Effect Of Long Non-coding RNA Research Articles

LncRNA FR215775 Regulates Th2 Differentiation in Murine Allergic Rhinitis.

To identify the effect of long noncoding RNA (lncRNA) FR215775 in regulating CD4+ T cells on murine models of allergic rhinitis (AR), the expression of lncRNA FR215775 in primary Th2 cells was detected through qRT-PCR. After knocking down the expression of lncRNA FR215775 via Sh-FR215775-Ads, Cell Counting Kit-8, cytometric bead array, and fluorescence-activated cell sorting were performed to determine its functions in vitro. Moreover, lncRNA FR215775-silencing or nonsilencing cells were injected intravenously into AR mice. Then, hematoxylin and eosin, Alcian blue-periodic acid Schiff, and toluidine blue staining were performed, and the levels of IL-2, IL-4, IL-5, IL-6, IL-10, IL-17A, IFN-γ, and TNF in the AR mice were also determined. We found that the expression of lncRNA FR215775 was specifically higher in the murine primary Th2 cells. After the knockdown of lncRNA FR215775, the proliferation of CD4+ T cells was inhibited, and the expressions of IL-4 and IL-5 in the cell culture supernatant were significantly decreased (P < 0.001), along with the percentage of Th2 cells (P < 0.05). The lncRNA FR215775-silencing AR group showed less serious allergic symptoms and a low level of ovalbumin-specific immunoglobulin E (P < 0.01). Meanwhile, the eosinophilia inflammation, goblet cell hyperplasia, and mast cell inflammation in the nasal mucosa all decreased, which indicated attenuated allergic inflammation in the lncRNA FR215775-silencing AR group. In addition, the Th2-related cytokines IL-4 and IL-5 were downregulated in the serum and nasal lavage fluid of this group (P < 0.01). In conclusion, lncRNA FR215775 may play a vital role in the function and differentiation of Th2 cells, which may encourage allergic inflammation. These results may provide significant insights into AR pathogenesis and offer new treatment targets for alleviating AR.

Study the relationship between long non-coding RNA (CCAT1) expression and CDK4 expression levels in Egyptian patients with preeclampsia

BackgroundMaternal and perinatal mortality is caused by a variety of factors, including preeclampsia. PE's onset and progression may be influenced by lncRNAs. The effect of long non-coding RNA (lncRNA) Colon cancer-associated transcription factor 1 (CCAT1) expression in the placenta of preeclampsia patients on preeclampsia progression was the focus of this investigation. ObjectivesThe aim of the current study is to check if the levels of expression of Colon cancer-associated transcription factor 1 (CCAT1) and Cyclin-dependent protein kinase 4 (CDK4) are associated with preeclampsia vulnerability and biogenesis. Subjectsand methods: This work included the participation of 160 people. Eighty of the patients had preeclampsia. The control group included 80 normal pregnant women. The two groups were almost of the same age. A thorough clinical examination was performed in all groups (including taking a detailed history, concentrating on parity, age and previous background of diabetes or hypertension). The expression levels of CCAT1 and CDK4 in placental tissue were determined using a real-time q PCR technique. ResultsExpression levels of CCAT1 and CDK4 differed significantly between the study groups. preeclamptic patients having the highest level of CCAT1in comparison with control group, However, preeclamptic patients having lower level of CDK4 than controls. There was a strong negative association between CDK4 expression level and DBP, SBP, creatinine, urea and CCAT1 level of expression in the preeclamptic group, whereas there was a positive correlation between CCAT1 level of expression and DBP, SBP, urea and creatinine in patients group. ConclusionBased on the findings of this study, it is possible that CCAT1 and CDK4 expression levels could be used to aid in the diagnosis and biogenesis of preeclampsia.

