulated in HNSCC cells, and miR-299-5p could bind with LINC00467. Furthermore, USP48 was conspicuously overexpressed in HNSCC cells and capable of binding with miR-299-5p. LINC00467 could upregulate USP48 expression via sponging miR-299-5p. Finally, rescue assays proved that USP48 overexpression could compensate for the suppressive effects on HNSCC progression mediated by LINC00467 deficiency. CONCLUSIONS: LINC00467 enhances HNSCC progression by serving as a sponge of miR-299-5p to increase USP48 expression.

LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) has been recognized as a member of the most common human malignant tumors globally. According to multiple studies, long noncoding RNAs (lncRNAs) have been defined as vital regulators in tumor progression. Although previous studies have indicated that lncRNA long intergenic non-protein coding RNA 467 (LINC00467) exerts oncogenic effect in tumorigenesis and the development of cancers, the specific function that LINC00467 induces in HCC remains obscure. METHODS: LINC00467 expression was examined by a quantitative reverse transcriptase-polymerase chain reaction. CCK-8, EdU, transwell, western blotting and caspase-3 activity analyses were utilized to testify the role of LINC00467 in HCC. The interaction between IGF2BP3 and LINC00467 (or TRAF5) was investigated by luciferase reporter, RIP and RNA pull-down assays. RESULTS: LINC00467 upregulation in HCC tissues and cells was observed. LINC00467 silencing suppressed cell proliferation and metastasis, whereas it facilitated cell apoptosis in HCC. The gene for tumor necrosis factor receptor-associated factor 5 (TRAF5) was a neighboring gene of that for LINC00467 and its expression was positively modulated by LINC00467 in HCC. TRAF5 knockdown inhibited HCC progression. LINC00467 deficiency could decrease the mRNA stability of TRAF5 in HCC. Insulin-like growth factor-2 messenger RNA-binding protein 3 (IGF2BP3) could bind with LINC00467 and its depletion could lower TRAF5 mRNA stability in HCC. Final rescue assays further indicated that downregulation of IGF2BP3 or TRAF5 acted against LINC00467 upregulation-mediated function on HCC progression. CONCLUSIONS: LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in HCC.

STAT1-induced upregulation of LINC00467 promotes the proliferation migration of lung adenocarcinoma cells by epigenetically silencing DKK1 to activate Wnt/ß-catenin signaling pathway.

Long non-coding RNAs (lncRNAs) have been reported as essential regulators in human cancers, including lung adenocarcinoma (LUAD). In the present study, we found that lncRNA long intergenic non-protein coding RNA 467 (LINC00467) was expressed higher in TCGA LUAD samples and predicted poor prognosis in LUAD patients. High expression of LINC00467 was further detected in LUAD cell lines. Functionally, high expression level of LINC00467 promoted LUAD cell proliferation and migration, indicating that LINC00467 exerted oncogenic functions in LUAD progression. Considering the upregulation of LINC00467 in LUAD, we further detected the activator of LINC00467 promoter. Combining with bioinformatics analysis and mechanism experiments, we determined that LINC00467 was activated by STAT1 in LUAD. Moreover, high expression of LINC00467 was found to be associated with the activation of Wnt/ß-catenin signaling pathway. Rescue assays demonstrated that dickkopf WNT signaling pathway inhibitor 1 (DKK1; an inhibitor of Wnt/ß-catenin signaling pathway) and Wnt/ß-catenin signaling involved in DKK1-mediated LUAD cell proliferation and migration. Furthermore, LINC00467 was located in the nucleus of LUAD cell lines and negatively regulated DKK1 in LUAD cells. Mechanistically, we determined that LINC00467 epigenetically silenced DKK1 by recruiting enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) to DKK1 promoter. Collectively, we determined that STAT1-induced upregulation of LINC00467 promoted LUAD progression by epigenetically silencing DKK1 to activate Wnt/ß-catenin signaling pathway.

LINC00467 mediates the 5-fluorouracil resistance in breast cancer cells.

Breast cancer is a prevalent global disease that requires the development of effective therapeutic approaches. The occurrence of 5-fluorouracil (5-FU) resistance in breast cancer is emerging, which urgently needs new way to overcome the obstacle. In this study, we validated that the expression of LINC00467 is up-regulated in the breast cancer patients and breast cancer cells. In addition, the high expression of LINC00467 is associated with the 5-FU resistance of breast cancer cells. Interestingly, LINC00467 induced the homologous recombination (HR) repair via promoting the expression of NBS1 in 5-FU resistant breast cancer cells. Furthermore, miR-205 was validated as a common target of LINC00467 and NBS1, indicating that LINC00467 may induce NBS1 via the miRNA-mRNA target. Importantly, we identified that XBP1, as a transcription factor, induced the expression of LINC00467, which resulted in the enhanced HR efficiency and 5-FU resistance. Silencing XBP1 sensitized the 5-FU resistant breast cancer cells to the 5-FU treatment, whereas the ectopic expression of LINC00467 abrogated the effect of XBP1 silencing. In conclusion, LINC00467 enhances the 5-FU resistance by inducing NBS1-mediated DNA repair. LINC00467 also mediates the function of XBP1 in 5-FU resistance in breast cancer cells.

lncRNA Biomarkers of Glioblastoma Multiforme.

