Non-coding RNA CASC2 Research Articles

Retraction Note: Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5

Retraction Note: Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5

RETRACTION: Long noncoding RNA CASC9 promotes the proliferation and metastasis of papillary thyroid cancer via sponging miR-488-3p.

Retraction: Y. Chen, Y. Li, and H. Gao, "Long Noncoding RNA CASC9 Promotes the Proliferation and Metastasis of Papillary Thyroid Cancer Via Sponging miR-488-3p," Cancer Medicine 9, no. 5 (2020): 1830-1841. https://doi.org/10.1002/cam4.2839. The above article, published online on 13 January 2020, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Stephen Tait, and John Wiley & Sons Ltd. A report submitted by a third party noted image duplications with other articles by different author groups. Specifically, the report found image duplications with other published articles in Figures2D, 3C, 4B, 4C, 5C and 7B. The report also found image overlap between images in Figures2C and 6H. The retraction has been agreed to because the evidence of image duplication across different articles, each of which describes different experimental conditions, fundamentally compromises the editors' confidence in the conclusions presented. The authors did not respond to our notice regarding the retraction.

Abstract 76: CASC15 lncRNA as a Mediator of Vascular Senescence in the Renin-Angiotensin System

The renin-angiotensin system (RAS) regulates vascular function and maintains blood pressure homeostasis. Angiotensin-II (Ang-II) and angiotensin-1-7 (Ang-1-7) have opposing effects on vascular health. Ang-II promotes vascular senescence and pathophysiological remodeling by inducing oxidative stress, inflammation, vascular hypertrophy, and endothelial dysfunction. In contrast, Ang-1-7, known for its vasodilatory, anti-inflammatory, and antioxidative properties, counteracts these detrimental effects, enhancing endothelial function, reducing oxidative stress, and inhibiting inflammation. Our laboratory has identified the long non-coding RNA CASC15 as a critical regulatory element within the RAS. CASC15 expression is significantly repressed by Ang-II in aortic vascular smooth muscle cells (SMCs), showing a 59.25% decrease compared to the vehicle control (n=10, p=0.000333). Loss of CASC15 induces cellular senescence, increasing senescent cells from a mean of 14.09% (control inhibitor, n=9, SEM=4.824) to 57.79% (CASC15 inhibitor, n=9, SEM=6.420, p<0.0001), and leads to vascular hypertrophy, with cell area increasing from a mean of 46.89% (control inhibitor, n=8, SEM=9.229) to 221.2% (CASC15 inhibitor, n=9, SEM=67.53, p=0.0300). We hypothesize that CASC15 repression by Ang-II (1 µM) contributes to vascular senescence and increased DNA damage, while Ang-1-7 (1 µM) preserves CASC15 expression and mitigates these effects. Pro-senescent stressors like hydrogen peroxide and doxorubicin also repress CASC15 expression in SMCs. Using RT-qPCR, we observed decreases in CASC15 expression by 29.56% (hydrogen peroxide vs. vehicle, n=4, p=0.0790) and 44.09% (doxorubicin vs. vehicle, n=3, p=0.0733). Ang-1-7 alone did not significantly change CASC15 expression, but combined with Ang-II, it showed potential recovery from 40% repression to 94% recovery. Further research is needed. Immunofluorescence against gamma-H2AX revealed increased DNA damage in SMCs lacking CASC15, with positive foci increasing from 26.27% (control inhibitor, n=4, SEM=1.459) to 63.71% (CASC15 inhibitor, n=4, SEM=1.806, p=0.0009). In conclusion, CASC15 is a crucial regulator within the RAS. Its repression by Ang-II promotes vascular senescence, hypertrophy, and DNA damage, effects countered by Ang-1-7. Targeting CASC15 could offer new strategies for mitigating vascular aging and improving vascular health, particularly in chronic kidney disease.

A study of the prognostic value of long non-coding RNA CASC15 in human solid tumors utilizing The Cancer Genome Atlas (TCGA) datasets and a meta-analysis.