Long non-coding RNA Gm37494 alleviates osteoarthritis chondrocyte injury via the microRNA-181a-5p/GABRA1 axis

ObjectiveThis study was conducted to investigate the effect of long non-coding RNA (lncRNA) Gm37494 on osteoarthritis (OA) and its related molecular mechanism.MethodsThe cartilage tissues were obtained from OA patients, and an OA mouse model was induced by the destabilization of the medial meniscus, followed by measurement of Gm37494, microRNA (miR)-181a-5p, GABRA1 mRNA, and the encoded GABAARα1 protein expression. Thereafter, a cellular model was induced by interleukin-1β (IL-1β) treatment in chondrocytes, followed by ectopic and silencing experiments. Chondrocyte proliferation was detected by CCK-8 and EdU assays, chondrocyte apoptosis by flow cytometry and western blot, and the levels of inflammatory factors by ELISA. The binding of Gm37494 to miR-181a-5p was evaluated by dual-luciferase reporter gene and RIP assays, and that of GABRA1 to miR-181a-5p by dual-luciferase reporter gene and RNA pull-down assays.ResultsOA patients and mice had decreased GABRA1 mRNA and GABAARα1 protein levels and elevated miR-181a-5p expression in cartilage tissues. Additionally, Gm37494 was poorly expressed in OA mice. Mechanistically, Gm37494 directly bound to and inversely modulated miR-181a-5p that negatively targeted GABRA1. In IL-1β-induced chondrocytes, Gm37494 overexpression enhanced cell proliferation and suppressed cell apoptosis and inflammation, whereas further miR-181a-5p up-regulation or GABRA1 silencing abolished these trends.ConclusionsConclusively, Gm37494 elevated GABRA1 expression by binding to miR-181a-5p, thus ameliorating OA-induced chondrocyte damage.

Effect and Mechanism of lncRNA CERS6-AS1 on the Biological Behavior of Prostate Cancer Cell.

Objective To investigate the effect of long noncoding RNA (lncRNA) CERS6 antisense RNA1 (CERS6-AS1) on the biological behavior of prostate cancer cells DU145 and its mechanism. Methods RT-PCR was used to detect the relative level of CERS6-AS1 and miR-16-5p in prostate cancer tissues, adjacent tissues, prostate cancer cells DU145, and human normal prostate epithelial cells RWPE-1. DU145 cells were divided into control group, si-CERS6-AS1 group, si-NC group, miR-16-5p mimic group, miR-NC group, and si-CERS6-AS1+miR-16-5p inhibitor group. And CCK-8 method and colony formation test was applied to detect cell proliferation ability, flow cytometry was selected to calculate cell apoptosis, and scratch healing test was employed to assess cell migration ability. Western blot was determined to detect high mobility protein A2 (HMGA2) expression. RT-PCR and dual-luciferase reporter experiments were used to analyze the targeting relationship among CERS6-AS1, miR-16-5p, and HMGA2. Results Compared with the adjacent tissues, the relative level of CERS6-AS1 in prostate cancer tissue was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05). Compared with RWPE-1 cells, the relative level of CERS6-AS1 in DU145 cells was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05). Compared with the control group and the si-NC group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1 group and the miR-16-5p mimic group were reduced (P < 0.05), and the relative level of miR-16-5p and the proliferation inhibition rate and apoptosis were increased (P < 0.05). miR-16-5p is specifically bound to CERS6-AS1 and HMGA2, respectively. Compared with the si-CERS6-AS1 group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1+miR-16-5p inhibitor group were increased (P < 0.05), and the cell proliferation inhibition rate and apoptosis rate were reduced (P < 0.05). Conclusion Silencing CERS6-AS1 can inhibit the proliferation and migration of prostate cancer cell DU145 and induce cell apoptosis, the mechanism is related to the regulation of the miR-16-5p/HMGA2 axis.

Study on the Role and Mechanism of LncRNA ZFasL in Renal Carcinoma.

