scholarly journals Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Dahai Liu ◽  
Jianfeng Wang ◽  
Meihan Liu
Keyword(s):  
Multiple Myeloma ◽  
Cell Lines ◽  
Histone Deacetylases ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
Real Time Quantitative Pcr ◽  
Rna Immunoprecipitation

Abstract Background: Long non-coding RNA taurine up-regulated gene 1 (TUG1) was reportedly involved in initiation and development of several cancers. However, its function and molecular mechanisms in multiple myeloma (MM) are still unclear. The present study aimed to determine the expression status, biological function, and potential mechanisms of TUG1 in the progression of MM. Materials and methods: The expression levels of TUG1 were examined in MM samples and cell lines by real-time quantitative PCR. The effects of TUG1 on MM cells proliferation and apoptosis were assessed using Cell Counting Kit-8 assay and flow cytometry respectively. MiRNAs-targeted sites in TUG1 were screened by Starbase2.0 and were identified by RNA immunoprecipitation assay combined with luciferase reporter assay. Results: The expression levels of TUG1 were markedly increased in MM samples and cell lines. Knockdown of TUG1 significantly suppressed the proliferation, induced cell cycle arrest at G1/G0 phase, and promoted apoptosis of MM cells. In exploring the regulatory mechanism, miR-29b-3p was confirmed to be a direct target of TUG1, and repression of miR-29b-3p could partially rescue the effect TUG1 knockdown on MM cell proliferation, cycle, and apoptosis. In addition, TUG1 positively modulated histone deacetylases 4 (HDAC4, a target of miR-29b-3p) expression through sponging of miR-29b-3p in MM cells. Conclusion: These findings suggested that TUG1 exerted an oncogenic role in MM by acting as a competing endogenous RNA of miR-29b-3p, and implied the potential application of TUG1 in treatment for MM.

scholarly journals LncRNA DANCR functions as a competing endogenous RNA to regulate RAB1A expression by sponging miR-634 in glioma

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Dawei Xu ◽  
Jian Yu ◽  
Guojun Gao ◽  
Guangjian Lu ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Cell Lines ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Glioma Cells ◽  
Tumor Grade ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Biological Functions ◽  
Advanced Tumor ◽  
Rna Immunoprecipitation

Long noncoding RNA (lncRNA) differentiation antagonizing nonprotein coding RNA (DANCR) plays important regulatory roles in many solid tumors. However, the effect of DANCR in glioma progression and underlying molecular mechanisms were not entirely explored. In the present study, we determined the expression of DANCR in glioma tissues and cell lines using qRT-PCR and further defined the biological functions. Furthermore, we used luciferase reporter assay, Western blot, and RNA immunoprecipitation (RIP) to explore the underlying mechanism. Our results showed that DANCR was significantly up-regulated in glioma tissues and cell lines (U251, U118, LN229, and U87MG). High DANCR expression was correlated with advanced tumor grade. Inhibition of DANCR suppressed the glioma cells proliferation and induced cells arrested in the G0/G1 phase. In addition, we verified that DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression. The present study demonstrated that DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma, and DANCR might potentially serve as a therapeutic target for the treatment of glioma patients.

scholarly journals LncRNA SNHG15 contributes to doxorubicin resistance of osteosarcoma cells through targeting the miR-381-3p/GFRA1 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 871-883
Author(s):  
Jinshan Zhang ◽  
Dan Rao ◽  
Haibo Ma ◽  
Defeng Kong ◽  
Xiaoming Xu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Inhibitory Effect ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells

AbstractBackgroundOsteosarcoma is a common primary malignant bone cancer. Long noncoding RNA small nucleolar RNA host gene 15 (SNHG15) has been reported to play an oncogenic role in many cancers. Nevertheless, the role of SNHG15 in the doxorubicin (DXR) resistance of osteosarcoma cells has not been fully addressed.MethodsCell Counting Kit-8 assay was conducted to measure the half-maximal inhibitory concentration value of DXR in osteosarcoma cells. Western blotting was carried out to examine the levels of autophagy-related proteins and GDNF family receptor alpha-1 (GFRA1). Quantitative reverse transcription-polymerase chain reaction was performed to determine the levels of SNHG15, miR-381-3p, and GFRA1. The proliferation of osteosarcoma cells was measured by MTT assay. The binding sites between miR-381-3p and SNHG15 or GFRA1 were predicted by Starbase bioinformatics software, and the interaction was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to validate the function of SNHG15 in vivo.ResultsAutophagy inhibitor 3-methyladenine sensitized DXR-resistant osteosarcoma cell lines to DXR. SNHG15 was upregulated in DXR-resistant osteosarcoma tissues and cell lines. SNHG15 knockdown inhibited the proliferation, DXR resistance, and autophagy of osteosarcoma cells. MiR-381-3p was a direct target of SNHG15, and GFRA1 bound to miR-381-3p in osteosarcoma cells. SNHG15 contributed to DXR resistance through the miR-381-3p/GFRA1 axis in vitro. SNHG15 depletion contributed to the inhibitory effect of DXR on osteosarcoma tumor growth through the miR-381-3p/GFRA1 axis in vivo.ConclusionsSNHG15 enhanced the DXR resistance of osteosarcoma cells through elevating the autophagy via targeting the miR-381-3p/GFRA1 axis. Restoration of miR-381-3p expression might be an underlying therapeutic strategy to overcome the DXR resistance of osteosarcoma.