Several malignant solid tumors have been reported to have an abnormal expression of the long non-coding RNA CASC15 (lncRNA CASC15). However, the clinicopathologic and prognostic importance of CASC15 in solid tumors are unknown. As a result, we examined the interrelationship between CASC15, overall survival length, and clinicopathological attributes of cancers affecting humans by analyzing various studies and The Cancer Genome Atlas (TCGA) data related to CASC15 expression. Web of Science, PubMed, Cochrane Library, Embase, Chinese WanFang, and Chinese CNKI databases were used to conduct a literature search. Hazard ratios (HRs) and Pooled odds ratios (ORs) were calculated taking 95% confidence intervals (CIs). The results of the current meta-analysis were further validated using TCGA datasets. A total of 12 eligible studies enrolling 767 patients were included in this meta-analysis. Findings of the analysis showed that CASC15 expression had a significant relation to the metastasis of lymph node (OR = 3.30, 95%CI = 1.88-5.81, p < 0.001), distant metastasis (OR = 2.64, 95%CI = 1.24-5.63, p = 0.012), and high TNM/clinical stage (OR = 2.67, 95%CI = 1.34-5.32, p = 0.005). Additionally, we found that a poor outcome for overall survival (OS) was predicted by an elevation in CASC15 expression (HR = 2.01, 95%CI = 1.71-2.36, p < 0.001). Further investigation of the TCGA dataset revealed that CASC15 had abnormal expression in many cancers, which at least partially validated the findings of the current meta-analysis. According to the latest meta-analysis and systematic review, high expression levels of CASC15 are associated with poor survival outcomes for solid tumor patients, and the use of CASC15 as a solid tumor prognostic predictor has a solid theoretical foundation.

Long noncoding RNA CASC2 protect ROS-induced oxidative stress in myocardial infarction by miR-18a/SIRT2.

We aimed to investigate the function and its possible mechanisms of long noncoding RNA (lncRNA) in acute myocardial infarction (AMI) model. Patients with AMI and normal volunteers were selected from our hospital. Sprague-Dawley rats were induced into in vivo model of AMI. H9c2 cells were treated with H2 O2 to generate injury model. A significantly lower serum gene expression of lncRNA CASC2 was detected. In rat models of AMI, lncRNA CASC2 gene expressions in heart tissue of mice with AMI were decreased. In in vitro model, downregulation of lncRNA CASC2 increased reactive oxygen species (ROS)-induced oxidative stress; lncRNA CASC2 induced NADPH oxidase (NOX-2) expression and suppressed miR-18a expression; MiR-18a promoted ROS-induced oxidative stress; downregulation of miR-18a decreased ROS-induced oxidative stress. The inhibition of miR-18a reversed the effects of CASC2 downregulation on ROS-induced oxidative stress in in vitro model of AMI. The activation of miR-18a reversed the effects of CASC2 on ROS-induced oxidative stress in in vitro model of AMI. These data for the first time suggest that lncRNA CASC2 have better protective effects on AMI, which could reduce oxidative stress through their carried miR-18a and subsequently downregulating the SIRT2/ROS pathway.

Berberine enhances the sensitivity of temozolomide to chemotherapy for glioma

Objective To investigate whether berberine can enhance the chemotherapeutic sensitivity of temozolomide to glioma cells and its mechanism. Methods CCK-8 method was used to determine the effect of Ber and TMZ at different concentrations on glioma cell proliferation, and to evaluate the combined effect of Ber and TMZ. Flow cytometry was used to detect the effects of different concentrations of Ber, TMZ and the combination of the two on apoptosis and cell cycle of glioma cells. The expression of long non-coding RNA (LncRNA) CASC-2 in glioma cells was determined by RT-PCR. Results CCK 8 determination results show that the single use of Ber (5, 10, 20, 40, 80, 160 umol/L) and TMZ (25, 50, 100, 200, 400, 800 umol/L) separate effect on gliomas are a dose dependent inhibition of glioma proliferation, and concentration of Ber for 40 umol/L on glioma U87 cells as well as a significant inhibition will not lead to a large number of cell death, so after the experiment we use 40 umol/L study on combination of Ber. After 40umol/L Ber was combined with TMZ at different concentrations, cell survival rate decreased significantly compared with TMZ alone at the same concentration. The cell cycle detection by flow cytometry showed that after the action of Ber combined with TMZ on glioma, glioma cells could be largely blocked in S phase and inhibited to enter the proliferation phase. The results of flow cytometry showed that after TMZ combined with Ber, the apoptosis rate of glioma cells significantly increased compared with TMZ alone. The results of RT-PCR showed that the expression of CASC-2 in the combination group was higher than that in the single group, and it was significantly higher than that before the treatment. Conclusion Berberine can sensitize TMZ to the effect of chemotherapy on glioma. Berberine can increase the sensitivity of glioma to TMZ by up-regulating the expression of LncRNA CASC-2 gene。

Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p, by D.-J. Yu, M. Zhong, W.-L. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7943-7949-DOI: 10.26355/eurrev_201909_19010-PMID: 31599419" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18857.

Long non-coding RNA CASC15 promotes nasopharyngeal carcinoma cell proliferation and metastasis by downregulating miR-101-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA CASC15 promotes nasopharyngeal carcinoma cell proliferation and metastasis by downregulating miR-101-3p, by M.-Y. Xue, H.-X. Cao, published in Eur Rev Med Pharmacol Sci 2019; 23 (20): 8897-8904-DOI: 10.26355/eurrev_201910_19285-PMID: 31696476" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19285.

Long non-coding RNA CASC9 promotes tumor progression in oral squamous cell carcinoma by regulating microRNA-545-3p/laminin subunit gamma 2

ABSTRACT Long non-coding RNA (lncRNA) CASC9 is reported to be a tumor promoter in oral cancer, but its mechanism in oral squamous cell carcinoma (OSCC) has not been fully explored. Our study aimed to identify the interaction between lncRNA CASC9, microRNA-545-3p (miR-545-3p), and laminin subunit gamma 2 (LAMC2) in OSCC cells. Our study confirmed that lncRNA CASC9 and LAMC2 were upregulated in OSCC, whereas miR-545-3p expression was reduced. After performing a series of cell functional experiments, it was found that knockdown of lncRNA CASC9 or LAMC2 resulted in the inhibition of proliferation, colony formation, and migration of OSCC cells, but their negative effects could be partly impaired by the miR-545-3p inhibitor. In addition, we proved for the first time that lncRNA CASC9 can sponge miR-545-3p to upregulate LAMC2. In conclusion, our study revealed that lncRNA CASC9 promotes the malignancy of OSCC cells by sponging miR-545-3p to enhance LAMC2 expression, implying that lncRNA CASC9/miR-545-3p/LAMC2 may be an intervention approach in OSCC therapy.

Long noncoding RNA CASC2 alleviates the growth, migration and invasion of oral squamous cell carcinoma via downregulating CDK1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA CASC2 alleviates the growth, migration and invasion of oral squamous cell carcinoma via downregulating CDK1, by H.-B. Xing, H.-M. Qiu, Y. Li, P.-F. Dong, X.-M. Zhu, published in Eur Rev Med Pharmacol Sci 2019; 23 (11): 4777-4783-DOI: 10.26355/eurrev_201906 _18060-PMID: 31210307" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18060.

Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3

Increasing studies have shown that long non-coding RNAs (lncRNAs) are regarded as important regulators in the occurrence and development of colorectal cancer (CRC). Although lncRNA CASC9 has been studied in CRC, the detailed regulatory mechanism of CASC9 in CRC is still unclear. In this study, we found that CASC9 was significantly upregulated in CRC tissues and cell lines compared to normal controls and that aberrant expression was associated with the tumor-node-metastasis (TNM) stage of CRC. Functionally, CASC9 depletion efficiently inhibited the proliferation of CRC cells and induced cell apoptosis in vitro. Mechanistically, CASC9 was mainly enriched in the cytoplasm of CRC cells and interacted directly with miR-576-5p. Downregulation of miR-576-5p reversed the inhibitory effect of CASC9 siRNA on CRC cell progression. Furthermore, AKT3 has been identified as a downstream target of miR-576-5p. Spearman’s correlation analysis revealed that AKT3 was negatively correlated with miR-576-5p but positively correlated with CASC9. Downregulation of miR-576-5p restored the effect of CASC9 silencing on AKT3 expression. Therefore, silencing CASC9 could downregulate the expression of AKT3 by reducing the competitive binding of CASC9 to miR-576-5p, thus suppressing CRC cell proliferation and promoting cell apoptosis. In summary, we identified CASC9 as an oncogenic lncRNA in CRC and defined the CASC9/miR-576-5p/AKT3 axis, which might be considered a potential therapeutic target for CRC patients, as a novel molecular mechanism implicated in the proliferation and apoptosis of CRC.