Background Renal carcinoma is the 7th most common cancer in the world, with the 7th and 6th highest incidence and mortality rates worldwide. Although great progress has been made in the diagnosis and treatment of renal carcinoma, its prognosis is still unsatisfactory. It is important to study the molecular mechanisms of renal carcinoma occurrence and development and to find potential therapeutic targets. Objective The main objective is to investigate the effects of long noncoding RNA (lncRNA) ZFAS1 (lncZFAS1) on the proliferation, apoptosis, and migration of renal carcinoma cells and to preliminarily explore its mechanism. Methods A qRT-PCR method was used to detect the expression of lncZFAS1 in renal carcinoma tissues and renal carcinoma cells. After shRNA interference with lncZFAS1 expression, the effects of lncZFAS1 on cell proliferation, apoptosis, migration, and invasion were detected by CCK-8 method, flow cytometry, scratch test, and Transwell assay. The effect of the knockdown of lncZFAS1 on the growth of transplanted tumors was examined. The expression of lncZFAS1 in renal carcinoma tissues and renal carcinoma cells was significantly higher than that in paracancerous tissues and normal esophageal epithelial cells. Knockdown of lncZFAS1 significantly inhibited the proliferation, migration, and invasive ability of renal carcinoma cells; upregulated miR-150-5P expression and downregulated HMGA2 expression in renal carcinoma cells; and significantly inhibited the growth of transplanted tumors in nude mice. Conclusion Upregulation of miR-150-5P expression was detected after knockdown of lncZFAS1 in renal carcinoma cells, while both mRNA and protein expression levels of HMGA2 were decreased. lncZFAS1 can promote the proliferation and migration of renal carcinoma cells, and the mechanism may be related to the regulation of the miR-150-5P/HMGA2 molecular axis.

Research Progress on the Inflammatory Effects of Long Non-coding RNA in Traumatic Brain Injury.

Globally, traumatic brain injury (TBI) is an acute clinical event and an important cause of death and long-term disability. However, the underlying mechanism of the pathophysiological has not been fully elucidated and the lack of effective treatment a huge burden to individuals, families, and society. Several studies have shown that long non-coding RNAs (lncRNAs) might play a crucial role in TBI; they are abundant in the central nervous system (CNS) and participate in a variety of pathophysiological processes, including oxidative stress, inflammation, apoptosis, blood-brain barrier protection, angiogenesis, and neurogenesis. Some lncRNAs modulate multiple therapeutic targets after TBI, including inflammation, thus, these lncRNAs have tremendous therapeutic potential for TBI, as they are promising biomarkers for TBI diagnosis, treatment, and prognosis prediction. This review discusses the differential expression of different lncRNAs in brain tissue during TBI, which is likely related to the physiological and pathological processes involved in TBI. These findings may provide new targets for further scientific research on the molecular mechanisms of TBI and potential therapeutic interventions.

Knockdown of lncRNA LINC00662 suppresses malignant behaviour of osteosarcoma cells via competition with miR-30b-3p to regulate ELK1 expression

PurposeOsteosarcoma is a type of bone malignancy that mainly occurred in teenagers. This investigation is aimed to clarify the effect of long non-coding RNA (lncRNA) LINC00662 on the proliferation, migration, and invasion in osteosarcoma and explore the underlying action mechanisms.MethodsThe mRNA expression of LINC00662 was determined by real-time quantitative polymerase chain reaction. Cell proliferation, migration, and invasion were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, and transwell assays, respectively. A dual-luciferase reporter assay was used to validate the target relationships Between microRNA (miR)-30b-3p and LINC00662/ ETS domain-containing protein 1 (ELK1). Western blotting was performed to determine the protein expression of ELK1. Xenograft model was established to evaluate the effects of LINC00662 silencing on tumor growth in vivo.ResultsLncRNA LINC00662 and ELK1 were significantly increased, while miR-30b-3p was reduced in osteosarcoma tissues. The results of functional experiments indicated that transfection of small hairpin (sh)-LINC00662 and miR-30b-3p mimics repressed the migration, invasion, and proliferation of osteosarcoma cells. LncRNA LINC00662 also appeared to sponge miR-30b-3p in order to affect the expression of ELK1. Simultaneously, there were weak negative correlations between the expression of miR-30b-3p and LINC00662/ELK1 in osteosarcoma tissues. Rescue experiments suggested that ELK1 overexpression and downregulation of miR-30b-3p reversed the suppressive effects of sh-LINC00662 on the cell migration, invasion, and proliferation in osteosarcoma.ConclusionsThe current study indicated that knockdown of LINC00662 repressed cell migration, invasion, and proliferation through sponging miR-30b-3p to regulate the expression of ELK1 in osteosarcoma. These results may uncover a promising target for the treatment of osteosarcoma.