Long Noncoding RNA TTC39A-AS1 Promotes Breast Cancer Tumorigenicity by Sponging MicroRNA-483-3p and Thereby Upregulating MTA2

Pharmacology ◽  
2021 ◽  
pp. 1-15
Author(s):  
Zhaohui Zhou ◽  
Ping Yang ◽  
Binming Zhang ◽  
Maohui Yao ◽  
Yali Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Noncoding Rna ◽  
Flow Cytometric Analysis ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rna Immunoprecipitation ◽  
Anticancer Treatment ◽  
High Level

<b><i>Introduction:</i></b> In recent years, the regulatory activities of long noncoding RNAs have received increasing attention as an important research focus. This study aimed to characterize the expression and detailed roles of TTC39A antisense RNA 1 (TTC39A-AS1) in breast cancer (BC), in addition to concentrating on its downstream mechanisms. <b><i>Methods:</i></b> Quantitative RT-PCR was performed to determine the expression levels of TTC39A-AS1, microRNA-483-3p (miR-483-3p), and metastasis-associated gene 2 (MTA2). Further, the detailed functions of TTC39A-AS1 in BC cells were confirmed using the Cell Counting Kit 8 assay, flow cytometric analysis, and Transwell cell migration and invasion assays. The targeting relationship between TTC39A-AS1, miR-483-3p, and MTA2 in BC was predicted via bioinformatics analysis and further confirmed by performing the luciferase reporter assay and RNA immunoprecipitation. <b><i>Results:</i></b> TTC39A-AS1 was present in high levels in BC; this result was confirmed in our sample cohort and The Cancer Genome Atlas database. Patients with BC with a high level of TTC39A-AS1 had a shorter overall survival than those with a low level of TTC39A-AS1. Functionally, the absence of TTC39A-AS1 accelerated cell apo­ptosis but retained cell proliferation, migration, and invasion. Mechanistically, TTC39A-AS1 functioned as a competing endogenous RNA in BC by sponging miR-483-3p and thereby indirectly increasing MTA2 expression. Finally, rescue experiments revealed that the tumor-inhibiting actions of TTC39A-AS1 knockdown on the malignant characteristics of BC cells could be reversed by inhibiting miR-483-3p or upregulating MTA2. <b><i>Conclusion:</i></b> The newly identified TTC39A-AS1/miR-483-3p/MTA2 pathway was revealed to be a critical regulator in the tumorigenicity of BC, possibly offering a novel therapeutic direction for the anticancer treatment of BC.

scholarly journals Inhibition of apoptosis may lead to the development of bortezomib resistance in multiple myeloma cancer cells

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Emine Öksüzoğlu ◽  
Gül Kozalak
Keyword(s):  
Multiple Myeloma ◽  
Drug Resistance ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Plasma Cells ◽  
Expression Levels ◽  
Diphenyltetrazolium Bromide ◽  
Apoptotic Pathways ◽  
Resistant Cells

AbstractBackgroundMultiple myeloma (MM), a malignancy of plasma cells, is the second most prevalent hematological cancer. Bortezomib is the most effective chemotherapeutic drug used in treatment. However, drug-resistance prevents success of chemotherapy. One of the factors causing drug-resistance is dysfunction of apoptotic-pathways. This study aimed to evaluate the relationship between expression levels of Bcl-2, Bax, caspase-3 and p-53 genes involved in apoptosis and the development of bortezomib-resistance in MM cell lines.Materials and methodsMultiple myeloma KMS20 (bortezomib-resistant) and KMS28 (bortezomib-sensitive) cell lines were used. 3-[4,5-Dimethylthiazol-2-yl] 1-2,5-diphenyltetrazolium bromide (MTT) assay was performed to determine IC50 values of bortezomib. RNAs were isolated from bortezomib-treated cell lines, followed by cDNA synthesis. Expression levels of the genes were analyzed by using q-Realtime-PCR.ResultsAs a result, Bcl-2/Bax ratio was higher in KMS20 (resistant) cells than in KMS28 (sensitive) cells. Expression of caspase-3 decreased in KMS20-cells, whereas increased in KMS28-cells. The results indicate that apoptosis was suppressed in resistant cells.ConclusionThese findings will enable us to understand the molecular mechanisms leading to drug-resistance in MM cells and to develop new methods to prevent the resistance. Consequently, preventing the development of bortezomib resistance by eliminating the factors which suppress apoptosis may be a new hope for MM treatment.