Long Non-coding RNA CASC15 Promotes Intrahepatic Cholangiocarcinoma Possibly through Inducing PRDX2/PI3K/AKT Axis.

PurposeIntrahepatic cholangiocarcinoma (ICC) is one of the most common liver primary tumors but its treatments are limited. Bioinformatics showed that the expression level of long non-coding RNA cancer-associated susceptibility 15 gene (CASC15) is correlated with ICC progression, but its functional mechanism remains unclear.Materials and MethodsTissues from ICC patients, tumor and adjacent tissue, were used for detection of the expression of CASC15. Clinical data were also collected for clinicopathologic and survival analysis. Short interfering RNA and lentiviral short hairpin RNA were used to knock down CASC15 and PRDX2 expression in ICC cell lines, for the analysis of changes of cell function and xenografts. RNA-pulldown and RNA immunoprecipitation assays were used to detect RNA-binding protein, PRDX2. Male nude mice were used for ICC xenografts, and livers were collected after 4 weeks for immunohistochemistry.ResultsCASC15 is highly expressed in ICC tissues and is related to higher TNM stage. Knockdown of CASC15 in ICC cells reduced cell proliferation, migration, invasiveness and increased apoptosis, and G1/S block. PRDX2 bound to CASC15. Knockdown of CASC15 decreased PRDX2 expression which was rescued by the inhibition of proteasome formation. Downregulation of PRDX2 resulted in G1/S block, reduced ICC cell invasion. Downregulation of CASC15 inhibited phosphoinositide 3-kinase (PI3K)/AKT/c-Myc pathway through downregulating of PRDX2 and overexpressed PRDX2 rescued the block. CASC15 knockout in ICC xenografts suppressed tumor development in vivo, decreased the expression of PRDX2 and Ki67 and inhibited PI3K/AKT pathway.ConclusionCASC15 promotes ICC possibly by targeting PRDX2 via the PI3K/AKT pathway, indicating poor prognosis and high degree of malignancy of ICC.

Long non-coding RNA CASC9 promotes gefitinib resistance in NSCLC by epigenetic repression of DUSP1

Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib, has greatly affected clinical outcomes in non-small cell lung cancer (NSCLC) patients. The long noncoding RNAs (lncRNAs) are known to regulate tumorigenesis and cancer progression, but their contributions to NSCLC gefitinib resistance remain poorly understood. In this study, by analyzing the differentially expressed lncRNAs in gefitinib-resistant cells and gefitinib-sensitive cells in the National Institute of Health GEO dataset, we found that lncRNA CASC9 expression was upregulated, and this was also verified in resistant tissues. Gain and loss of function studies showed that CASC9 inhibition restored gefitinib sensitivity both in vitro and in vivo, whereas CASC9 overexpression promoted gefitinib resistance. Mechanistically, CASC9 repressed the tumor suppressor DUSP1 by recruiting histone methyltransferase EZH2, thereby increasing the resistance to gefitinib. Furthermore, ectopic expression of DUSP1 increased gefitinib sensitivity by inactivating the ERK pathway. Our results highlight the essential role of CASC9 in gefitinib resistance, suggesting that the CASC9/EZH2/DUSP1 axis might be a novel target for overcoming EGFR-TKI resistance in NSCLC.

Long non-coding RNA CASC2 enhances irradiation-induced endoplasmic reticulum stress in NSCLC cells through PERK signaling.