Long Non-coding RNA TPT1-AS1 Suppresses APC Transcription in a STAT1-Dependent Manner to Increase the Stemness of Colorectal Cancer Stem Cells.

Cancer stem cells (CSCs) are the major culprits leading to a new level of complexity and the consequential therapy resistance and disease recurrence in colorectal cancer (CRC). This study focuses on the effect of long non-coding RNA (lncRNA) TPT1-AS1 and its associated molecules on the stemness maintenance of CRC stem cells. TPT1-AS1 was identified as a significantly upregulated gene in CRC using the GSE146587 dataset. Stem cells from CRC HCT116 and CACO2 cells were isolated. TPT1-AS1 was significantly highly expressed in the CSCs compared to non-stem cells. Downregulation of TPT1-AS1 reduced the stemness of the CRC stem cells. TPT1-AS1 recruited STAT1 to the promoter region of APC to suppress APC transcription. Further upregulation of STAT1 or downregulation of APC blocked the role of TPT1-AS1 silencing and restored the malignant behaviors of CSC stem cells. APC inactivated the Wnt/β-catenin pathway. Overexpression of STAT1 restored the levels of cyclin D1 and β-catenin in cells suppressed by TPT1-AS1 silencing. In summary, this work demonstrates that TPT1-AS1 recruits STAT1 to suppress APC transcription and increase the stemness of colorectal CSCs via Wnt/β-catenin activation.

Long non-coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR-214.

The maxillofacial region in the human body is susceptible to fracture and corresponding soft tissue injury. In the current study, the effect of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) on maxillofacial fracture development was investigated. In total, 50 patients diagnosed with maxillary fracture and 50 healthy volunteers were enrolled in this study. Participants' TUG1 expression level in serum was measured using reverse transcription-quantitative (RT-q)PCR. After transfection with small interfering (si)-TUG1, microRNA (miR)-214 mimic, miR-214 inhibitor, bone morphogenetic protein 2 (BMP2) mimic or a combination, the biological behavior of osteoblasts was evaluated using MTT, Transwell assays, RT-qPCR, flow cytometry and western blot analysis. Recovery experiments were used to explore the potential mechanism. Results demonstrated that TUG1 expression was decreased in the serum of patients with maxillary fractures. Knockdown of TUG1 repressed viability, migration and differentiation and induced apoptosis of osteoblasts. StarBase v2.0 revealed that TUG1 served as a sponge for miR-214 and BMP2 is a direct target of miR-214. Altogether, it was revealed that TUG1 expression was decreased in patients with maxillary fractures and TUG1 knockdown repressed the biological process of osteoblasts by sponging miR-214.

LncRNA SNHG12 in extracellular vesicles derived from carcinoma-associated fibroblasts promotes cisplatin resistance in non-small cell lung cancer cells

ABSTRACT Non-small-cell lung cancer (NSCLC) is defined as the most universally diagnosed class of lung cancer. Cisplatin (DDP) is an effective drug for NSCLC, but tumors are prone to drug resistance. The current study set out to evaluate the regulatory effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) in extracellular vesicles (EVs) derived from carcinoma-associated fibroblasts (CAFs) on DDP resistance in NSCLC cells. Firstly, NSCLC cells were treated with EVs, followed by detection of cell activity, IC50 values, cell proliferation and apoptosis, and Cy3-SNHG12. We observed that CAFs-EVs promoted IC50 values and cell proliferation and inhibited apoptosis. In addition, we learned that lncRNA SNHG12 carried by CAFs-EVs into NSCLC facilitated DDP resistance of NSCLC cells. Furthermore, ELAV like RNA binding protein 1 (HuR/ELAVL1) binding to lncRNA SNHG12 and X-linked inhibitor of apoptosis (XIAP) was verified and RNA stability of XIAP was also verified CAFs-EVs promoted RNA stability and transcription of XIAP, while silencing HuR could partially-reverse this promoting effect. Further joint experimentation showed that silencing XIAP partially inhibited DDP resistance in NSCLC cells. Additionally, the tumor growth and the positive rate of Ki67 and HuR were detected, which showed that CAFs-oe-EVs promoted the tumor and the positive rate of Ki67, as well as the levels of lncRNA SNHG12, HuR, and XIAP in vivo. Collectively, our findings indicated that lncRNA SNHG12 carried by CAFs-EVs into NSCLC cells promoted RNA stability and XIAP transcription by binding to HuR, thus augmenting DDP resistance in NSCLC cells.