scholarly journals Ginsenoside Rg3 alleviates septic liver injury by regulating the lncRNA TUG1/miR-200c-3p/SIRT1 axis

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Pan Wu ◽  
Xiao Yu ◽  
Yue Peng ◽  
Qian-Lu Wang ◽  
Long-Tian Deng ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mitochondrial Dysfunction ◽  
Noncoding Rna ◽  
Protective Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Ampk Pathway ◽  
Rna Immunoprecipitation ◽  
Hepatocyte Damage ◽  
Amp Activated Protein Kinase

Abstract Background Studies have shown that ginsenoside R3 (Rg3) plays a protective role in sepsis-induced organ injuries and mitochondrial dysfunction. Long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) is regarded as a regulator in sepsis. However, the association between TUG1 and Rg3 remains elusive. Methods A sepsis mouse model was established by caecal ligation and puncture (CLP), and liver injury was induced by haematoxylin-eosin (H&E) staining. Lipopolysaccharide (LPS) was used to induce hepatocyte damage. The expression levels of TUG1, microRNA (miR)-200a-3p, and silencing information regulator 1 (SIRT1) were examined by quantitative real-time polymerase chain reaction (qRT–PCR) assays. Cell viability was monitored using the Cell Counting Kit-8 (CCK-8) assay. MitoSOX Red staining and CBIC2 (JC-1) dye were employed to detect mitochondrial reactive oxygen species (ROS) and mitochondrial transmembrane potential (MTP) levels, respectively. The interaction between miR-200a-3p and TUG1 or SIRT1 was confirmed via dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. Results Rg3 upregulated TUG1 expression in liver tissues of CLP mice and LPS-induced hepatocytes. Rg3 could activate autophagy to improve mitochondrial dysfunction in LPS-treated hepatocytes, which was partially reversed by TUG1 depletion or miR-200a-3p overexpression. Importantly, TUG1 targeted miR-200a-3p to activate the SIRT1/AMP-activated protein kinase (AMPK) pathway in LPS-treated hepatocytes. Moreover, gain of TUG1 ameliorated mitochondrial dysfunction in LPS-treated hepatocytes by sequestering miR-200a-3p. Conclusion Our study revealed that Rg3 increased TUG1 expression and reduced miR-200a-3p expression to stimulate the SIRT1/AMPK pathway, thereby enhancing autophagy to improve sepsis-induced liver injury and mitochondrial dysfunction.

scholarly journals Mutant NPM1-regulated lncRNA HOTAIRM1 promotes leukemia cell autophagy and proliferation by targeting EGR1 and ULK3

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Yipei Jing ◽  
Xueke Jiang ◽  
Li Lei ◽  
Meixi Peng ◽  
Jun Ren ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Animal Studies ◽  
Leukemia Cell ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Promising Therapeutic Target ◽  
Rna Immunoprecipitation ◽  
Incorporation Assay

Abstract Background Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1), which displays a distinct long noncoding RNA (lncRNA) expression profile, has been defined as a unique subgroup in the new classification of myeloid neoplasms. However, the biological roles of key lncRNAs in the development of NPM1-mutated AML are currently unclear. Here, we aimed to investigate the functional and mechanistic roles of the lncRNA HOTAIRM1 in NPM1-mutated AML. Methods The expression of HOTAIRM1 was analyzed with a public database and further determined by qRT-PCR in NPM1-mutated AML samples and cell lines. The cause of upregulated HOTAIRM1 expression was investigated by luciferase reporter, chromatin immunoprecipitation and ubiquitination assays. The functional role of HOTAIRM1 in autophagy and proliferation was evaluated using western blot analysis, immunofluorescence staining, a Cell Counting Kit-8 (CCK-8) assay, a 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay, flow cytometric analyses and animal studies. The action mechanism of HOTAIRM1 was explored through RNA fluorescence in situ hybridization, RNA pulldown and RNA immunoprecipitation assays. Results HOTAIRM1 was highly expressed in NPM1-mutated AML. High HOTAIRM1 expression was induced in part by mutant NPM1 via KLF5-dependent transcriptional regulation. Importantly, HOTAIRM1 promoted autophagy and proliferation both in vitro and in vivo. Mechanistic investigations demonstrated that nuclear HOTAIRM1 promoted EGR1 degradation by serving as a scaffold to facilitate MDM2-EGR1 complex formation, while cytoplasmic HOTAIRM1 acted as a sponge for miR-152-3p to increase ULK3 expression. Conclusions Taken together, our findings identify two oncogenic regulatory axes in NPM1-mutated AML centered on HOTAIRM1: one involving EGR1 and MDM2 in the nucleus and the other involving the miR-152-3p/ULK3 axis in the cytoplasm. Our study indicates that HOTAIRM1 may be a promising therapeutic target for this distinct leukemia subtype.