Long noncoding RNAs (lncRNAs) are RNA molecules of 200 nucleotides or more in length that are not translated into proteins. Their expression is tissue-specific, with the vast majority involved in the regulation of cellular processes and functions. Many human diseases, including cancer, have been shown to be associated with deregulated lncRNAs, rendering them potential therapeutic targets and biomarkers for differential diagnosis. The expression of lncRNAs in the nervous system varies in different cell types, implicated in mechanisms of neurons and glia, with effects on the development and functioning of the brain. Reports have also shown a link between changes in lncRNA molecules and the etiopathogenesis of brain neoplasia, including glioblastoma multiforme (GBM). GBM is an aggressive variant of brain cancer with an unfavourable prognosis and a median survival of 14-16 months. It is considered a brain-specific disease with the highly invasive malignant cells spreading throughout the neural tissue, impeding the complete resection, and leading to post-surgery recurrences, which are the prime cause of mortality. The early diagnosis of GBM could improve the treatment and extend survival, with the lncRNA profiling of biological fluids promising the detection of neoplastic changes at their initial stages and more effective therapeutic interventions. This review presents a systematic overview of GBM-associated deregulation of lncRNAs with a focus on lncRNA fingerprints in patients' blood.

LINC00467 induces melanoma deterioration by targeting miR-485-5p/p21 activated kinase 1.

Background: The purpose of the current research was to investigate the biological roles of LINC00467 in inducing melanoma deterioration. Methods: Differential level of LINC00467 in melanoma tissues and its prognostic value were analyzed in GEPIA, which were further confirmed in clinical samples we collected. Regulatory effects of LINC00467 on proliferation, migration and invasion capacities of A375 and SKMEL1 cell lines were examined by a series of functional experiments. Potential downstream targets of LINC00467 were identified through dual-luciferase reporter assay, and their synergistic role in melanoma process was finally explored by rescue experiments. Results: LINC00467 was up-regulated in melanoma samples, but it did not have a prognostic potential in melanoma. LINC00467 has the capacities to stimulate proliferation, migration and invasion of A375 and SKMEL1 cell lines. The feedback loop LINC00467/miR-485-5p/PAK1 was identified, which was responsible for inducing melanoma deterioration. Conclusions: LINC00467 stimulates proliferation, migration and invasion capacities of melanoma via targeting miR-485-5p to upregulate PAK1, which provides potential targets for treatment of melanoma.

Paired Box 5-Induced LINC00467 Upregulation Promotes the Progression of Laryngeal Squamous Cell Cancer by Triggering the MicroRNA-4735-3p/TNF Alpha-Induced Protein 3 Pathway.

LINC00467 was reported as an oncogenic gene in different types of human cancers. In this study, we investigated the molecular mechanisms of LINC00467 in the tumorigenesis of laryngeal squamous cell cancer (LSCC). RT-qPCR was utilized to detect the mRNA expression of genes, and western blot assay was used to determine the protein levels of TNF alpha-induced protein 3 (TNFAIP3). The cell viability was detected by CCK-8 assay. Transwell assays were conducted to determine the cell migration and invasion of LSCC cells, and the cell cycle was assessed by flow cytometry. The association between paired box 5 (PAX5), LINC00467, miR-4735-3p, and TNFAIP3 was verified using ChIP, RNA pull-down, or luciferase reporter assays. In our study, we found that LINC00467 was upregulated in LSCC, and knockdown of LINC00467 suppressed cell viability and metastasis of LSCC. Besides, LINC00467 transcription could be activated by PAX5 in LSCC. Furthermore, LINC00467 acted as competitive endogenous RNA (ceRNA) for miR-4735-3p to accelerate LSCC progression. In the meantime, TNFAIP3 was identified as a downstream gene of miR-4735-3p. Finally, TNFAIP3 overexpression could overturn the effects of miR-4735-3p mimic on LSCC cellular activities. In conclusion, our results demonstrated that PAX5-induced LINC00467 facilitated LSCC progression by inhibiting miR-4735-3p to increase TNFAIP3 expression.

LINC00467: A key oncogenic long non-coding RNA.