LncRNA SNHG8 sponges miR-449c-5p and regulates the SIRT1/FoxO1 pathway to affect microglia activation and blood-brain barrier permeability in ischemic stroke.

Ischemic stroke (IS) can cause disability and death, and microglia as the immune component of the CNS can release inflammatory factors and participate in blood-brain barrier (BBB) dysfunction. This study aimed to investigate the effects of long noncoding RNA (lncRNA) SNHG8 on microglia activation and BBB permeability in IS. A rat model of permanent middle cerebral artery occlusion (p-MCAO) and a cell model of oxygen and glucose deprivation (OGD) in microglia were established, followed by evaluation of neurobehavioral function, BBB permeability, brain edema, and pathologic changes of microglia in brain tissue. The activation status of microglia and expressions of inflammatory factors were detected. Cell viability and integrity of microglia membrane were assessed. The downstream microRNA (miR), gene, and pathway of SNHG8 were analyzed. LncRNA SNHG8 was down-regulated in MCAO rats. Overexpression of SNHG8 improved the neural function defect, reduced brain water content, BBB permeability, brain tissue damage and inflammation, and inhibited microglia activation. In OGD-induced microglia, overexpression of SNHG8 or miR-449c-5p down-regulation increased cell viability and decreased lactate dehydrogenase activity. Moreover, SNHG8 sponged miR-449c-5p to regulate SIRT1. Overexpression of SNHG8 increased the expression of SIRT1 and FoxO1. MiR-449c-5p mimic could annul the effect of SNHG8 overexpression on ischemic microglia. Collectively, SNHG8 inhibits microglia activation and BBB permeability via the miR-449c-5p/SIRT1/FoxO1 pathway, thus eliciting protective effects on ischemic brain injury.

Long non-cording RNA XIST promoted cell proliferation and suppressed apoptosis by miR-423-5p/HMGA2 axis in diabetic nephropathy.

This research studied the effect of long non-coding RNA X-inactive-specific transcript (XIST) on DN. The effect of high glucose (HG) on the expression of XIST and miR-423-5p was detected by quantitative real-time PCR (qRT-PCR) in human kidney (HK) cells (human glomerular mesangial cells (HMCs) and human kidney-2 (HK-2) cells). The effect of XIST depletion and miR-423-5p inhibition or overexpression on high mobility group protein A2 (HMGA2) protein level was examined by western blot in HG-induced HK cells. The impacts of XIST depletion on viability and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and flow cytometry assays in HG-induced HK cells. We found the expression of XIST and HMGA2 protein was significantly upregulated in DN tissues and cells. Moreover, HG treatment induced the upregulation of XIST and HMGA2 protein level in HK cells. Besides, both XIST depletion and HMGA2 depletion decreased cell proliferation but increased apoptosis in HG-treated HK cells. Furthermore, HMGA2 upregulation or miR-423-5p inhibition partly eliminated the effects of XIST depletion on cell proliferation, apoptosis of HG-treated HK cells. Interestingly, HMGA2 upregulation partly reversed miR-423-5p overexpression-mediated suppression on viability and promotion on apoptosis in HG-treated HK cells. Mechanistically, XIST sponged miR-423-5p to regulate HMGA2 expression in DN cells. Taken together, XIST depletion suppressed proliferation and promoted apoptosis via miR-423-5p/HMGA2 axis in HG-treated HK cells, which may provide a potential therapeutic target for DN.