scholarly journals The Effect of lncRNA SNHG3 Overexpression on Lung Adenocarcinoma by Regulating the Expression of miR-890

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Baojie Kang ◽  
Caihong Qiu ◽  
Ying Zhang
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Bioinformatics Analysis ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Reverse Transcription Quantitative Pcr ◽  
Dual Luciferase Reporter Assay

The lncRNA small nucleolar host gene 3 (SNHG3) was discovered to play an important role in the occurrence and development of lung adenocarcinoma (LUAD). However, the underlying molecular mechanism of SNHG3 in LUAD remains unclear. In the present study, SNHG3 expression levels in LUAD tissues and cell lines were analyzed using reverse transcription-quantitative PCR. The effects of SNHG3 on the proliferation, apoptosis, migration, and invasion of LUAD cells were determined using Cell Counting Kit-8, colony formation, flow cytometry, wound healing, and Transwell chamber assays, respectively. The specific underlying mechanism of SNHG3 in LUAD was investigated using bioinformatics analysis and a dual luciferase reporter assay. The results revealed that SNHG3 expression levels were downregulated in LUAD tissues and cell lines. Functionally, SNHG3 overexpression suppressed the proliferation, migration, and invasion of LUAD cells, while promoting apoptosis. Mechanistically, microRNA- (miR-) 890 was identified as a potential target of SNHG3, and its expression was negatively regulated by SNHG3. Notably, SNHG3 was found to promote LUAD progression by targeting miR-890. In conclusion, the findings of the present study revealed that lncRNA SNHG3 promoted the occurrence and progression of LUAD by regulating miR-890 expression.

scholarly journals SNHG9 Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

2021 ◽  
Author(s):  
Ramesh Bhandari ◽  
Sun Gui Feng ◽  
Liu Ya ◽  
Bian Zhixuan ◽  
Pan Quihui ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Pearson Correlation ◽  
Direct Interaction ◽  
Luciferase Reporter ◽  
Kaplan Meier ◽  
Rna Immunoprecipitation ◽  
Cellular Apoptosis

Abstract Background: Hepatoblastoma is common hepatic tumors occurring children between 0 – 5 years. Accumulating studies has shown lncRNA potential role in distinct cancers progression and development including the hepatoblastoma. SnoRNA host gene 9 (SNHG9) is associated the progression of distinct human cancers but, it`s specific molecular mechanisms in hepatoblastoma not unknown. Methods:In this study, we estimated SNHG9 expression on hepatoblastoma tissue and cell lines by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Next, we downregulated and upregulated the SNHG9 expression in hepatoblastoma cell lines and then determined the cell proliferation (CCK-8), colony formation, cellular apoptosis activity. The dual luciferase reporter activity, RNA immunoprecipitation (RIP), biotin RNA pulls down and Spemann’s Pearson correlation coefficient assay were performed to establish the interaction between the SNHG9, WNt3a and miR-23a-5p. Xenograft in-vivo tumorgenicity test was performed to elucidate therole of SNHG9 hepatoblastoma in tumorigenesis. SNHG9 role in Cisplatin drugs resistance in hepatoblastoma was also determined. Results:SNHG9 was significantly upregulated in hepatoblastoma tissue and cell lines. SNHG9 overexpression on HUH6 & HepG2 resulted in a significant increase in cell proliferation and clonogeneic while SNHG9 knock down resulted in a sustained inhibition of cell proliferation and clonogenic activity. Dual luciferase activity, RNA immunoprecipitation and biotin pull down confirmed the direct interaction of miR-23a-5p with SNHG9. In Xenograft tumorgenicity test showed SNHG9 downregulation significantly reduced the tumor growth on mice. ROC and Kaplan-Meier analysis showed potential prognostic and diagnostic importance of SNHG9 in hepatoblastoma.Conclusion: We concluded that SNHG9/miR-23a-5p/Wnt3a axis promotes the progression hepatoblastoma tumor.