Radiotherapy is instrumental in the treatment of inoperable non-small cell lung cancer (NSCLC). Studies have revealed that radiotherapy induces endoplasmic reticulum (ER) stress, which consequently induces apoptosis and sensitization of cancer cells. A recent study has revealed that long non-coding RNA (lncRNA) CASC2 is negatively correlated with the malignancy of NSCLC cells. The present study investigated the effects and molecular mechanisms of CASC2 on radiosensitivity and ER stress in NSCLC cells. The overexpression of CASC2 markedly decreased cell survival and increased apoptosis, expression of PERK, phosphorylated-eIF2α and CHOP in irradiated human NSCLC cells, whereas knocking down PERK reversed these effects. Moreover, CASC2 considerably promoted the stability of PERK mRNA, but had no effect on the activity of PERK gene promoter in irradiated NSCLC cells. Strikingly, CASC2 exhibited no apparent effect on non-irradiated NSCLC cells. This study demonstrated that lncRNA CASC2 increases the stability of PERK mRNA, which consequently triggers the PERK/eIF2α/CHOP ER stress pathway and promotes radiosensitivity or apoptosis in irradiated NSCLC cells. Results of the present study suggest that CASC2 can act as an effective therapeutic target to enhance the efficacy of radiotherapy in the treatment of NSCLC.

Long non-coding RNA CASC15 promotes proliferation and induces apoptosis of cervical cancer cells through targeting miR-101-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA CASC15 promotes proliferation and induces apoptosis of cervical cancer cells through targeting miR-101-3p, by Y.-N. Zhang, B. Liu, T. Jiang, Q. Li, published in Eur Rev Med Pharmacol Sci 2020; 24 (2): 611-618-DOI: 10.26355/eurrev_202001_20037-PMID: 32016962" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20037.

LncRNA CASC2 inhibits cell proliferation, metastasis and EMT through miR-18a/SOCS5 axis in cholangiocarcinoma.

Cholangiocarcinoma (CCA) is one of the tumors with high malignancy of the liver and bile system, whose development and prognosis mechanisms are still not clear. Here, a preliminary illustration was made on the expression and function of long non-coding RNA (lncRNA) CASC2 and the relevant mechanism of its function. Expression of CASC2 in CCA tissues and cells were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation ability was detected using colony formation and Cell Counting Kit-8 (CCK-8) assays while cell invasion and migration abilities were measured using transwell and Matrigel assays. Using bioinformatic analysis, underlying downstream molecules of CASC2 were predicted and by Dual-Luciferase assay and Western blot. It was found that CASC2 was expressed at a significantly lower level in CCA tissues and cell lines. The overexpression of CASC2 inhibited QBC939 cell proliferation, invasion and migration when the knockdown of CASC2 accelerated HUCCT1 cell growth and metastasis. Besides, miR-18a was identified as a direct target for CASC2, and SOCS5 as target for miR-18a. Moreover, CASC2 functioned as a sponge of miR-18a to promote the SOCS5 expression, then, slowed down the epithelial-to-mesenchymal transition (EMT) progression. CASC2 was downregulated in CCA tissues and cells. It could inhibit cell proliferation, invasion, migration and EMT via sponging miR-18a/SOCS5 axis. This might provide a novel target for CCA diagnosis and treatment.

RETRACTED ARTICLE: Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5

BackgroundStudies have demonstrated that long noncoding RNAs (lncRNAs) have essential impacts on the development of atherosclerosis (AS). This study aimed to identify the role and functional mechanism of lncRNA CASC2 in the development and migration of vascular smooth muscle cells (VSMCs).MethodThe serum of 40 pairs of AS patients and healthy volunteers were collected and the expression of CASC2 was evaluated. qRT-PCR and western blotting were carried out to examine the expression levels of at mRNA and protein level, repectively. Cell proliferation assay, colony formation assay, transwell migration assay, dual-luciferase reporter assay, and wound healing assay were conducted to evaluate cell proliferation, colony formation, migration, transcription, targeting, and self-restoration.ResultsThe expression levels of CASC2 were decreased, while the expression levels of miR-532-3p were elevated in AS patient samples and VSMCs. Overexpression of CASC2 inhibited the proliferation and migration of VSMCs and enhanced cell apoptosis. CASC2 inhibited the expression of miR-532-3p, and inversely upregulated the expression of PAPD5, which was a target of miR-532-3p. In addition, knockdown of miR-532-3p-mimic and PAPD5 could attenuate the impact of overexpression of CASC2 on proliferation, migration, and apoptosis in ox-LDL-VSMCs.ConclusionCASC2 suppressed cell reproduction and promoted cell apoptosis by regulating the miR-532-3p/PAPD5 axis in ox-LDL-mediated VSMCs. This might be important for AS therapeutics.