LncRNA PVT1 Knockdown Ameliorates Myocardial Ischemia Reperfusion Damage via Suppressing Gasdermin D-Mediated Pyroptosis in Cardiomyocytes.

Objective: Myocardial ischemia reperfusion (I/R) damage is a life-threatening vascular emergency after myocardial infarction. Here, we observed the cardioprotective effect of long non-coding RNA (lncRNA) PVT1 knockdown against myocardial I/R damage.Methods: This study constructed a myocardial I/R-induced mouse model and a hypoxia/reoxygenation (H/R)-treated H9C2 cells. PVT1 expression was examined via RT-qPCR. After silencing PVT1 via shRNA against PVT1, H&E, and Masson staining was performed to observe myocardial I/R damage. Indicators of myocardial injury including cTnI, LDH, BNP, and CK-MB were examined by ELISA. Inflammatory factors (TNF-α, IL-1β, and IL-6), Gasdermin D (GSDMD), and Caspase1 were detected via RT-qPCR, western blot, immunohistochemistry, or immunofluorescence. Furthermore, CCK-8 and flow cytometry were presented for detecting cell viability and apoptosis.Results: LncRNA PVT1 was markedly up-regulated in myocardial I/R tissue specimens as well as H/R-induced H9C2 cells. Silencing PVT1 significantly lowered serum levels of cTnI, LDH, BNP, and CK-MB in myocardial I/R mice. H&E and Masson staining showed that silencing PVT1 alleviated myocardial I/R injury. PVT1 knockdown significantly lowered the production and release of inflammatory factors as well as inhibited the expression of GSDMD-N and Caspase1 in myocardial I/R tissue specimens as well as H/R-induced H9C2 cells. Moreover, silencing PVT1 facilitated cell viability and induced apoptosis of H/R-treated H9C2 cells.Conclusion: Our findings demonstrated that silencing PVT1 could alleviate myocardial I/R damage through suppressing GSDMD-mediated pyroptosis in vivo and in vitro. Thus, PVT1 knockdown may offer an alternative therapeutic strategy against myocardial I/R damage.

LncRNA XIST restrains the activation of Müller cells and inflammation in diabetic retinopathy via stabilizing SIRT1

Background Recent studies have provided strong evidence that lncRNAs play a functional regulatory role in diabetic retinopathy (DR). The purpose of this study was to investigate the effect of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) in DR. Methods A DR mouse model was established by intraperitoneal injection of streptozotocin (STZ), and then the mouse retinal Müller cells (mMCs) were isolated from retina tissues of mice. Human retinal Müller cell line (HMCs) and mMCs and were treated with high glucose (HG) to simulate an in vitro DR model. XIST expression was detected by qRT-PCR. Next, XIST overexpression was performed in mMCs and HMCs to examine its effect on the activation of Müller cells and production of pro-inflammatory cytokines. Subsequently, the interaction between XIST and SIRT1 was verified, and the ubiquitination level of SIRT1 as well as the stability of SIRT1 protein were assessed. Results XIST was down-regulated in retinal tissues of DR mice and HG-induced HMCs. Overexpression of XIST inhibited HG-induced activation of mMCs and HMCs, and reduced the production of pro-inflammatory cytokines. XIST promoted SIRT1 expression via interacting with SIRT1 and inhibiting the ubiquitination of SIRT1. Furthermore, SIRT1 silencing partly abrogated the effect of XIST overexpression on the activation of mMCs and HMCs as well as the production of pro-inflammatory cytokines induced by HG. Conclusion We concluded that XIST restrained the activation of Müller cells and the production of pro-inflammatory cytokines via stabilizing SIRT1.

Long non-coding RNA KTN1-AS1 promotes progression in pancreatic cancer through regulating microRNA-23b-3p/high-mobility group box 2 axis.