scholarly journals circAkap17b acts as a miR-7 family molecular sponge to regulate FSH secretion in rat pituitary cells

2020 ◽  
Vol 65 (4) ◽  
pp. 135-148
Author(s):  
Chang-Jiang Wang ◽  
Fei Gao ◽  
Yi-Jie Huang ◽  
Dong-Xu Han ◽  
Yi Zheng ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rna Immunoprecipitation ◽  
Rat Pituitary Cells

The pituitary gland functions as a prominent regulator of diverse physiologic processes by secreting multiple hormones. Circular RNAs (circRNAs) are an emerging novel type of endogenous noncoding RNA that have recently been recognized as powerful regulators participating in various biological processes. However, the physiological roles and molecular mechanisms of circRNAs in pituitary remain largely unclear. Herein, we concentrated on expounding the biological function and molecular mechanism of circRNA in rat pituitary. In this study, we identified a novel circRNA in pituitary tissue, circAkap17b, which was pituitary- and stage-specific. Then, we designed circAkap17b siRNA and constructed an overexpression plasmid to evaluate the effect of loss- and gain-of-circAkap17b function on FSH secretion. Interestingly, silencing circAkakp17b significantly inhibited FSH expression and secretion, while overexpression of circAkap17b enhanced FSH expression and secretion. Furthermore, dual luciferase reporter and RNA immunoprecipitation (RIP) assays confirmed that circAkap17b could serve as miR-7 sponge to regulate target genes. Additionally, miR-7b suppressed FSH expression and secretion by directly targeting Fshb through the dual luciferase reporter and RT-qPCR analysis. Additionally, rescue experiments showed that circAkap17b could regulate FSH secretion in pituitary cells through a circAkap17b-miR-7-Fshb axis. Collectively, we demonstrated that circAkap17b could act as a molecular sponge of miR-7 to upregulate expression of the target gene Fshb and facilitate FSH secretion. These findings provide evidence for a novel regulatory role of circRNAs in pituitary.

scholarly journals Mechanism and Role of the Neuropeptide LGI1 Receptor ADAM23 in Regulating Biomarkers of Ferroptosis and Progression of Esophageal Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Chen Chen ◽  
Jun Zhao ◽  
Jing-ni Liu ◽  
Chenyu Sun
Keyword(s):  
Esophageal Cancer ◽  
Cell Lines ◽  
Noncoding Rna ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cerna Network ◽  
And Migration ◽  
Proliferation And Migration

Background. According to recent studies, ferroptosis is closely related to the efficacy and prognosis of tumour treatment. However, the role of ferroptosis in esophageal squamous cell carcinoma (ESCC) has not been explored comprehensively. Materials and Methods. The esophageal cancer (EC) transcriptome data was downloaded from The Cancer Genome Atlas (TCGA), then analyzed, to obtain the differentially expressed messenger RNA (mRNA), microRNA (miRNA), and long noncoding RNA (lncRNA) between groups with the low and high Ferroptosis Potential Index (FPI) and construct a ferroptosis-associated ceRNA network. In addition, the expression of ARHGEF26-AS1 and miR-372-3p in ESCC cell lines was assessed, and the appropriate cell lines were selected. The interaction between ARHGEF26-AS1, miR-372-3p, and ADAM23 was also determined through a dual-luciferase reporter assay. Moreover, the Western blot, Cell Counting Kit-8 (CCK-8), wound healing, cell viability, and cell death assays were conducted to establish the biological functions of the ARHGEF26-AS1/miR-372-3p/ADAM23 pathway in ESCCs. Results. An FPI scoring model reflecting the activity of the ferroptosis pathway was constructed, and a ferroptosis-associated ceRNA network was established. The findings revealed that low expression of ADAM23 and ARHGEF26-AS1 as well as high expression of miR-372-3p was associated with poor prognosis and a lower FPI score in EC patients. Functionally, overexpression of ADAM23 and ARHGEF26-AS1 and the miR-372-3p inhibitor not only promoted ferroptosis in ESCC cells in vitro but also inhibited the proliferation and migration of cells. Mechanistically, ARHGEF26-AS1 upregulated the expression of ADAM23 by competitively binding to miR-372-3p. Conclusions. The study showed that the lncRNA, ARHGEF26-AS1 acts as a miR-372-3p sponge that regulates the neuropeptide LGI1 receptor ADAM23 expression. This in turn not only inhibits the proliferation and migration of ESCC cells but also upregulates the ferroptosis pathway. A neuropeptide-related ferroptosis regulatory pathway was identified in this study.

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