The significance of long non-coding RNAs (lncRNAs) in the development and progression of human cancers has attracted increasing attention in recent years of investigations. Having versatile interactions and diverse functions, lncRNAs can act as oncogenes or tumor-suppressors to actively regulate cell proliferation, survival, stemness, drug resistance, invasion and metastasis. LINC00467, an oncogenic member of long intergenic non-coding RNAs, is upregulated in numerous malignancies and its high expression is often related to poor clinicopathological features. LINC00467 facilitates the progression of cancer via sponging tumor-suppressive microRNAs, inhibiting cell death cascade, modulating cell cycle controllers, and regulating signalling pathways including AKT, STAT3, NF-κB and Wnt/ß-catenin. A growing number of studies have revealed that LINC00467 may serve as a novel prognostic biomarker and its inhibitory targeting has a valuable therapeutic potential to suppress the malignant phenotypes of cancer cells. In the present review, we discuss the importance of LINC00467 and provide a comprehensive collection of its functions and molecular mechanisms in a variety of cancer types.

Long intergenic non-protein-coding RNA 467 promotes tumor progression and angiogenesis via the microRNA-128-3p/vascular endothelial growth factor C axis in colorectal cancer.

Long non-coding RNAs (lncRNAs) are important regulators and biomarkers of tumorigenesis and tumor metastasis. Long intergenic non-protein-coding RNA 467 (LINC00467) is associated with various cancers. However, the role and mechanism of LINC00467 in colorectal cancer (CRC) promotion are poorly understood. This study aimed to present new details of LINC00467 in the progression of CRC. Reverse transcription-polymerase chain reaction demonstrated that the expression level of LINC00467 in CRC tissues and cell lines was significantly upregulated, which was closely related to the clinical features of CRC. Cell and animal studies showed that the downregulation of LINC00467 expression in CRC cells significantly inhibited cell proliferation, metastasis, and angiogenesis. Moreover, the overexpression of LINC00467 accelerated CRC promotion. Bioinformatics analysis and luciferase reporter assay confirmed that LINC00467 binds to miR-128-3p. Rescue experiments manifested that decreased miR-128-3p level reversed CRC cell inhibition by silencing LINC00467. Furthermore, vascular endothelial growth factor C (VEGFC) was identified as a target of miR-128-3p that could reverse the inhibition of cell growth that is mediated by miR-128-3p. Altogether, our results showed that LINC00467 contributes to CRC progression and angiogenesis via the miR-128-3p/VEGFC axis. Our findings expand the understanding of the mechanisms underlying CRC and suggest potential targets for clinical strategies against CRC.

Long Noncoding RNA LINC00467: Role in Various Human Cancers.

Intricate genetic mutations promote the progression of different cancer types. Long noncoding RNAs (lncRNAs) have been widely demonstrated to participate in the genomic activities of various human cancers. Long intergenic non-coding RNA 467 (LINC00467) is an upregulated lncRNA in diverse diseases, especially in several types of cancers. Functional experiments of LINC00467 revealed that LINC00467 overexpression enhanced cell chemoresistance, proliferation, migration, and invasion in several types of cancers. Moreover, overexpressed LINC00467 was associated with a poor clinical prognosis. The present evidence suggests that LINC00467 may serve as a promising prognostic indicator and become a novel cancer therapeutic target. In this review, we introduce the biologic functions of lncRNAs and describe the molecular mechanism and clinical significance of LINC00467 in detail.

Downregulated Reprimo by LINC00467 participates in the growth and metastasis of gastric cancer.

Gastric cancer (GC) as an aggressive malignancy still causes a global health problem. It has been documented that long noncoding RNAs are involved in GC development. Therefore, this research was designed to explore the role of LINC00467 in the growth and metastasis of GC. The expression of LINC00467 and Reprimo in GC tissues and cells was detected. The binding relationship among LINC00467, DNA methyltransferase 1 (DNMT1) and Reprimo was assessed following. Reprimo promoter methylation was detected by methylation sequencing. GC cell lines overexpressing or knock downing LINC00467 were constructed for pinpointing the effect of LINC00467 on cell functions as well as growth and metastasis of GC cells in vivo. LINC00467 was highly expressed, whereas Reprimo was poorly expressed in GC tissues and cells. Mechanically, LINC00467 promoted the methylation and decreased the expression of Reprimo promoter by recruiting DNMT1 in GC cells. Knockdown of LINC00467 diminished the malignant properties of GC cells. Knockdown of LINC00467 reduced tumorigenesis and metastasis of GC cells in vivo. LINC00467 might exert oncogenic effects in GC via Reprimo downregulation by recruiting DNMT1.

LINC00467 facilitates the proliferation, migration and invasion of glioma via promoting the expression of inositol hexakisphosphate kinase 2 by binding to miR-339-3p.