To explore the inhibitory effect of long non-coding RNA (LncRNA) antisense of KTN1 (KTN1-AS1) on the growth of pancreatic cancer (PC) cells by regulating the microRNA-23b-3p (miR-23b-3p)/high-mobility group box 2 (HMGB2) axis. The expression of KTN1-AS1 in tissues and cells was detected by qRT-PCR, and the relationship between KTN1-AS1 and clinicopathological data of patients with PC was analyzed. In addition, stable and transient overexpression and inhibition vectors were established and transfected into PC cells PANC-1, BxPC-3. CCK-8, transwell, and flow cytometry were responsible for the detection of proliferation, invasion, and apoptosis of transfected cells, respectively. The correlation of miR-23b-3p between KTN1-AS1 and HMGB2 was determined by dual luciferase reports, and the relationship between KTN1-AS1 and miR-23b-3p was further verified by RNA immunoprecipitation (RIP). The highly expressed KTN1-AS1 in PC patients was indicative of its high diagnostic value in this disease. Besides, it was found that KTN1-AS1 was linked with the pathological stage, differentiation degree and lymph node metastasis (LNM) of PC patients. Underexpressed KTN1-AS1 led to decreased proliferation and invasion ability of cells and increased apoptosis rate, while the effect of further overexpression of KTN1-AS1 on cells was the opposite. Dual luciferase reporter (DLR) assay confirmed that KTN1-AS1 could target miR-23b-3p, while miR-23b-3p could target HMGB2. Functional analysis showed that the overexpression of miR-23b-3p inhibited the expression of HMGB2 in PC cells and affected cell proliferation, invasion and apoptosis. Co-transfection of Sh-KTN1-AS1 and miR-23b-3p-mimics exhibited that up-regulation of KTN1-AS1 expression could reverse the effect of miR-23b-3p-mimics on PC cells.

Retraction

Retraction: "Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma," by Xin Wen, Xin-Rui Han, Yong-Jian Wang, Shao-Hua Fan, Juan Zhuang, Zi-Feng Zhang, Qun Shan, Meng-Qiu Li, Bin Hu, Chun-Hui Sun, Qiao Wu, Jun-Hua Tan, Dong-Mei Wu, Jun Lu, Yuan-Lin Zheng, J Cell Biochem. 2018; 1827-1840: The above article, published online on 10 August 2017 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcb.26344) has been retracted by agreement between the the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid.

Long Noncoding RNA GAS5 Targeting miR-221-3p/Cyclin-Dependent Kinase Inhibitor 2B Axis Regulates Follicular Thyroid Carcinoma Cell Cycle and Proliferation

Introduction: Follicular thyroid carcinoma (FTC) is more aggressive than the most common papillary thyroid carcinoma (PTC). However, the current research on FTC is less than PTC. Here, we investigated the effects of long noncoding RNA (lncRNA) GAS5 and miR-221-3p in FTC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect GAS5 and miR-221-3p expression in the FTC tissues and cells. Cell proliferation was assessed by CCK8 and EdU assays. Flow cytometry was performed to determine the cell cycle. The dual-luciferase reporter assay was employed to validate the binding relationship of GAS5/miR-221-3p and miR-221-3p/cyclin-dependent kinase inhibitor 2B (CDKN2B). Western blot was conducted to measure the protein level of CDKN2B. Results: Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells. What’s more, overexpression of GAS5 or miR-221-3p inhibition induced G0/G1 phase arrest and inhibited cell proliferation of FTC cells. GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p. Additionally, GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression. Conclusion: GAS5 induced G0/G1 phase arrest and inhibited cell proliferation via targeting miR-221-3p/CDKN2B axis in FTC. Thus, GAS5 may be a potential therapeutic target for the treatment of FTC.

Long non-coding RNA X-inactive specific transcript promotes osteosarcoma metastasis via modulating microRNA-758/Rab16.