Long noncoding RNA CASC15 is upregulated in glioma and facilitates cell proliferation and metastasis via targeting miR-130b-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA CASC15 is upregulated in glioma and facilitates cell proliferation and metastasis via targeting miR-130b-3p, by Y. Xie, Y. Cheng, published in Eur Rev Med Pharmacol Sci 2019; 23 (17): 7475-7481-DOI: 10.26355/eurrev_201909_18857-PMID: 31539135" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18857.

Long Non-Coding RNA (LncRNA) CASC15 Is Upregulated in Diabetes-Induced Chronic Renal Failure and Regulates Podocyte Apoptosis.

BackgroundCASC15 has been recently characterized as an oncogenic lncRNA. This study aimed to investigate the role of CASC15 in diabetic patients complicated with chronic renal failure (DCRF).Material/MethodsLevels of CASC15 in plasma derived from 3 groups of participants were measured by qPCR and compared by ANOVA and Tukey test. The interaction between CASC15 and miR-34c was analyzed by performing cell transfections. Cell apoptosis assay was performed to analyze the effects of transfections on the apoptosis of CIHP-1 cells (podocytes).ResultsWe found that CASC15 in plasma was upregulated in DCRF compared with diabetic patients (no obvious complications) and healthy controls. Upregulation of CASC15 distinguished DCRF patients from healthy controls and diabetic patients. High D-glucose environment induced the upregulation of CASC15 in cells of the human podocyte cell line CIHP-1. Overexpression of CASC15 did not affect miR-34c in CIHP-1 cells, but bioinformatics analysis showed that CASC15 can sponge miR-34c. Overexpression of CASC15 led to an increased apoptotic rate of CIHP-1 cells, and miR-34c overexpression led to a decreased apoptotic rate of CIHP-1 cells. In addition, CASC15 overexpression attenuated the effects of miR-34c overexpression on cell apoptosis.ConclusionsTherefore, CASC15 is upregulated in DCRF patients and promotes the apoptosis of podocytes by sponging miR-34c. Our study adds to our understanding of the pathogenesis of DCRF and suggests that CASC15 could serve as a potential therapeutic target of DCRF.

Long non-coding RNA CASC15 promotes proliferation and induces apoptosis of cervical cancer cells through targeting miR-101-3p.

Cervical cancer (CC) is a common type of fatal gynecological cancer worldwide. The aim of this study was to identify the exact role of lncRNA CASC15 in the progression of CC and to explore the possible underlying mechanism. Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect CASC15 expression in 4 CC cell lines, and 54 paired CC tissue samples. The roles of CASC15 in CC were explored through apoptosis assay, colony formation assay, and proliferation assay in vitro, respectively. Furthermore, the underlying mechanism of CASC15 in CC was explored by luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. CASC15 expression in CC tissues was remarkably higher than that of adjacent normal tissues. The knockdown of CASC15 significantly inhibited CC cell proliferation, whereas induced cell apoptosis in vitro. Meanwhile, CC cell proliferation was remarkably promoted, and cell apoptosis was inhibited by overexpression of CASC15 in vitro. In addition, miR-101-3p was up-regulated and down-regulated after knockdown and overexpression of CASC15 in vitro, respectively. Furthermore, bioinformatics analysis and mechanism assays revealed that miR-101-3p was a direct target of CASC15 in CC tumorigenesis. CASC15 could promote proliferation and inhibit apoptosis of CC cells by targeting miR-101-3p. Our findings suggested that CASC15 might offer a new therapeutic intervention for CC patients.