Our previous studies indicate that long noncoding RNA (lncRNA) LINC00467 can act as an oncogene to participate in the malignant progression of glioma, but the underlying molecular mechanism remains to be studied further. This study aimed to explore the biological role of the LINC00467/miR-339-3p/ inositol hexakisphosphate kinase 2 (IP6K2) regulatory axis in glioma. The Cancer Genome Atlas (TCGA), Oncomine databases and reverse transcription­quantitative PCR (RT­qPCR) were used to analyze IP6K2 expression in glioma. RT-PCR, EdU and transwell assays were conducted to observe the effect of IP6K2 on glioma cell proliferation, migration and invasion. Using bioinformatics analysis, RT-PCR, and dual luciferase reporter gene assay, the potential role of the LINC00467/miR-339-3p/IP6K2 regulatory axis in glioma was verified. The results showed that IP6K2 was up-regulated in glioma tissues and cell lines. Moreover, the expression level of IP6K2 was correlated with the clinical features of glioma patients. In vitro and in vivo experiments indicated that IP6K2 overexpression could promote the proliferation, migration, and invasion of glioma cells. Further bioinformatics analysis and in vitro assays revealed that LINC00467 could promote IP6K2 expression by binding to miR-339-3p and promote the malignant progression of glioma. Overall, LINC00467 could upregulate IP6K2 by binding to miR-339-3p and promote the proliferation, migration, and invasion of glioma cells. The LINC00467/miR-339-3p/IP6K2 regulatory axis might be a potential therapeutic target for glioma.

Circulating plasma exosomal long non-coding RNAs LINC00265, LINC00467, UCA1, and SNHG1 as biomarkers for diagnosis and treatment monitoring of acute myeloid leukemia.

Exosomal long non-coding RNAs (lncRNAs) have emerged as a cell-free biomarker for clinical evaluation of cancers. However, the potential clinical applications of exosomal lncRNAs in acute myeloid leukemia (AML) remain unclear. Herein, we attempted to identify plasma exosomal lncRNAs as prospective biomarkers for AML. In this study, plasma exosomes were first successfully extracted from AML patients and healthy donors (HD). Subsequently, the downregulated plasma exosomal lncRNAs (LINC00265, LINC00467, and UCA1) and the upregulated plasma exosomal lncRNA (SNHG1) were identified in AML patients (n=65) compared to HD (n=20). Notably, individual exosomal LINC00265, LINC00467, UCA1, or SNHG1 had a capability for discriminating AML patients from HD, and their combination displayed better efficiency. Furthermore, exosomal LINC00265 and LINC00467 were increased expressed in patients achieving complete remission after chemotherapy. Importantly, there was upregulation of exosomal LINC00265 and downregulation of exosomal SNHG1 upon allogeneic hematopoietic stem cell transplantation. Additionally, these lncRNAs were high stability in plasma exosomes. Exosomal LINC00265, LINC00467, UCA1, and SNHG1 may act as promising cell-free biomarkers for AML diagnosis and treatment monitoring and provide a new frontier of liquid biopsy for this type of cancer.

LINC00467 Promotes Tumor Progression via Regulation of the NF-kb Signal Axis in Bladder Cancer.

PURPOSE: Long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of bladder cancer, but the underlying molecular mechanisms remain largely unknown. In this study, we found that LINC00467 was significantly highly expressed in bladder cancer through bioinformatic analysis. The present study aimed to explore the role of LINC00467 in bladder cancer and its possible underlying molecular mechanisms. METHODS: The expression of LINC00467 was obtained from GEO (GSE31189), the TCGA database, and qRT-PCR. The role of LINC00467 in bladder cancer was assessed both in vitro and in vivo. RIP, RNA pulldown, and CO-IP were used to demonstrate the potential mechanism by which LINC00467 regulates the progression of bladder cancer. RESULTS: Through the analysis of GEO (GSE133624) and the TCGA database, it was found that LINC00467 was highly expressed in bladder cancer tissues and that the expression of LINC00467 was significantly negatively correlated with patient prognosis. Cell and animal experiments suggest that LINC00467 promotes the proliferation and invasion of bladder cancer cells. On the one hand, LINC00467 can directly bind to NF-kb-p65 mRNA to stabilize its expression. On the other hand, LINC00467 can directly bind to NF-kb-p65 to promote its translocation into the nucleus to activate the NF-κB signaling pathway, which promotes the progression of bladder cancer. CONCLUSIONS: LINC00467 is highly expressed in bladder cancer and can promote the progression of bladder cancer by regulating the NF-κB signaling pathway. Therefore, targeting LINC00467 is very likely to provide a new strategy for the treatment of bladder cancer and for improving patient prognosis.