BackgroundAs a common malignant bone sarcoma, osteosarcoma (OS) affects the health and lives of many people. Here, we probed the effects of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and microRNA-758 (miR-758) on OS metastasis, and examined possible downstream effector.MethodsQuantitative reverse transcription PCR (qRT-PCR) was performed to detect the expressions of XIST and miR-758 in OS tissues and cells. Cell transfection was carried out to alter the levels of XIST and miR-758 in OS cells, and cell viability, migration, and invasion were assessed. Subsequently, qRT-PCR and a dual-luciferase reporter assay were conducted to analyze the regulatory effects of XIST on miR-758 and miR-758 on Rab16. Finally, we investigated whether Rab16 was the downstream effector of XIST/miR-758 axis.ResultsXIST was highly expressed in OS tissues and cells, but the opposite was seen for miR-758. In OS cells, migration, invasion, and epithelial-mesenchymal transformation (EMT) was promoted by overexpression of XIST and miR-758 inhibitor, but were inhibited by XIST knockdown and miR-758 mimics. XIST regulated miR-758 expression, and miR-758 regulated Rab16 expression in OS cells. Overexpression of Rab16 reversed the effects of miR-758 mimics on OS cell migration and invasion.ConclusionsXIST contributed to OS cell migration, invasion, and EMT via regulation of miR-758/Rab16.

Effects of long noncoding RNA on prognosis of oral squamous cell carcinoma: A protocol for systematic review and meta analysis.

Background:Long noncoding RNA (lncRNA) is reported to be upregulated in many tumors. Although the expression of lncRNA in oral squamous cell carcinoma has been assessed, the association between lncRNA expression and prognosis or clinicopathological feature still remains controversial. Therefore, we conducted a meta-analysis to verify whether lncRNA expression was related to prognosis or clinicopathological features in patients with oral squamous cell carcinoma.Methods:We searched Embase, PubMed, Web of Science, Cochrane library, Chinese National Knowledge Infrastructure, and Wanfang databases from inception to February 2021. The language included Chinese and English. The published literature on lncRNA expression and prognosis or clinicopathological characteristics of patients with oral squamous cell carcinoma was statistically analyzed. The combination of hazard ratios (HRs), odds ratios (OR), and 95% confidence intervals (95% CIs) were applied to evaluate the effects of lncRNA on the prognosis and clinicopathological features of oral squamous cell carcinoma.Results:This study could provide a comprehensive review of the available evidence of lncRNA on the prognosis and clinicopathological features of oral squamous cell carcinoma.Conclusion:The conclusion of our study will provide the updated evidence to judge the lncRNA on the prognosis and clinicopathological features of oral squamous cell carcinoma.

Promotive effects of HOXA10 antisense RNA on the stemness of oral squamous cell carcinoma stem cells through a microRNA-29a/MCL-1/phosphatidyl inositol 3-kinase/protein kinase B axis

ObjectiveThe aim of this study was to investigate the effects of long non-coding RNA (lncRNA) HOXA10 antisense RNA (HOXA10-AS) on the properties of oral squamous cell carcinoma (OSCC) stem cells and the molecular mechanism. DesignTumor and the paracancerous tissues were collected from 83 patients with OSCC. OSCC stem cells were extracted from a human OSCC cell line Tca8113. Silencing of HOXA10-AS was introduced in stem cells and then the malignant behaviors of cells were determined. The target transcripts of HOXA10-AS were predicted using integrated bioinformatics analyses. The interactions among HOXA10-AS, microRNA (miR)-29a and MCL-1 were validated, and their functions in stem cell behaviors in vivo and in vitro were explored. ResultsHOXA10-AS and MCL-1 were highly expressed while miR-29a was poorly expressed in the collected tumor tissues and the extracted OSCC stem cells. High expression of HOXA10-AS and MCL-1, while poor expression of miR-29a was relevant to poor prognosis in patients. Silencing of HOXA10-AS suppressed proliferation and tumor sphere formation ability of stem cells, and it reduced growth and metastasis of tumors in animals. HOXA10-AS served as a sponge for miR-29a and upregulated MCL-1 mRNA expression. Inhibition of miR-29a promoted, while silencing of MCL-1 suppressed the malignant behaviors of OSCC stem cells. In addition, HOXA-10-AS and MCL-1 were found to activate the phosphatidyl inositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. ConclusionThis study evidenced that HOXA10-AS enhances the stem cell property of OSCC stem cells through the miR-29a/MCL-1/PI3K/AKT axis.